- Email: [email protected]
PERSON-TO-PERSON SPREAD OF SALMONELLA: A PROBLEM IN HOSPITALS?
1001
and occipital capillary haemangiomata were present. Neurological examination revealed decorticate rigidity, hyperacusia, and myoclonic jerk-like seizures. Chromosome studies
evaluated by
patients
us
were carried and disclosed
out no
on
all three
abnormality.
Discussion The pattern of altered growth and morphogenesis in the two newborn babies we describe is strikingly similar to that of the previously reported children with the fetal alcohol syndrome. Pertinent additional findings include the following: both newborn infants had serious problems of respiratory adaptation, and one of them had problems with biochemical adaptation, as shown by hypoglycaemia, hypocalcxmia, and hyperbilirubinxmia. The observation of mild microphthalmia in both newborn babies tends to accord with the suggestion that the consistently short palpebral fissures in this syndrome are secondary to reduced ocular growth. All three patients were judged to have a cardiac anomaly, further emphasising the frequency of this defect in the fetal alcohol syndrome. Two of them had a cleft soft palate, a new observation in this disorder. The findings in the brain of patient 2, the first case of the fetal alcohol syndrome on whom a necropsy There was was performed, are of special relevance. serious disorientation of both neuronal and glial elements as well as incomplete development of the brain which must have started before 80 days’ gestation, judging from the absence of the corpus callosum. Some of the functional and structural abnormalities in this syndrome may relate to the types of aberration in brain morphogenesis observed in this patient. These secondary features include microcephaly, developmental delay, and fine-motor dysfunction, which showed itself in early infancy by tremulousness. Some of the joint anomalies could be related to neurological impairment of the fetus, including
reduced The
movement.
profound degree of prenatal-onset growth deficiency yet noted in the fetal alcohol syndrome occurred in patient 3. The findings in patient 3, most
who at 7 months of age was still below normal newborn size and showed no growth response to highcaloric feedings, provide further evidence of the immutable nature of the adverse prenatal effect on growth-rate in this disorder. The findings in the two newborn infants accorded with the previous observation that prenatal growth in length is more severely affected than weight gain. The mother of patient 1 provided us with the first opportunity to study the nutritional status of a chronically alcoholic woman at the time of birth of her affected child, and of investigating the suggestion that a secondary nutritional deficiency could be the cause of the syndrome. Serious iron deficiency was the only abnormality detected. Since neither this degree of growth deficiency nor this pattern of malformation have to our knowledge been noted in offspring of iron-deficient ansemic women who were non-alcoholic, it seems unlikely that iron-deficiency anaemia is the cause of this disorder. The risk of the initial diagnosis being wrong is
high.
For
example,
the 18
trisomy syndrome
and
Cornelia de Lang syndrome were seriously considered by the physicians who initially evaluated these patients. An incorrect diagnosis could lead to inappropriate advice about the risk of malformation in future children. Risk of fetal alcohol syndrome in future children is potentially high, as indicated by patient 3, unless maternal alcoholism is controlled. Additional studies are needed to determine the incidence of the fetal alcohol syndrome in offspring of alcoholic mothers. Preliminary data from the collaborative study of the National Institute of Neurologic Disease and Stroke indicate a 32% incidence of this condition in offspring of women whose chronic alcoholism was ascertained during their pregnancy. The results of that study will form the basis of a future report. We thank Dr John Opitz for calling to our attention patient 3, whom we had previously evaluated; Dr Frederick Harvey who performed the ncuropathological evaluation of patient 2; Mrs Mary Ann Harvey and Dr Gordon Green, Dr K. M. Laurance, and Dr Jan Langman for making us aware of pertinent historical data; Mrs Lyle Harrah, research librarian; Mrs Christine Hansen for secretarial assistance; and Mr Bradley Gong for the photography. This study was supported by grants from the Maternal and Child Health Services, the National Institutes of Health, and the National FoundationMarch of Dimes.
