Case Report / Kasuistik D. E. Greydanus, T. F. Smith, G. B. Stickler

Acute Encephalopathy with Liver Dysfunction, Chylous Ascites and Cytomegalovirus Infection Summary: A child with acute encephalopathy and liver dysfunction subsequently developed acute chylous ascites. Titers for cytomegalovirus increased from less than 1 ! 2 to 1 : 3 2 during the illness, and cytomegalovirus was isolated from the urine. This case is the first one possibly linking cytomegalovirus with acute encephalopathy and liver dysfunction in a child. In our patient, enlargement of the abdominal lymph nodes, as seen on a lymphangiogram, resulted in a severe obstruction of abdominal lymphatic flow, producing a transudation of lymph into the peritoneal cavity. The acute chylous ascites associated with mesenteric Iymphadenitis was likely caused by the cytomegalovirus infection.

A patient suffered acute e n e e p h a t o p a t h y with liver dysfunction. A f t e r the patient r e c o v e r e d rapidly f r o m this episode, acute chylous ascites developed, probably f r o m mesenteric lymphadenitis. Infection with cytomegalovirus was documented.

Report of a Case A 5-year-old girl had nausea, vomiting, and muscular pain 4 days before admission. Thirty-six hours before our evaluation, she had a temperature of 40.5 °C and vomited with increasing frequency; she rapidly became lethargic. On arrival, she had been semicomatose for the preceding 24 hours and reacted to painful stimuli only. Her temperature was 39.5 °C, and her weight was 19.5; kg. The liver was palpated 5 cm below the right costal margin, and the spleen was 2 cm below the left costal margin. The important laboratory findings are summarized in Table 1. Results of the liver function tests were abnormal. The level of blood ammonia was elevated to 48 /zg/dl, and the serum glucose level was 67 mg/dl. An electroencephalogram showed diffuse neuronal disturbance. Acute encephalopathy with liver dysfunction was diagnosed, and 10% glucose in water was given intravenously. Pronounced clinical improvement was noted within 24 hours; the patient was alert and oriented 48 hours after admission. Transfusions were not necessary. Another electroencephalogram done 36 hours after hospitalization demonstrated significant improvement (Table 1). The serum titer to cytomegalovirus using the complement-fixation test was less than 1 : 2 . When dismissed on the eighth hospital day (or the 12th day of illness), she weighed 19.5 kg. She was seen seven days later (on the 19th day of illness) and was doing well. Her weight had remained at 19.5 kg, the liver was 2 cm below the fight costal margin, and the spleen was 1 cm below the left costal margin. On the 23rd day of illness, the patient experienced anorexia, mild abdominal pain, and swelling under the eyes. On the 25th day of illness, there was severe abdominal distention, and the patient was rehospitalized. At this time, she was alert but

Zusammenfassung: Akute Enzephatopathie mit Leberdysfunktion, chyI6sem Aszites und Zytomegatie-Virusinfektion. Ein Kind mit akuter Enzephalopathie und Leberdysfunktion entwickelte allmghlich einen chyliSsen Aszites. Die Titer fiir das Zytomegalievirus stiegen yon weniger als 1 : 2 bis 1 : 32 wiihrend der Erkrankung an; Zytomegalievirus wurde aus dem Urin isoliert. Dieser Fall ist m/Sgticherweise der erste, bei dem in Verbindung mit dem Zytomegalievirus eine akute Enzephalopathie und Leberdysfunktion bei einem Kind auftraten. Bei unserem Patienten kam es zu einer Vergr6gerung der abdominellen Lymphknoten- dargesteIlt mit Hilfe eines Lymphangiogramms - , so dab sic in einer schweren Obstruktion des abdominellen Lymphabflusses resultierte und dadurch eine Transsudation der Lymphe in den Peritonealraum bewirkte. Der akute chyRise Aszites, verbunden mit der Mesenteriallymphadenitis, war wahrscheinlich durch das Zytomegalievirus verursacht. uncomfortable because of her enlarged abdomen. Her weight was 22 kg. Severe periorbital edema and pitting pedal edema were noted, in addition to the abdominal distention. Results of liver function tests were normal; the levels of total protein and albumin were low (Table 1). Abdominal paracentesis revealed a milky fluid that contained lipids in the chylomicron form, specifically resembling lymph. The cholesterol level was 11 mg/dl, level of triglycerides 88 mg/dl, protein 0.266 g/dl, and specific gravity 1.01.7. Cultures for acid-fast bacilli, general bacteria, and anaerobes were negative. A lymphangiogram done on the seventh hospital day (or 32nd day of illness) showed enlarged lymph nodes from T-12 to L-4. The cytomegalovirus complement-fixation titer on the 25th day of illness was 1 : 16. The diagnosis at this time was acute chylous ascites probably due to mesenteric lymphadenitis. The edematous state gradually resolved. No specific treatment was given, and she was dismissed eight days after admission, on the 33rd day of illness. Her weight was 20 kg. The patient was seen on the 41st day of illness and was doing well. She had no evidence of periorbital swelling or of ascitic fluid. Her weight was 20.5 kg. The level of total protein had increased to 6.16 g/dl and the albumin level to 2.83 g/dl. The cytomegalovirus complement-fixation titer was 1 : 3 2 , and the virus was isolated from a urine sample by use of WI-38 (human embryonic lung) cell cultures.

