Figure: Comparison of systolic and diastolic flow after LAST
procedure in LIMA-LAD graft and ungrafted right internal
mammary artery (RIMA)
patency of the LIMA to LAD can be immediately assessed
at the end of the procedure with a transthoracic pulse-wave
doppler. This procedure will show a greatly increased
the LIMA compared with
predominantly systolic flow in the ungrafted right internal
mammary artery, confirming patency (figure).
In our experience so far, this minimally invasive approach
is safe and should be regarded as the primary intervention in
the management of patients with isolated LAD disease, or as
a method of achieving partial revascularisation in those
patients in whom there are contraindications to conventional
cardiac surgical approaches. Furthermore, the protection
conferred by a patent LIMA-LAD graft may allow safe
angioplasty revascularisation to the proximal LAD or to
other diseased coronary arteries.
Antonio Maria Calafiore, *G D Angelini
Department of Cardiac Surgery, San Camillo de’Lellis Hospital, Chieti, Italy; and
Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW, UK
Stanbridge R De L, Symons GV, Banwell PE. Minimal-access surgery
for coronary artery revascularisation. Lancet 1995; 346: 837.
Dopamine receptors in schizophrenia
SiR-Gjedde and colleagues (Nov 11, p 1302)’ make three
critical remarks concerning our Sept 16 review.
First, our PET studies of D dopamine receptors in drug
naive schizophrenic patients certainly indicate a substantial
reduction of Dl dopamine receptor binding, both in the
striatum and in the frontal cortex. We apologise for the error
in table 1: the data show mean values with SD and not SE.
Second, the controversy concerning D
in schizophrenia was discussed extensively in the paper by
Nordstrom et al. Our main objective concerns the variability
obtained with the method used by Wong et al. Our own
studies will certainly also in the future deal with possible
alterations of D
dopamine receptors in schizophrenia.
Lastly, we agree with Gjedde and colleagues’ statement that
one study indicates a therapeutic potential of glycine in
schizophrenic negative symptomatology. However, these
clinical results certainly do not prove that this effect is
mediated by stimulation of glutamate transmission.
Although glycine interacts synergistically with glutamate
receptors by modulating a heterotopic glycine receptor, it
does not seem correct to classify glycine as a glutamate
Göran Sedvall, Lars Farde
Department of Clinical Neuroscience, Psychiatry Section, Karolinska Hospital,
S-171 76 Stockholm, Sweden
1 Gjedde A, Reith J, Wong D. Dopamine receptors in schizophrenia.
Lancet 1995; 346: 1302-03.
2 Sedvaal G, Farde L. Chemical brain anatomy in schizophrenia. Lancet
1996; 346: 743-49
HIV co-infection with a currently
SIR-HIV and Leishmayzia infantuna co-infection is common in
characterising parasite variability among them,= we found an
unusual Leishmania-like parasite.
A 35-year-old female intravenous drug user living in
Madrid was diagnosed HIV-positive in 1986. Her medical
history included herpes zoster infections in 1985 and 1987.
The patient had fever for 2 months before admission
pneumonia, and herpes labialis were diagnosed. Visceral
leishmaniasis was suspected because of clinical and laboratory
findings: 1450 leucocytes/l, packed cell volume 27-5%,
platelets 75 000/[tl’, total protein (71 g/L). CD4 count was
150/13. Immunofluorescence antibody test for leishmaniasis
was borderline, with a titre of 1/80. Amastigotes were not seen
in bone-marrow aspirate although flagellates were isolated.
The patient was treated for 21 days with meglumine
antimoniate (20 mg/kg per day) and recovered fully; 3 years
after treatment no relapses were detected.
Giemsa-stained preparations from cultured promastigotes
excluded Trypanosoma infection (figure). When the stock was
typed by isoenzyme electrophoresis, it showed a different
pattern to that of Leishmania reference strains. Furthermore,
kDNA and nDNA from this stock did not hybridise with
kDNA (307/K-l)-specific and nDNA (7-059, pDk20,
ultrastructure was examined by transmission and scanning
electron microscopy but was non-contributory. Promastigotes
did not infect Balb/c mice or Syrian golden hamsters.