Requests for reprints should be addressed to K. L. J., University of Washington, RR 234 Health Sciences RD-20, Seattle, Washington 98195, U.S.A. REFERENCES 1. 2.
3.
4. 5. 6.
7. 8. 9. 10.
11.
Jones, K. L., Smith, D. W., Ulleland, C. N., Streissguth, A. P. Lancet, 1973, i, 1267. Haggard, H. W., Jellinek, E. M. Alcohol Explored. Garden City, New York, 1942. Report on drunkenness presented to the House of Commons by the Select Committee, 1834. Sullivan, W. C. Med. Temp. Rev. 1900, 3, 72. Ladraque, P. Alcoholisme et enfants. Paris, 1901. Roe, A. Q. Jl Stud. Alcohol, 1944, 5, 378. Lecomte, M. Scalpel, Brux. 1950, 103, 1133. Christiaens, L., Mizon, J. D., Delmarle, G. Sem. Hôp. Paris, 1960, 36, 37. Sandor, S. Rev. roum. Embryol. Cytol. Sér. Embryol. 1968, 5, 1, 51. Sandor, S. ibid. p. 167. Sandor, S., Amels, D. ibid. 1971, 8, 105.
PERSON-TO-PERSON SPREAD OF SALMONELLA: A PROBLEM IN HOSPITALS? ROB ROY MACGREGOR
JUDITH REINHART Infectious Diseases Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, U.S.A. Summary
8
patients with acute diarrhœa were to hospital and appropriate
admitted
techniques were not used to avoid seconThese patients later proved to have salmonellosis. Their surroundings were extensively contaminated, exposing 265 patients and staff to infected fæces. No case of symptomatic or asymptostool-barrier
dary spread.
matic salmonellosis was found as a result of personto-person spread. It is concluded that person-toperson spread of salmonella in hospital is difficult to accomplish without an intermediary common vehicle.
1002 SALMONELLA CASES ADMITTED WITHOUT ENTERIC PRECAUTIONS
Introduction THE debate
is
acquired l,2
over
has
the way
prompted hospital cases.
by
which salmonellosis.
us to
report
our
experi-
with Since epidemics of salmonellosis do occur in hospitals,;-’ enteric precautions are normally taken to avoid person-to-person spread of salmonella when patients with diarrhoea are admitted to hospital. Occasionally an infectious agent is not initially suspected and the hospital staff and other patients are directly exposed to infected fxces or fxcally contaminated materials. ence
Patients
During the past eighteen months, despite our hospital’s policy to isolate febrile patients with diarrhoea of unknown cause, 8 patients with diarrhoea, in whom enteric precautions were not started for more than seventy-two hours, proved to have salmonellosis. Before their isolation, patients variably had sigmoidoscopy, barium enema, rectal examination, or had their rectal temperature taken; all had fsecal incontinence, some were comatose, and there was major f2ecal soilage of their immediate surroundings. When the cause of their diarrhoea became obvious, all staff who had had physical contact with the patient or his contaminated materials, without using proper barrier techniques, were asked to provide a stool sample for culture. Those with diarrhoea were kept from work until results of their cultures were known. In addition, all patients sharing the same room as the index case gave stools for culture, as did any other patients in the same unit in whom diarrhoea developed; the latter were put on stool isolation pending results of culture. We were surprised to find that no secondary spread of salmonellae could be detected from any of our 8 cases. Our results suggest that direct, personto-person spread of the organism is difficult to accomplish, even in vulnerable hospital patients.
salmonella organism isolated. Over two-thirds of the cultures were received in the first half of each culture period-e.g., more than 30 of the 52 contacts of patient 3 had cultures taken within seven days of their Diarrheca-rates among conexposure to infection. tacts varied from 0 to 19 %, depending on the time of year (more in winter), number of patients in the exposed group (patients had higher diarrhoea-rates than staff), and how the contacts defined diarrhoea (staff were simply asked " have you had any diarrhoea ?").
