845
RELAPSING CLOSTRIDIUM DIFFICILE
ENTEROCOLITIS CURED BY RECTAL INFUSION OF
HOMOLOGOUS FAECES
SIR,-Recurrent Clostridium difficile associated enterocolitis is
uncommon but troublesome for the patient. The patient described
here received vancomycin treatment several times but always
relapsed with C difficile enterocolitis 2-3 weeks after
discontinuation of treatment.
A 65-year-old woman with a lifelong history of irritable colon also
had diverticulosis of the colon and diverticulitis of increasing
severity. A partial colectomy was done to remove the diseased
part of the sigmoid colon. She was given routine preoperative
treatment with neomycin and metronidazole. 1 week
she given co-trimoxazole because of
postoperatively was pulmonary
infection. She responded well at first but 3 weeks later she had
frequent diarrhoea and fever and C difficile enterocolitis was
diagnosed. Stool cultures grew C dzfficile and its cytotoxin was
demonstrated. Vancomycin was given for 7 days and proved
effective. 2 weeks later, however, the patient had a relapse. C
difficile and its cytotoxin was again demonstrated in the stool.
Vancomycin was given with prompt response. The patient had
another four relapses of Cdifficile enterocolitis, also after prolonged
(4 month’s) vancomycin therapy.
Since the patient was faced with the unattractive prospect of
lifelong vancomycin treatment we decided to try to achieve a normal
bowel flora by infusing faeces, hoping that C difficile would be
suppressed and a normal flora established.
Enemas were prepared in an anaerobic cabinet from fresh faeces
obtained from the patient’s husband. 4 days after the last (sixth)
course of vancomycin treatment two such enemas were given
immediately after preparation and 3 days apart. There were no
untoward reactions. The rectal infusion of normal faeces resulted in
prompt and complete normalisation of bowel function. Stools of
normal consistency, colour, and smell have thereafter been passed
daily or every other day. The follow-up period is now 9 months. The
patient feels well and has gained in weight from 41 to 47 kg.
Institute of Clinical Bacteriology,
Department of Paediatrics ANNA SCHWAN
and Department of Infectious Diseases
University Hospital, STIG SJOLIN
75122 Uppsala, Sweden ULLA TROTTESTAM
National Bacteriological Laboratory,
Stockholm BO ARONSSON
MUROID VIRUS NEPHROPATHIES
SIR,-Your editorial and the subsequent correspondence drew
attention to the haemorrhagic fever with renal syndrome (HFRS)
and the closely related nephropathia epidemica described by Scan-
dinavian workers.2,3 It seems that in Western Europe, outside Scan-
dinavia, HFRS acquired from laboratory rats has been observed
only in Belgium (Desmyler J, personal communication). In addition
antibodies to Hantaan virus, as well as antigen, have been detected in
a wild rodent, the red-backed vole (Clethrionomys glareolus), in
Belgium.4We have observed a case of HFRS in a French resident
after exposure to wild rodents. A previously healthy 29-year-old
man living in Paris was admitted to hospital on Nov 16, 1982,
because of fever, chills, profuse sweating, vomiting, and intense
lumbar pain which had appeared 4 days earlier. The only relevant
signs found on initial examination were bilateral conjunctival
haemorrhages and acute myopia. Blood pressure was 110/70 mm
Hg and remained normal throughout the course of the disease.
Laboratory data included haemoglobin 7 g/dl, leucocyte count
21 700/1, platelets 41 000/1, SGOT 65 IU/1, SGPT 67 IU/1, blood
1 Editorial Muroid virus nephropathies. Lancet 1982, ii: 1375-77.
2 Lähdevirta J Nephropathia epidemica in Finland. A clinical, histological and
epidemiological study. Ann Clin Res 1971, 3 (suppl 8). 1-154.
3 Lee HW, Lee PW, Lähdevirta J, Brummer-Korvenkontio M. Aetiological relation
between Korean haemorrhagic fever and nephropathia epidemica. Lancet 1979; ii:
186-87
4 Van der Groen G, Tkachenko EA, Ivanov AP, Verhagen R Haemorrhagic fever with
renal syndrome related virus in indigenous wild rodents in Belgium Lancet 1983; ii:
110-11
urea nitrogen 5’8mmol/l, serum creatinine 330 mol/1, and urine
analysis showing abundant proteinuria (2’5g/day) and microscopic
haematuria. Renal echography disclosed a symmetrical
of
enlargement both kidneys.
During the next 4 days symptoms regressed, whereas renal
function continued to deteriorate (serum creatinine peaked at 960
mol/1 on the 1 Oth day of the disease), urinary output was 800-1000
ml/day with a urinary sodium below 10 mmol/day and a moderate
proteinuria. On the 1 lth day diuresis occurred (3300 ml/day) and
persisted for 4 days, followed by a dramatic improvement of renal
function. By the l7th day serum creatinine and urinary sediment
had returned to normal; proteinuria was negative. 9 months later the
patient has no clinical or biochemical abnormality. A renal
percutaneous biopsy on day 10 showed conspicuous abnormalities
within the medulla, with diffuse oedema, hyperaemia, and
haemorrhages in the interstitium. There was also a pronounced
vacuolisation and swelling of tubular epithelial cells without
necrosis. Glomerular changes were minimal. Several capillary loops
were enlarged by numerous red cells; no hypercellularity was
present. Arteries and arterioles were normal. Immunofluorescence
for IgG, IgM, IgA, Clq, C3, and fibrinogen was negative. The
diagnosis of HFRS, which was strongly suggested by both clinical
and histological data,2,5 was confirmed by fluorescent-antibody test
in two different laboratories. A significant increase in antibodies to
vero E6 cells infected with strain 74-118 Hantaan virus (see figure)6
and to lung section of bank voles infected for nephropathia
epidemicawas detected.
not uec. idn. ai reu. mar. Apr. may
IgG and IgM titres to strain 76 - 118 Hantaan virus.
This case of HFRS is the first observed in France. The patient had
never travelled out of France or been exposed to laboratory rats.
However, he had worked for a day two weeks before onset in a barn
located in a small village 120 km north-east of Paris. It seems very
likely that he had acquired the infection from wild rodents which
were sometimes seen in the barn. An epidemiological survey has
been undertaken in this rural area. The occurrence of an infection of
man due to an HFRS-related virus acquired in France after
exposure to wild rodents obviously extends the boundary of
European endemic HFRS. This is not surprising, since field mice
(Apodemus), the reservoir of Hantaan virus, are common in France
as in other Western European countries.8 HFRS should be
5 Lee HW. Korean hemorrhagic fever. Prog Med Virol 1982, 28: 96-113.
6. McCormick JB, Sasso DR, Palmer EL, Kiley MP Morphological identification of the
agent of Korean haemorrhagic fever (Hantaan virus) as a member of the
Bunyaviridae Lancet 1982; i; 765-68
7 Brummer-Korvenkontio J, Vaheri A, Hovi T, et al. Nephropathia epidemica:
Detection of antigen m bank voles and serologic diagnosis of human infection J
Infect Dis 1980, 141: 131-34.
8. Nowak RM, Paradiso JL. Walker’s mammals of the world. Baltimore. Johns Hopkins
University Press, 1983