584 clerotic vascular disease (patients requiring surgery for peripheral arterial disease and patients with previous myocardial infarction). Thus the link between hypertension and immunoglobulins might be because high systemic pressures enhance atheroma formation and the immune processes which play a part in atherogenesis are reflected in the increased serum immunoglobulin levels. The old name for atheroma was "endarteritis chronicaa deformans",5 but this inflammatory element has been increasingly forgotten. The link between hypertension and enhanced immunoglobulin levels may serve to remind us of this neglected component of the atherosclerotic process. Department of Medicine, General Hospital, Nottingham NG1 6HA
J. R. A. MITCHELL
HYPERTENSION—SALT POISONING?
SIR,-The suggestion is offered in your editorial,6 that some of the discrepancy in published reports linking sodium ingestion to hypertension will be resolved by accepting heterogeneity of responsiveness. This should not be restricted to this particular putative hypertensinogenic stimulus. Part of the evidence offered to support the hypothesis that sodium ingestion causes hypertension in some people is Dahl’s demonstration that two strains of rats have opposite, genetically determined predispositions to salt-induced hypertension. Animals from the sensitive strain rapidly and predictably develop fulminant hypertension in response to a high-salt diet, while animals from the resistant strain are normotensive on the same diet. Sensitive-strain rats on a low-salt diet do not have significant hypertension but what was not mentioned was that when exposed to other types of stimulation (renal artery constricthese animals tion,8 cadmium,9 or psychological become hypertensive even on a low-salt diet. Cadmium and stress have been linked to hypertension but have achieved even less acceptance as aetiological factors than has salt. As you implied, much confusion could have been avoided by simply stating that excess sodium ingestion is likely to result in hypertension in only some individuals. We need to know what distinguishes susceptible people. Much the same can be said for other stimuli suspected of initiating or maintaining raised
stress )
blood-pressure. Medical Department, Brookhaven National Laboratory, Upton, New York 11793, U.S.A.
RICHARD FRIEDMAN JUNCHI IWAI
INTERCONTINENTAL NOSOCOMIAL INFECTIONS
SIR,-We have seen two seriously ill patients who arrived in South Africa from abroad and were infected with multiply resistant gram-negative bacilli. When this happens there may be undesirable additions to local bacterial resistance-gene inventories. The experience with typhoid fever’ supports this view. We have found that simple precautionary measures prevent these organisms becoming hospital residents. A male aged 35, was admitted to the Johannesburg Hospital 10 weeks after hsemorrhoidectomy in Sao Paulo, Brazil. The postoperative period had been complicated by nephrolithiasis, which required surgical treatment, and by severe perineal infection, which involved the left thigh and remained uncontrolled on admission. There was no evidence of diabetes mellitus or other underlying disease. He had been treated with several drugs, including cephalosporins, gentamicin and co-trimoxazole. Blood cultures taken at admission yielded Eschericia coli resistant to ampicillin, carbenicillin, cephalothin, strep4. 5.
Gray, M. V., Hill, J. D., Mitchell, J. R. A. Atherosclerosis (in the press). Virchow, R. Die cellular Pathologie. Berlin, 1858.
6. Lancet, 1978, i, 1136. 7. Dahl, L. K., Heine, M., Tassinari, L. J.J. exp. Med. 1962, 115, 1173. 8. Dahl, L. K., Heine, M., Tassinari, L. J. ibid. 1963, 118, 605. 9. Ohanian, E. V., Iwai, J., Leitl, G., Tuthill, R. Am. J. Physiol. (in the press). 10. Friedman, R., Iwai, J. Science, 1976, 193, 161.