Methods Stool samples were cultured as follows: approximately 1 g. of stool was emulsified in 5 ml. of ’GN’ (gram negative) broth (Baltimore Biological Laboratories) and streaked on MacConkey’s agar; the agar and the broth were incubated at 37 °C. After twenty-four hours, the ’GN ’’ broth was subcultured on to’XLD ’ (xylose/lysine/desoxycholate) agar (Baltimore Biological Laboratories) and both cultures then were held at 37 °C for forty-eight hours. Any non-lactose-fermenting colonies were further investigated by standard biochemical procedures.6 All presumptive salmonella: isolates were sent to the Pennsylvania State Laboratory for verification and serotyping. Exposure was judged to be significant if the individual actually handled the patient, his faeces, or any objects which might have been soiled with faeces (bedding, hospital gown, All room-mates of the patients were bedpan, &c.). believed to be at risk through the intermediary of common attendants and room materials.
Results
Between December, 1971, and May, 1973, 20 inpatients had Salmonella spp. isolated from their stool; 8 of these had diarrhoea for periods of three to ten days before proper enteric-isolation procedures were started (see accompanying table). Fellow patients constituted 19-2% of the individuals exposed to infection, while the remainder were physicians, nurses, and other ward staff. Over 90 % of contacts had at least one stool cultured; in no instance was a
Discussion In 1960, Datta and Pridie reported a hospital epidemic caused by Salmonella typhimurium which lasted for twenty weeks and involved over 250 cases.5 Their conclusion that this epidemic represented person-to-person spread in the hospital was based on the protracted duration of the outbreak, failure to grow the organism from food, and the potential transmission link represented by 154 symptom-free excreters, 68 of whom were involved in patient care. Datta and Pridie’s report, and other warnings of the highly contagious nature of salmonellosis in hospitals,’,’ led us to believe that our un-isolated patients posed a serious threat to other patients and staff. Secondary spread seemed almost inevitable, since fsecal soilage occurred in areas like our surgical intensive-care unit, a single large room with no natural barriers, and filled with desperately ill postoperative patients. These patients were thought to be especially vulnerable to cross-infection, since many were receiving antibiotics; and such treatment has been shown to reduce by 104 the inoculum of salmonellse required to infect laboratory animals.9 Therefore, with our first patient, we were quite surprised to be unable to detect a single symptomatic or symptom-free secondary case. Believing ourselves to be inordinately lucky, we continued to culture all contacts in successive cases of salmonellosis admitted without enteric
1003
episodes have now been single secondary case. Contrary to our earlier impression, transmission of salmonella from patient-to-patient seems difficult to achieve, even in the hospital situations which appear to favour spread. Schroeder et al. reported forty epidemics in institutions and hospitals,3 pointing out that cross-infection outbreaks were virtually confined to pqcdiatric populations,4,10 while a common vehicle was the mechanism of transmission for most hospital epidemics among adults. Moreover, on reviewing cases purporting to demonstrate patient-to-patient spread of salmonella in hospitals, one finds that a common vehicle has not been excluded. For example, Datta and Pridie5 note that another hospital in the same town was having an epidemic similar to theirs, which is consistent with a community focus such as contaminated water. In their not did remit for addition, epidemic twenty weeks despite stringent control measures to avoid person-to-person spread. In a six-week nursing-home epidemic involving 45 cases, Gotoff et al. argued that both the duration and the low attack-rate suggested person-to-person spread, but water, food, and other potential vehicles of infection were not investigated." Furthermore, there was no spread among the roommates of infected cases. Careful epidemiological analysis of outbreaks lacking an obvious common
precautions. Eight
similar
studied without finding
Preliminary Communication
a
vehicle of infection have shown that materials such
carmine dye,12 raw milk,13 and imported food 1 were actually responsible for these apparently sporadic and unrelated cases. Thus, some scepticism seems warranted about similar episodes which are claimed, because of inability to detect a common vehicle of infection, to prove patient-to-patient spread. Our as
results from situations where extensive environmental fscal contamination occurred suggest that it is difficult to achieve person-to-person spread of salmonella. even when dealing with patients vulnerable to crossinfection. Inoculation of the organisms into food or water, with subsequent multiplication up to an infecting dose, seems to be a necessary intermediate step in the development of an epidemic. Requests for reprints should be addressed