Likewise, it was not possible to establish infection in
promastigotes were found in the gut of Rhodnius prolixus.
Insect parasites known as "lower trypanosomatids" were
tested. Both kDNA and nDNA cross-hybridisation from the
current stock with several lower trypanosomatid genera
(Crithidia fasciculata, Herpetomonas muscarum, Leptomonas
ctenocephali, Blastocrithidia spp, and Sauroleishmania spp)and
other trypanosomatids (Trypanosoma cruzi, Phytomonas tomate,
and Endotrypanum schaudinna) did not reveal any homology.
Figure: Promastigote cultures
RPM]-10% FCS. Giemsa staining (X1250). A.-Leishmania infantum
reference stock (LEM-75). and B.-Non-Leishmania flagellate showing
blunt end and larger and more dense kinetoplast.
265 Download full-text
Data on the enzymatic polymorphism analysed with Jaccard’s
similarity index showed no close phylogenetic relationships
between the trypanosomatids studied and the sample.
Western-blot analysis of four sequential sera from the
patient against soluble antigens from the sample identified
43, 72, and 92 kDa bands, which are commonly found in
visceral Leishmaniasis. Sera from the patient recognised
weak L infantum antigen-bands but in a different pattern to
the one found with sample antigen.
These findings suggest that immunocompromised patients
could be vulnerable
other currently non-human
pathogenic trypanosomatids which provoke a clinical pattern
similar to Leishmania infection in HIV-infected patients. We
have previously suggested blood As a frequent source of
transmission for L infantum when shared syringes act as
vehicles for infected monocytes.’ In this case, it is difficult to
give an explanation for the transmission route of this
trypanosomatid. Perhaps our patient contracted infection
from washing syringes in water contaminated with faeces of
M I Jiménez, R López-Vélez, R Molina, C Cañavate, *J Alvar
*Laboratorio de Rererencia de Leishmaniasis, Servicio de Parasitología, Centro
Nacional de Microbiología, Instituto de Salud Carlos III, 28220 Majadahonda,
Madrid, Spain; and Unidad de Medicina Tropical y Parasitología Clínica,
Servicio de Microblología, Hospital Ramón y Cajal, Madrid
1 Alvar J. Leishmaniasis and AIDS co-infection: the Spanish example.
Parasitol Today 1994; 10: 160-63.
2 Jiménez MI, Ferrer-Dufol M, Cañavate C, et al. Variability of
Leishmania (Leishmania) infantum among stocks from
immunocompromised, immunocompetent patients and dogs in Spain.
FEMS Microbiol Lett 1995; 131: 197-204.
3 Alvar J, Jiménez MI. Could infected drug-abusers act as potential
L (L) infantum reservoirs? Aids 1994; 8: 854.
Pseudomonas aeruginosa exotoxin A
antibodies in rapidly deteriorating chronic leg
SiR-Chronic leg ulcers are colonised with saprophytic
bacteria that do not influence ulcer healing, and routine
discouraged.’ However, we have seen some chronic leg
ulcers colonised with Pseudomonas aeruginosa enlarge despite
treatment. This opportunistic pathogen produces several
extracellular virulence factors. We determined the antibody
response to alkaline proteinase, elastase, and exotoxin A in
patients with ulcers colonised by P aeruginosa.