SUSCEPTIBILITY OF IMPORTED ISOLATES TO SELECTED DRUGS
M.l.C.—Minimum inhibitory concentration in mg/1 M.B.c.-Minimum bactericidal concentration in mg/1
tomycin, gentamicin, kanamycin, tobramycin, amikacin, netilmicin, sulphonamides, co-trimoxazole, and chloramphenicol, and susceptible only to tetracyclines and polymyxins. Broth dilution sensitivities to selected drugs are shown in the table. The same organism was isolated from a septic left knee joint. Because of renal failure, the patient was treated with intravenous doxycycline. The initial clinical response was good, although the knee infection relapsed later. Subsequent testing had shown the organism to be sensitive to cefoxitin, which was then successfully used to control the infection. After many complications (including systemic candidosis) and orthopaedic operations, the patient is well, and free of the organism. Precautionary measures soon -after his admission-treating the patient in a single-bed room, and attention primarily to handcleansing by the staff-prevented dissemination of the bacterium in the hospital despite its persistence for weeks in wound-drainage material. A 37-year-old male, was admitted to a private hospital in Johannesburg about 6 weeks after a laparotomy for an acute abdomen in Tel Aviv, Israel. He had acute necrotising pancreatitis, no doubt related to an excessive alcohol intake. The pancreatic abscess was still draining through multiple sinuses on his arrival in Johannesburg. Culture of the pus yielded Providencia stuartii which was resistant to all available drugs except cefoxitin (see table). It was partially susceptible to cefamandole. The patient remained febrile and ill despite further drainage of the abscess, with persistent ansemia requiring transfusion. Cefoxitin and cefamandole were found to be synergistic against the organism by an agar-plate diffusion method, and their combined use resulted in rapid clinical improvement. Control procedures similar to those used in the first case were successful in preventing establishment of the organism in the hospital. However, while the patient is now well and back at work, he has a slowly closing abdominal sinus which is still colonised by P. stuartii. The potential for spread of the organism therefore remains. Both the organisms isolated from these patients were susceptible to nalidixic acid. Transfer rates of gentamicin resistance to nalidixic-acid-resistant E. coli K12 showed a rate of 0-5+10 for the Brazilian E. coli, while the Israeli P. stuartii did not transfer in our system (< 10-8). These cases illustrate the potential hazard of worldwide spread of nosocomial pathogens. We believe that national and international health authorities should recognise the problem, and investigate surveillance and control procedures. South African Institute for Medical Research, PO Box 1038, Johannesburg 2000, South Africa
Departments of Medicine and Surgery, University of the Witwatersrand and Johannesburg Hospital, Johannesburg 2001 Brenthurst Clinic, Johannesburg 2001 1. Anderson, E.
S., Smith,
H. R. Br.
C. S. BLOCK LAVINIA CLAUSEN S. KAY H. A. SEREBRO
med. J. 1972, in,
329.
J. R. A. MITCHELL
HYPERTENSION—SALT POISONING?
SIR,-The suggestion is offered in your editorial,6 that some of the discrepancy in published reports linking sodium ingestion to hypertension will be resolved by accepting heterogeneity of responsiveness. This should not be restricted to this particular putative hypertensinogenic stimulus. Part of the evidence offered to support the hypothesis that sodium ingestion causes hypertension in some people is Dahl’s demonstration that two strains of rats have opposite, genetically determined predispositions to salt-induced hypertension. Animals from the sensitive strain rapidly and predictably develop fulminant hypertension in response to a high-salt diet, while animals from the resistant strain are normotensive on the same diet. Sensitive-strain rats on a low-salt diet do not have significant hypertension but what was not mentioned was that when exposed to other types of stimulation (renal artery constricthese animals tion,8 cadmium,9 or psychological become hypertensive even on a low-salt diet. Cadmium and stress have been linked to hypertension but have achieved even less acceptance as aetiological factors than has salt. As you implied, much confusion could have been avoided by simply stating that excess sodium ingestion is likely to result in hypertension in only some individuals. We need to know what distinguishes susceptible people. Much the same can be said for other stimuli suspected of initiating or maintaining raised
stress )
blood-pressure. Medical Department, Brookhaven National Laboratory, Upton, New York 11793, U.S.A.