to
R. R. MacG.
CONVULSIONS AND ELECTROENCEPHALOGRAM ABNORMALITIES AFTER INTRA-AMNIOTIC PROSTAGLANDIN F2a R. C. LYNEHAM J. G. MCLEOD I. D. SMITH
Departments of Obstetrics and Gynæcology and Medicine, University of Sydney, King George V Memorial Hospital, and Royal Prince Alfred Hospital, Sydney, Australia of three hundred and twenty patients who had therapeutic secondtrimester abortion by intra-amniotic prostaglandin F2a (P.G.F2a) experienced major convulsions during the procedure. In four out of eight patients there were abnormalities in serial electroencephalograms performed within one to four hours of P.G.F.2a
Summary
1. 2. 3.
4. 5. 6.
Cherubin, C. E. Lancet, 1972, ii, 377. Gangarosa, E. J., Barker, W. H., Baine, W. B., Morris, G. K., Rice, P. A. ibid. 1973, i, 878. Schroeder, S. A., Aserhoff, B., Brachman, P. S. New Engl. J. Med. 1968, 279, 674. Jellard, C. H., Jolly, H., Brown, R. W. Lancet, 1959, i, 390. Datta, N., Pridie, R. B. J. Hyg., Camb. 1960, 58, 229. Edwards, E. in Identification of Enterobacteriaceæ. Minneapolis, 1972.
7.
8. 9. 10. 11.
12. 13.
Hook, E. W., Kaye, D. (editors). Proceedings of the National Conference on Salmonella, U.S. publ. Hlth Serv. Publ. 1965, no. 1262, p. 47. Benenson, A. S. in Control of Communicable Diseases in Man; p. 215. New York, 1970. Bohnhoff, M., Miller, C. P. J. infect. Dis. 1962, 111, 117. Szanton, U. L. Pediatrics, Springfield, 1957, 20, 794. Gotoff, S. P., Boring, J. R., Lepper, M. H. Am. J. med. Sci. 1966, 251, 16. Lang, D. J., Kunz, L. J., Martin, A. R. New Engl. J. Med. 1967, 276, 829. Centre for Disease Control. Morbid. Mortal. wkly Rep. 1966, 15,
385. 14. ibid. 1973,
22,
29.
Five
administration. INTRODUCTION
EVIDENCE suggests that prostaglandins (P.G.s) are involved in neuronal function. They are synthesised by the brain and are a natural constituent of 1 nervous tissue and cerebrospinal fluid. P.G.S have been available for clinical experimentation for some years, but we are unaware of any reports of major neurological side-effects. At King George V Memorial Hospital, Sydney, intra-amniotic p.G.F2rt has been used since March, 1972, as the method of choice for inducing second-trimester abortions. We report electroencephalogram (E.E.G.) after P.G. administration. The present study changes was undertaken because five of three hundred and had major contwenty patients treated with p.G.F2<1 vulsions. MATERIALS
AND
METHODS
Patients
Abortion REFERENCES
P. A. Low R. P. SHEARMAN A. R. KORDA
was
induced in three hundred and twenty Seven gave a history
patients, 14-20 weeks pregnant. of previous epileptic seizures.
Prostaglandin Administration After admission to hospital, a standard 17-gauge Tuohy epidural needle was inserted trans abdominally into the amniotic cavity and an epidural catheter (external diameter 1-02 mm.) was introduced through the needle. An initial injection of 30 mg. of P.G.F2a was given via the catheter; if abortion did not occur within 24 hours, a further 15 mg. was given and, if necessary, repeated 18 hours later. Drug therapy was restricted rigidly to pethidine for pain and metoclopramide for nausea.
E.E.G.
