1056

CYSTIC FIBROSIS IN KUWAIT

S:R,—Cystic fibrosis is well known in Europe and North Americabut it has not hitherto been reported in the Middle East. Wedescribe here two proven cases of this condition. The first was afemale baby who presented with small-intestinal obstruction. Atoperation meconium ileus was found and the standard Bishop-Koopileostomy was done. Postoperatively increasing respiratory distressdeveloped and, despite ventilation, the child died of pneumonia.The second child was a 12-month-old who came in with symptomsof respiratory difficulty. There had been several admissions for thesame illness. A sister had died of a similar illness at the age of 5months. The child had bronchiolitis, and, despite intensive

supportive treatment, died 2 weeks after admission. Both thesechildren were born to Arab parents (Kuwaiti or Syrian). At necropsyin both cases the classical findings of cystic fibrosis were noted bothmacroscopically and microscopically. In the first patient thesefindings affected pancreas, intestine, liver, and lungs, while in thesecond patient the most affected organs were the lungs andpancreas.

In neither case was cystic fibrosis suspected before death, thiscondition being thought not to occur in the Middle East. Thesecases are presented in the hope that, in future, physicians in theMiddle East and Asia will be alerted to make this diagnosis earlier.

Departments of Paediatric Surgery,and Pathology,

Al-Sabah Hospital,Kuwait

A P. R. ALUWIHARES. M ALIM. S. AHMADGALAL ABDULLA MIRGHANIJ. MOHACSY

*Present address: 132/7 Wariyapola Sri Sumangala Mawatha, Kandy, Sri Lanka

ANTIBACTERIAL ACTIVITY OF HYDROLYSEDLINSEED OIL AND LINOLENIC ACID AGAINSTMETHICILLIN-RESISTANT STAPHYLOCOCCUS

AUREUS

SiR,—Methicillin-resistant strains of Staphylococcus aureus

(MRSA), which are also resistant to most other anti-staphylococcalantibiotics, are currently causing a widespread epidemic of hospital-acquired infection in the State of Victoria. More than 31 metro-politan institutions are involved, together with a smaller number ofcountry base hospitals. In some Melbourne teaching hospitalsMRSA account for up to 50% of all isolates of Staph. aureus. Moststrains come from colonised patients, but severe infections do occurin debilitated and immunocompromised hosts, causing substantialmorbidity and mortality. 1,2

Patients who are colonised with MRSA appear to run a greaterrisk of infection after operative or other invasive procedures thando those who lack these strains. Colonised patients provide a focusfrom which MRSA can be disseminated to susceptible patients;thus, they are often refused admission to other institutions becauseof the risk of cross-infection.Conventional management of colonised patients includes the use

of topical antiseptics (e.g., hexachlorophene or chlorhexidine forskin colonisation) and/or a defined topical antibiotic which does nothave systemic use, such as framycetin or bacitracin for nasalcolonisation. Unfortunately, a proportion of patients cannot becleared by these measures, leaving long-term therapeutic andplacement problems.3 3

Recently, Lacey and Lord4 showed the Staph. aureus was

inhibited by linolenic acid, while Staph. epidermidis was relativelyresistant. Linolenic acid rapidly killed cultures of Staph. aureusapplied to the skin, and a therapeutic role for naturally occuring freefatty acids was suggested.

1 Health Commission of Victoria. staphylococcal infections in hospitals, 2nd ed. 1981.2. McDonald MI, Hurse A, Sim KN. Methicillin-resistant Staphylococcus aureus

bacteraemia. Med J Aust 1981, ii: 191-94.3. Gawler DM, Royle JP, Tosolini FA Intractable Nasal Carriage ofmethicillin-resistant

Staphylococcus aureus. Med J Aust 1980; i. 607-08.4. Lacey RM, Lord VL. Sensitivity of staphylococci to fatty acids Novel inactivation of

linolenic acid by serum. J Med Microbiol 1981; 14: 41-49.

Linseed oil contains 52% linolenic acid in the ester form and is

cheap and freely available. Alkaline hydrolysis is required toprovide a fatty acid with a free carboxyl group.We report here a comparison of the antibacterial activity of

hydrolysed linseed oil compared with pure linolenic acid against 91isolates of MRSA.

Staphylococci were obtained from a large diagnostic laboratoryand identification and sensitivity tests were done by standardmethods.5 Pure linolenic acid was obtained from Nuchek Prep(Minnesota) and linseed oil from Meggitt Ltd (Melbourne). Thelinseed oil was subjected to a standard alkaline hydrolysistechnique. Linolenic acid and hydrolysed linseed oil were

incorporated into molten nutrient agar base to final concentrationsofO-01,0-005, and 0-0025% v/v, and 0 - 025,0’01, and 0 005% v/v,respectively. (The nutrient agar base was composed of 2 5% w/vOxoid nutrient broth no. 2 with 0 3% w/v Oxoid yeast extract and1 - 2% w/v Oxoid agar no. 1.) After 18 h incubation at 37°C in brainheart infusion broth, the organisms were diluted in normal salinecontaining 1% peptone and inoculated onto the agar plates with aSteers replicator. Duplicate plates and controls were incubatedaerobically at both 30°C and 37°C for 48 h. A 95%, or greater,reduction in growth compared with the control was taken as

inhibition.The results are shown in the table.

PERCENTAGE OF 91 MRSA STRAINS INHIBITED BY LINOLENIC ACIDAND HYDROLYSED LINSEED OIL

At 0-025% (v/v) all strains of MRSA were inhibited by bothlinolenic acid and hydrolysed linseed oil. The antibacterial effect ofboth agents was greater at 37 °C than at 30 °C, although thedifference was more marked for linolenic acid at 0 - 005% (v/v). Thiswas reproducible in replicate experiments on different occasions.For many strains, at low concentrations of linolenic acid and

hydrolysed linseed oil, there was a striking reduction in the size ofthe colonies without 95% inhibition. Seven strains of Staph.epidermidis tested concurrently were resistant to both agents at aconcentration of 0’025% (v/v).Our data show that MRSA are sensitive to hydrolysed linseed oil

as well as linolenic acid. Preparations containing hydrolysed linseedoil may have a role in the eradication of the staphylococcal carrierstate and could also be useful for prophylaxis, especially indebilitated patients.

Microbiology Department,Royal Melbourne Hospital,Parkville, Victoria 3052, Australia

Veterinary Research Institute,Department of Agriculture,Parkville, Victoria

M. I. MCDONALDI. GRAHAMK. J. HARVEY

A. SINCLAIR

PYRAZINAMIDE FULMINANT HEPATITIS: AN OLDHEPATOTOXIN STRIKES AGAIN

SIR,-Discredited drugs, like old politicians, may become popularagain, once their faults have been forgotten. Introduced in 1952 asan antituberculosis agent, pyrazinamide was soon dismissed as ahepatotoxin. The drug increased transaminase activity in about10% of treated patients, produced jaundice in about 5%, and

5. Barry AL, Thornsberry C. In: Lennette EH, et al, eds. Manual of clinical microbiology,3rd ed. Washington, DC: American Society for Microbiology, 1980: 463-74.

6. Christie WR. Lipid analysis, Oxford Pergamon Press, 1973: 85-86.