Ten consecutive patients with chronic venous leg ulcers
colonised by P aeruginosa were studied. Because of rapid
enlargement of their ulcer two patients (1 and 2, table) had
the leg ulcer excised and skin grafted. A contributing factor
for grafting in patient 1 was declining general health and
anaemia requiring blood transfusions; both conditions
improved after the graft. One young man (patient 3) was
only grafted for cosmetic reasons. P aeruginosa isolates were
typed by serogrouping and phagetyping with a panel of 12
0-group serum samples and 22 phages.3 Antibody titres
against alkaline proteinase, elastase, and exotoxin A were
(Mediagnost GmbH, Tubingen, Germany) in a blinded
All antibody titres against alkaline proteinase or elastase
were negative. Antibody titres against exotoxin A antibody
were positive in patients 1 and 2 and were negative in
patients 3-10 (table). The two patients with rapidly
enlarging ulcers necessitating skin grafts were the only
patients with raised values of antibody to exotoxin A. These
two patients had identical P aeruginosa strains (serotype 11,
*The cutoff value (800) of the exotoxin A ELISA was calculated from sera obtained
from cystic fibrosis patients with and without known P aeruginosa lung infection and
results are given as reciprocal antibody titres.
tYoung man grafted for cosmetic reasons.
Table: Exotoxin A antibody titres in sera of 10 patients with
chronic leg ulcers colonised by Pseudomonas aeruginosa
phagetype col 21 and phagetype 21/col 21, respectively),
whereas the remaining 8 patients were colonised by other
Histological examination of the removed ulcers revealed
rods in the thickened endothelium of the capillaries of the
vital granulation tissue in patients 1 and 2; no bacteria were
seen in patient 3. This suggests that ulcer deterioration was
caused by an invasion of P aeruginosa into the surrounding
tissue leading to ulcer enlargement and antibody formation.
Serum antibodies to exotoxin A were not related to ulcer size
or length of colonisation with P aeruginosa.
Since the majority of P aeruginosa strains contain the
exotoxin A gene, the results suggest that either patients 1
and 2 were infected with
overproducing exotoxin A in vivo, or that the deteriorating
clinical situation allowed enhanced exotoxin A production
leading to antibody formation. Many in vivo and in vitro
studies have demonstrated pathogenic effects of exotoxin A,
such as retardation of wound healing with restoration of
normal healing with exotoxin A antibodies.4 Recently,
increased expression of exotoxin A mRNA in patients with
cystic fibrosis chronically infected with P aeruginosa has been
found to correlate with severe lung function deterioration.5
The finding of exotoxin A serum antibodies in patients with
chronic leg ulcers, infected with P aeruginosa, may provide a
marker for ulcer deterioration, and may support the decision
for skin grafting.
a highly virulent strain
The Study Group on Pseudomonas aeruginosa and leg ulcers includes the
authors and N Hoiby, E Gutschik, and S M Madsen.
*L Danielsen, H Westh, E Balselv, V T Rosdahl, G Döring
Departments of *Dermatology, Clinical Microbiology and Pathology,
Bispebjerg Hospital, Copenhagen, DK-2400 Denmark, Clinical Microbiology
Rigshospitalet and Division of Microbiology, Statens Seruminstitut, Copenhagen;
and University of Tübingen, Germany
Hansson C, Hoborn J, Moller A, Swanbeck G. The microbial flora in
venous leg ulcers without clinical signs of infections. Repeated culture
using a validated standardised microbiological technique. Acta Derm
Venereol 1995; 75: 24-30.
Döring G, Maier M, Müller E, Bibi Z, Tümmler B, Kharazmi A.
Virulence factors of Pseudomonas aeruginosa. Antibiot Chemother 1987;
Høiby N, Rosendal K. Epidemiology of Pseudomonas aeruginosa
infection in patients treated at a cystic fibrosis centre.
Acta Pathol Microbiol Scand B 1980; 88: 125-31.
4 Heggers JP, Haydon S, Ko F, Hayward PG, Carp S, Robson MC.
Pseudomonas aeruginosa exotoxin A: its role in retardation of wound
healing. J Burn Care Rehab 1992; 13: 512-18.
5 Storey DG, Ujack EE, Mitchell I. Comparison of Pseudomonas
aeruginosa virulence factor expression to the clinical presentation of a
pediatric population of cystic fibrosis patients. Pediatric Pulmonol 1995;
suppl 12: A239.