Study Eight patients, 16-19 weeks pregnant, who
were to be admitted for P.G. termination were studied. None gave a past or family history of epilepsy. 16-channel electroencephalography with routine- 21electrode placements was performed on each subject as an outpatient, before admission.
and occipital capillary haemangiomata were present. Neurological examination revealed decorticate rigidity, hyperacusia, and myoclonic jerk-like seizures. Chromosome studies
evaluated by
patients
us
were carried and disclosed
out no
on
all three
abnormality.
Discussion The pattern of altered growth and morphogenesis in the two newborn babies we describe is strikingly similar to that of the previously reported children with the fetal alcohol syndrome. Pertinent additional findings include the following: both newborn infants had serious problems of respiratory adaptation, and one of them had problems with biochemical adaptation, as shown by hypoglycaemia, hypocalcxmia, and hyperbilirubinxmia. The observation of mild microphthalmia in both newborn babies tends to accord with the suggestion that the consistently short palpebral fissures in this syndrome are secondary to reduced ocular growth. All three patients were judged to have a cardiac anomaly, further emphasising the frequency of this defect in the fetal alcohol syndrome. Two of them had a cleft soft palate, a new observation in this disorder. The findings in the brain of patient 2, the first case of the fetal alcohol syndrome on whom a necropsy There was was performed, are of special relevance. serious disorientation of both neuronal and glial elements as well as incomplete development of the brain which must have started before 80 days’ gestation, judging from the absence of the corpus callosum. Some of the functional and structural abnormalities in this syndrome may relate to the types of aberration in brain morphogenesis observed in this patient. These secondary features include microcephaly, developmental delay, and fine-motor dysfunction, which showed itself in early infancy by tremulousness. Some of the joint anomalies could be related to neurological impairment of the fetus, including
reduced The
movement.
profound degree of prenatal-onset growth deficiency yet noted in the fetal alcohol syndrome occurred in patient 3. The findings in patient 3, most
who at 7 months of age was still below normal newborn size and showed no growth response to highcaloric feedings, provide further evidence of the immutable nature of the adverse prenatal effect on growth-rate in this disorder. The findings in the two newborn infants accorded with the previous observation that prenatal growth in length is more severely affected than weight gain. The mother of patient 1 provided us with the first opportunity to study the nutritional status of a chronically alcoholic woman at the time of birth of her affected child, and of investigating the suggestion that a secondary nutritional deficiency could be the cause of the syndrome. Serious iron deficiency was the only abnormality detected. Since neither this degree of growth deficiency nor this pattern of malformation have to our knowledge been noted in offspring of iron-deficient ansemic women who were non-alcoholic, it seems unlikely that iron-deficiency anaemia is the cause of this disorder. The risk of the initial diagnosis being wrong is
high.
For
example,
the 18
trisomy syndrome
and
Cornelia de Lang syndrome were seriously considered by the physicians who initially evaluated these patients. An incorrect diagnosis could lead to inappropriate advice about the risk of malformation in future children. Risk of fetal alcohol syndrome in future children is potentially high, as indicated by patient 3, unless maternal alcoholism is controlled. Additional studies are needed to determine the incidence of the fetal alcohol syndrome in offspring of alcoholic mothers. Preliminary data from the collaborative study of the National Institute of Neurologic Disease and Stroke indicate a 32% incidence of this condition in offspring of women whose chronic alcoholism was ascertained during their pregnancy. The results of that study will form the basis of a future report. We thank Dr John Opitz for calling to our attention patient 3, whom we had previously evaluated; Dr Frederick Harvey who performed the ncuropathological evaluation of patient 2; Mrs Mary Ann Harvey and Dr Gordon Green, Dr K. M. Laurance, and Dr Jan Langman for making us aware of pertinent historical data; Mrs Lyle Harrah, research librarian; Mrs Christine Hansen for secretarial assistance; and Mr Bradley Gong for the photography. This study was supported by grants from the Maternal and Child Health Services, the National Institutes of Health, and the National FoundationMarch of Dimes.
Requests for reprints should be addressed to K. L. J., University of Washington, RR 234 Health Sciences RD-20, Seattle, Washington 98195, U.S.A. REFERENCES 1. 2.