RICHARD FRIEDMAN JUNCHI IWAI
INTERCONTINENTAL NOSOCOMIAL INFECTIONS
SIR,-We have seen two seriously ill patients who arrived in South Africa from abroad and were infected with multiply resistant gram-negative bacilli. When this happens there may be undesirable additions to local bacterial resistance-gene inventories. The experience with typhoid fever’ supports this view. We have found that simple precautionary measures prevent these organisms becoming hospital residents. A male aged 35, was admitted to the Johannesburg Hospital 10 weeks after hsemorrhoidectomy in Sao Paulo, Brazil. The postoperative period had been complicated by nephrolithiasis, which required surgical treatment, and by severe perineal infection, which involved the left thigh and remained uncontrolled on admission. There was no evidence of diabetes mellitus or other underlying disease. He had been treated with several drugs, including cephalosporins, gentamicin and co-trimoxazole. Blood cultures taken at admission yielded Eschericia coli resistant to ampicillin, carbenicillin, cephalothin, strep4. 5.
Gray, M. V., Hill, J. D., Mitchell, J. R. A. Atherosclerosis (in the press). Virchow, R. Die cellular Pathologie. Berlin, 1858.
6. Lancet, 1978, i, 1136. 7. Dahl, L. K., Heine, M., Tassinari, L. J.J. exp. Med. 1962, 115, 1173. 8. Dahl, L. K., Heine, M., Tassinari, L. J. ibid. 1963, 118, 605. 9. Ohanian, E. V., Iwai, J., Leitl, G., Tuthill, R. Am. J. Physiol. (in the press). 10. Friedman, R., Iwai, J. Science, 1976, 193, 161.
SUSCEPTIBILITY OF IMPORTED ISOLATES TO SELECTED DRUGS
M.l.C.—Minimum inhibitory concentration in mg/1 M.B.c.-Minimum bactericidal concentration in mg/1
tomycin, gentamicin, kanamycin, tobramycin, amikacin, netilmicin, sulphonamides, co-trimoxazole, and chloramphenicol, and susceptible only to tetracyclines and polymyxins. Broth dilution sensitivities to selected drugs are shown in the table. The same organism was isolated from a septic left knee joint. Because of renal failure, the patient was treated with intravenous doxycycline. The initial clinical response was good, although the knee infection relapsed later. Subsequent testing had shown the organism to be sensitive to cefoxitin, which was then successfully used to control the infection. After many complications (including systemic candidosis) and orthopaedic operations, the patient is well, and free of the organism. Precautionary measures soon -after his admission-treating the patient in a single-bed room, and attention primarily to handcleansing by the staff-prevented dissemination of the bacterium in the hospital despite its persistence for weeks in wound-drainage material. A 37-year-old male, was admitted to a private hospital in Johannesburg about 6 weeks after a laparotomy for an acute abdomen in Tel Aviv, Israel. He had acute necrotising pancreatitis, no doubt related to an excessive alcohol intake. The pancreatic abscess was still draining through multiple sinuses on his arrival in Johannesburg. Culture of the pus yielded Providencia stuartii which was resistant to all available drugs except cefoxitin (see table). It was partially susceptible to cefamandole. The patient remained febrile and ill despite further drainage of the abscess, with persistent ansemia requiring transfusion. Cefoxitin and cefamandole were found to be synergistic against the organism by an agar-plate diffusion method, and their combined use resulted in rapid clinical improvement. Control procedures similar to those used in the first case were successful in preventing establishment of the organism in the hospital. However, while the patient is now well and back at work, he has a slowly closing abdominal sinus which is still colonised by P. stuartii. The potential for spread of the organism therefore remains. Both the organisms isolated from these patients were susceptible to nalidixic acid. Transfer rates of gentamicin resistance to nalidixic-acid-resistant E. coli K12 showed a rate of 0-5+10 for the Brazilian E. coli, while the Israeli P. stuartii did not transfer in our system (< 10-8). These cases illustrate the potential hazard of worldwide spread of nosocomial pathogens. We believe that national and international health authorities should recognise the problem, and investigate surveillance and control procedures. South African Institute for Medical Research, PO Box 1038, Johannesburg 2000, South Africa
Departments of Medicine and Surgery, University of the Witwatersrand and Johannesburg Hospital, Johannesburg 2001 Brenthurst Clinic, Johannesburg 2001 1. Anderson, E.
S., Smith,
H. R. Br.
C. S. BLOCK LAVINIA CLAUSEN S. KAY H. A. SEREBRO
med. J. 1972, in,
329.
