445 of the 20 cases of sporadic NANBH and in 3 of the 113 cases of type A hepatitis. In contrast 4 cases of severe hepatitis were observed in the 38 patients with post-transfusion NANBH (data not
only 1 in
table).
An unexplained high case fatality rate in epidemic NANBH has been reported in pregnant women. Fortunately, we have not seen any instance of NANBH associated with shellfish consumption during pregnancy. We have never observed chronic evolution in a patient with sporadic NANBH or type A hepatitis associated with
faecal-oral spread. By contrast chronic hepatitis was histologically confirmed in 16 (42%) of the 38 patients with post-transfusion NANBH. These observations support the hypothesis that NANBH associated with shellfish consumption may be sporadic cases of epidemic waterborne NANBH. Immunological and virological confirmation will be possible only when specific, reliable, and reproducible diagnostic tests are available. FRANCESCO CAREDDA SPINELLO ANTINORI TIZIANA RE CARLA PASTECCHIA CLAUDIO ZAVAGLIA MAURO MORONI
Infectious Diseases Clinic,
University of Milan, Ospedale L Sacco, 20157 Milan, Italy
1. Tabor E. The three viruses of non-A, non-B hepatitis. Lancet 1985; i: 743-45. 2. Caredda F, d’Arminio Monforte A, Rossi E, Lopez S, Moroni M Non-A, non-B
hepatitis in Milan. 3 Khuroo MS.
human
Lancet
1981;
ii:
section,
TR 1-5 s, TE 28 ms,
on
Note the patchy bilateral reduction of resonance region and white matter.
day 9.
intensity in the thalamic
48.
Study of an epidemic of non-A,
non-B hepatitis. Possibility of another hepatitis virus distinct from post-transfusion non-A, non-B type. Am J Med
NMR STUDIES IN THALAMIC-STRIATAL NECROSIS
SiR,-Dr Trounce and colleagues (Jan 26, p 160) have drawn attention to a new clinical disorder-thalamic haemorrhage in the newborn. In their patients the underlying pathophysiology remained unclear, but earlier reportsl-3and the discussion of their communication (March 16, p 635; April 6, p 823) indicate that
haemorrhage
or
haemorrhage
secondary
to
anoxic/ischaemic injury of the thalamus are important disorders in term infants. We have recently followed up with NMR scans one of the three term neonates whose ultrasound, cranial computed tomograms, and necropsy findings showed bithalamic haemorrhage and/or necrosis. The 2660 g boy was delivered by caesarean section at 37 weeks of gestation because of abnormalities in fetal heart rate. Apgar scores were 1 and 2 at 1 and 5 min after birth, and pH was 7 16. 6 h later the child was transferred to our intensive-care unit with respiratory insufficiency. Muscle tone was flaccid, the pupils small but reactive to light, and the anterior fontanelle was tense. Despite prompt restoration of blood gases to normal after the start of artificial ventilation the child had strabismus divergens, diminished arousal reaction, tonic-clonic seizures, and inadequate antidiuretichormone secretion during the first week of life. He died after 6 weeks. On day 3 cranial ultrasound showed slit-like ventricles suggestive of brain oedema. 6 days later, we observed striking bilateral echodensity of brainstem, thalamus, nucleus caudatus, and striatum. The coronal sections showed a bulb-like formation due to a separation of the hyperechoic thalamus and striatum by a hypoechoic band of tissue, presumably the internal capsule. NMR imaging with a 0 - 35tesla supraconductive imaging system on day 9 revealed decreased resonance intensity of the thalamus and basal ganglia as well as of the entire white matter, while the internal capsule showed intense resonance. A NMR follow-up study on day 24 revealed leucomalacia of the whole white matter. The thalamic and striatal tissue had become similar in resonance to the dissolving white matter, while the structures of the internal capsule were still distinct in their high resonance intensity. Unlike the patients reported so far, our patient showed no evidence of haemorrhage, although we think that the pattern of his thalamic-striatal damage is similar to that found in the other patients. Furthermore, the bulb-like distribution of the tissue damage, sparing the internal capsule, and the accompanying
of
large
et
al,l
areas of the brain, accord with the findings of Donn et al,2 and Kreusser et awl. We want to emphasise that all of our three patients as well as those reported by the other three groups underwent a period of partial (intrauterine) asphyxia, then a period of total asphyxia. This may be of considerable aetiological importance, because in a comparable animal model basal ganglia injury has been observed only in rhesus monkeys subjected to a "partial plus total asphyxia" model and not in those animals who had total asphyxia alone. We cannot explain why in our patient, as in all but one of the patients reported so far, the sonographic detection of the thalamic damage was delayed until 4 to 14 days after the hypoxic period. It must therefore be asked which biochemical mechanisms could lead to a perpetuation or even exacerbation of the initial ischaemic insult, and how these mechanisms could be counteracted by therapeutic
damage Kotagal
1980, 68: 818-24.
primary
NMR coronal
measures.
Department of Pediatrics, University of Dusseldorf, and Institute of Radiology, Grafenberger Allee 63, D 4000 1.
Dusseldorf, FRG
THOMAS VOIT PETER LEMBURG WOLFGANG STORK
Kotagal S, Toce S, Kotagal P, Archer C. Symmetric bithalamic and striatal hemorrhage following perinatal hypoxia m a term infant J Comput Assist Tomography 1983; 7:
353-55.
SM, Bowerman RA, DiPietro MA, Gebraski SS. Sonographic appearance of neonatal thalamic-striatal hemorrhage J Ultrasound Med 1984; 3: 231-34. 3. Kreusser KL, Schmidt RE, Shackelford GD, Volpe JJ Value of ultrasound for identification of acute hemorrhagic necrosis of thalamus and basal ganglia in an asphyxiated term infant. Ann Neurol 1984; 16: 361-63 4. Myers RE Four patterns of perinatal brain damage and their conditions of occurrence in primates. Adv Neurol 1975; 10: 223-34. 2 Donn
FAECAL CARRIAGE OF METHICILLIN-RESISTANT STAPHYLOCOCCI a!R,—Dr Waish and colleagues (july 21, p 21’:1) may well be that the epidemiological importance of faecal carriage of methicillin-resistant Staphylococcus aureus (MRSA), in the absence of nasal carriage, has been underestimated. In a study of nasal and faecal carriage of S aureus in infants with and without Escherichia coli enteritis, we found a significantly higher carriage rate of both antibiotic sensitive staphylococci and MRSA amongst infants with enteritis.] Moreover, these infants carried S azireus in far greater numbers in the faeces when compared with matched controls without enteritis. Phage typing of nasal and faecal strains indicated that these were often dissimilar. correct