3.
4. 5. 6.
7. 8. 9. 10.
11.
Jones, K. L., Smith, D. W., Ulleland, C. N., Streissguth, A. P. Lancet, 1973, i, 1267. Haggard, H. W., Jellinek, E. M. Alcohol Explored. Garden City, New York, 1942. Report on drunkenness presented to the House of Commons by the Select Committee, 1834. Sullivan, W. C. Med. Temp. Rev. 1900, 3, 72. Ladraque, P. Alcoholisme et enfants. Paris, 1901. Roe, A. Q. Jl Stud. Alcohol, 1944, 5, 378. Lecomte, M. Scalpel, Brux. 1950, 103, 1133. Christiaens, L., Mizon, J. D., Delmarle, G. Sem. Hôp. Paris, 1960, 36, 37. Sandor, S. Rev. roum. Embryol. Cytol. Sér. Embryol. 1968, 5, 1, 51. Sandor, S. ibid. p. 167. Sandor, S., Amels, D. ibid. 1971, 8, 105.
PERSON-TO-PERSON SPREAD OF SALMONELLA: A PROBLEM IN HOSPITALS? ROB ROY MACGREGOR
JUDITH REINHART Infectious Diseases Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, U.S.A. Summary
8
patients with acute diarrhœa were to hospital and appropriate
admitted
techniques were not used to avoid seconThese patients later proved to have salmonellosis. Their surroundings were extensively contaminated, exposing 265 patients and staff to infected fæces. No case of symptomatic or asymptostool-barrier
dary spread.
matic salmonellosis was found as a result of personto-person spread. It is concluded that person-toperson spread of salmonella in hospital is difficult to accomplish without an intermediary common vehicle.
1002 SALMONELLA CASES ADMITTED WITHOUT ENTERIC PRECAUTIONS
Introduction THE debate
is
acquired l,2
over
has
the way
prompted hospital cases.
by
which salmonellosis.
us to
report
our
experi-
with Since epidemics of salmonellosis do occur in hospitals,;-’ enteric precautions are normally taken to avoid person-to-person spread of salmonella when patients with diarrhoea are admitted to hospital. Occasionally an infectious agent is not initially suspected and the hospital staff and other patients are directly exposed to infected fxces or fxcally contaminated materials. ence
Patients
During the past eighteen months, despite our hospital’s policy to isolate febrile patients with diarrhoea of unknown cause, 8 patients with diarrhoea, in whom enteric precautions were not started for more than seventy-two hours, proved to have salmonellosis. Before their isolation, patients variably had sigmoidoscopy, barium enema, rectal examination, or had their rectal temperature taken; all had fsecal incontinence, some were comatose, and there was major f2ecal soilage of their immediate surroundings. When the cause of their diarrhoea became obvious, all staff who had had physical contact with the patient or his contaminated materials, without using proper barrier techniques, were asked to provide a stool sample for culture. Those with diarrhoea were kept from work until results of their cultures were known. In addition, all patients sharing the same room as the index case gave stools for culture, as did any other patients in the same unit in whom diarrhoea developed; the latter were put on stool isolation pending results of culture. We were surprised to find that no secondary spread of salmonellae could be detected from any of our 8 cases. Our results suggest that direct, personto-person spread of the organism is difficult to accomplish, even in vulnerable hospital patients.
salmonella organism isolated. Over two-thirds of the cultures were received in the first half of each culture period-e.g., more than 30 of the 52 contacts of patient 3 had cultures taken within seven days of their Diarrheca-rates among conexposure to infection. tacts varied from 0 to 19 %, depending on the time of year (more in winter), number of patients in the exposed group (patients had higher diarrhoea-rates than staff), and how the contacts defined diarrhoea (staff were simply asked " have you had any diarrhoea ?").
Methods Stool samples were cultured as follows: approximately 1 g. of stool was emulsified in 5 ml. of ’GN’ (gram negative) broth (Baltimore Biological Laboratories) and streaked on MacConkey’s agar; the agar and the broth were incubated at 37 °C. After twenty-four hours, the ’GN ’’ broth was subcultured on to’XLD ’ (xylose/lysine/desoxycholate) agar (Baltimore Biological Laboratories) and both cultures then were held at 37 °C for forty-eight hours. Any non-lactose-fermenting colonies were further investigated by standard biochemical procedures.6 All presumptive salmonella: isolates were sent to the Pennsylvania State Laboratory for verification and serotyping. Exposure was judged to be significant if the individual actually handled the patient, his faeces, or any objects which might have been soiled with faeces (bedding, hospital gown, All room-mates of the patients were bedpan, &c.). believed to be at risk through the intermediary of common attendants and room materials.
Results
Between December, 1971, and May, 1973, 20 inpatients had Salmonella spp. isolated from their stool; 8 of these had diarrhoea for periods of three to ten days before proper enteric-isolation procedures were started (see accompanying table). Fellow patients constituted 19-2% of the individuals exposed to infection, while the remainder were physicians, nurses, and other ward staff. Over 90 % of contacts had at least one stool cultured; in no instance was a
Discussion In 1960, Datta and Pridie reported a hospital epidemic caused by Salmonella typhimurium which lasted for twenty weeks and involved over 250 cases.5 Their conclusion that this epidemic represented person-to-person spread in the hospital was based on the protracted duration of the outbreak, failure to grow the organism from food, and the potential transmission link represented by 154 symptom-free excreters, 68 of whom were involved in patient care. Datta and Pridie’s report, and other warnings of the highly contagious nature of salmonellosis in hospitals,’,’ led us to believe that our un-isolated patients posed a serious threat to other patients and staff. Secondary spread seemed almost inevitable, since fsecal soilage occurred in areas like our surgical intensive-care unit, a single large room with no natural barriers, and filled with desperately ill postoperative patients. These patients were thought to be especially vulnerable to cross-infection, since many were receiving antibiotics; and such treatment has been shown to reduce by 104 the inoculum of salmonellse required to infect laboratory animals.9 Therefore, with our first patient, we were quite surprised to be unable to detect a single symptomatic or symptom-free secondary case. Believing ourselves to be inordinately lucky, we continued to culture all contacts in successive cases of salmonellosis admitted without enteric
1003
episodes have now been single secondary case. Contrary to our earlier impression, transmission of salmonella from patient-to-patient seems difficult to achieve, even in the hospital situations which appear to favour spread. Schroeder et al. reported forty epidemics in institutions and hospitals,3 pointing out that cross-infection outbreaks were virtually confined to pqcdiatric populations,4,10 while a common vehicle was the mechanism of transmission for most hospital epidemics among adults. Moreover, on reviewing cases purporting to demonstrate patient-to-patient spread of salmonella in hospitals, one finds that a common vehicle has not been excluded. For example, Datta and Pridie5 note that another hospital in the same town was having an epidemic similar to theirs, which is consistent with a community focus such as contaminated water. In their not did remit for addition, epidemic twenty weeks despite stringent control measures to avoid person-to-person spread. In a six-week nursing-home epidemic involving 45 cases, Gotoff et al. argued that both the duration and the low attack-rate suggested person-to-person spread, but water, food, and other potential vehicles of infection were not investigated." Furthermore, there was no spread among the roommates of infected cases. Careful epidemiological analysis of outbreaks lacking an obvious common
precautions. Eight
similar
studied without finding
Preliminary Communication
a
vehicle of infection have shown that materials such
carmine dye,12 raw milk,13 and imported food 1 were actually responsible for these apparently sporadic and unrelated cases. Thus, some scepticism seems warranted about similar episodes which are claimed, because of inability to detect a common vehicle of infection, to prove patient-to-patient spread. Our as
results from situations where extensive environmental fscal contamination occurred suggest that it is difficult to achieve person-to-person spread of salmonella. even when dealing with patients vulnerable to crossinfection. Inoculation of the organisms into food or water, with subsequent multiplication up to an infecting dose, seems to be a necessary intermediate step in the development of an epidemic. Requests for reprints should be addressed
to
R. R. MacG.
CONVULSIONS AND ELECTROENCEPHALOGRAM ABNORMALITIES AFTER INTRA-AMNIOTIC PROSTAGLANDIN F2a R. C. LYNEHAM J. G. MCLEOD I. D. SMITH
Departments of Obstetrics and Gynæcology and Medicine, University of Sydney, King George V Memorial Hospital, and Royal Prince Alfred Hospital, Sydney, Australia of three hundred and twenty patients who had therapeutic secondtrimester abortion by intra-amniotic prostaglandin F2a (P.G.F2a) experienced major convulsions during the procedure. In four out of eight patients there were abnormalities in serial electroencephalograms performed within one to four hours of P.G.F.2a
Summary
1. 2. 3.
4. 5. 6.
Cherubin, C. E. Lancet, 1972, ii, 377. Gangarosa, E. J., Barker, W. H., Baine, W. B., Morris, G. K., Rice, P. A. ibid. 1973, i, 878. Schroeder, S. A., Aserhoff, B., Brachman, P. S. New Engl. J. Med. 1968, 279, 674. Jellard, C. H., Jolly, H., Brown, R. W. Lancet, 1959, i, 390. Datta, N., Pridie, R. B. J. Hyg., Camb. 1960, 58, 229. Edwards, E. in Identification of Enterobacteriaceæ. Minneapolis, 1972.
7.
8. 9. 10. 11.
12. 13.
Hook, E. W., Kaye, D. (editors). Proceedings of the National Conference on Salmonella, U.S. publ. Hlth Serv. Publ. 1965, no. 1262, p. 47. Benenson, A. S. in Control of Communicable Diseases in Man; p. 215. New York, 1970. Bohnhoff, M., Miller, C. P. J. infect. Dis. 1962, 111, 117. Szanton, U. L. Pediatrics, Springfield, 1957, 20, 794. Gotoff, S. P., Boring, J. R., Lepper, M. H. Am. J. med. Sci. 1966, 251, 16. Lang, D. J., Kunz, L. J., Martin, A. R. New Engl. J. Med. 1967, 276, 829. Centre for Disease Control. Morbid. Mortal. wkly Rep. 1966, 15,
385. 14. ibid. 1973,
22,
29.
Five
administration. INTRODUCTION
EVIDENCE suggests that prostaglandins (P.G.s) are involved in neuronal function. They are synthesised by the brain and are a natural constituent of 1 nervous tissue and cerebrospinal fluid. P.G.S have been available for clinical experimentation for some years, but we are unaware of any reports of major neurological side-effects. At King George V Memorial Hospital, Sydney, intra-amniotic p.G.F2rt has been used since March, 1972, as the method of choice for inducing second-trimester abortions. We report electroencephalogram (E.E.G.) after P.G. administration. The present study changes was undertaken because five of three hundred and had major contwenty patients treated with p.G.F2<1 vulsions. MATERIALS
AND
METHODS
Patients
Abortion REFERENCES
P. A. Low R. P. SHEARMAN A. R. KORDA
was
induced in three hundred and twenty Seven gave a history
patients, 14-20 weeks pregnant. of previous epileptic seizures.
Prostaglandin Administration After admission to hospital, a standard 17-gauge Tuohy epidural needle was inserted trans abdominally into the amniotic cavity and an epidural catheter (external diameter 1-02 mm.) was introduced through the needle. An initial injection of 30 mg. of P.G.F2a was given via the catheter; if abortion did not occur within 24 hours, a further 15 mg. was given and, if necessary, repeated 18 hours later. Drug therapy was restricted rigidly to pethidine for pain and metoclopramide for nausea.
E.E.G.
Study Eight patients, 16-19 weeks pregnant, who
were to be admitted for P.G. termination were studied. None gave a past or family history of epilepsy. 16-channel electroencephalography with routine- 21electrode placements was performed on each subject as an outpatient, before admission.