Discussion Our patient had evidence of acute e n c e p h a l o p a t h y w i t h liver dysfunction, followed by acute chylous ascites. W h e t h e r this liver dysfunction represented R e y e - J o h n s o n

Received: 4 JuIy 1977 Dr. D. E. Greydanus, Dr. T. F. Smith, Dr. G. B. Stickler, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, Minn., 55901, USA. Reprints: Dr. G. B. Stickler.

Infection 5 (t977) Nr, 4

255

D. E. Greydanus, T. F. Smith, G. B. Stickler: Acute Encephalopathy, Liver Dysfunction and Chylous Ascites

Table 1: Laboratory data on a patient with acute encephalopathy associated with liver dysfunction, chylous ascites, and cytomegalovirus infection.

Day of illness 5* Peripheral smear

Bilirubin (mg/dl) direct indirect SGOT (IUJL) Prothrombin time (sec) (normal 10-12 sec) Serum protein (g/dl) Serum albumin (g/dl) CMV titer Isolation of CMV (urine)

6

7**

41

abundant atypical lymphocytes

abundant atypical lymphocytes 1.5 0.5 2,764

1,296

15.9

13.4

-~1:2

25***

-

-

150

normal

3.17 1.64 1:16 -

normal

6.16 2.83 1:32 pos.

* Day 5: normal hemoglobin and lumbar puncture; negative Australia antigen, heterophil titer, direct Coombs' test, and leptospirosis titer; negative bacterial cultures from blood, spinal fluid, urine, and stool; negative viral cultures from throat and stool. ** Day 7: negative heterophil titer. *** Day 25: normal hemoglobin and immunoglobulins and negative 24-hour urine collection for protein. syndrome (1) or a variant (2) is not clear because liver biopsy was not done. Cytomegalovirus has not been considered to be a cause of acute encephalopathy with liver dysfunction, but its isolation in our patient indicates that this important member of the herpes virus family might be included in the list of causes. Since serum was not analyzed specifically for hepatitis A or B viruses, adenovirus, or Epstein-Barr virus, our patient also may have had hepatic inflammation due to one of these agents. Congenital cytomegalovirus infections associated with chronic intrauterine encephalitis and subsequent neonatal and infantile neurologic sequelae are well known (3). Our case may be an unusual one of acquired cytomegatovirus infection and encephalopathy. Yet there is ample documentation for acquired cytomegalovirus infection and liver inflammation (4, 5, 6). Cytomegalovirus mononucleosis (7) has been associated with atypical lymphocytosis, abnormal liver function test results, and splenomegaly. A patient with cytomegalovirus mononucleosis can clinically resemble a patient with infectious or serum hepatitis. Indeed, our patient may have had cytomegalovirus mononucleosis complicated by encephalopathy. This possible association of neurologic and hepatic dysfunction with cytomegalovirus infection is very unusual. The additional development of acute chylous ascites due to cytomegalovirus in this five-year-old girl is unique. A survey of the literature reveals only two other patients (8, 9) with acute chylous ascRes and documented cytomegalovirus infection; both of these patients were in-, fants. Chylous ascites is the presence of lymphatic fluid in the peritoneal cavity. It is usually diagnosed after paracente-

256

Infection 5 (1977) Nr. 4

sis reveals a milky fluid that is alkaline and contains lymphocytes. This fluid may have a fat content greater than that in serum and a protein content less than that in serum (I0). This fat content may be much less if the chylous ascites is the result of a transudation of fluid through the lymphatic walls. Disruption of abdominal lymphatic flow results in acute Chylous ascites. Vasko and Tapper (11) reviewed a series of 59 children with acute chylous ascites. They noted congenital anomalies, including stenosis of lymphatic vessels, mesenteric cysts, and gastrointestinal tract malrotation in 23 patients. Five suffered trauma, that is, rupture of the thoracic duct or lymphatic structures secondary to external trauma or to the laceration of the thoracic duct at surgery. They also found 2 patients with neoplasms, 20 with idiopathic causes, and 9 with inflammatory causes (peritoneal adhesions, cirrhosis, tuberculosis, and lymphadenitis). Boysen (12) discussed traumatic chylous ascites as part of the battered child syndrome. In contrast to that in adults, neoplasms are very rare causes of acute chylous ascites in children, and sporadic case reports have included a hemangiolymphangioma (11), cystic lymphangiomatosis (13), and an unspecified abdominal neoplasm (11). Obstruction of lymphatic vessels in fitariasis and schistosomiasis also has been reported (10). Another unusual cause of acute chylous ascites in children is obstruction of abdominal lymphatic vessels, often associated with mesenteric lymphadenitis. Although Huber and Silver (14) were the first to describe a child with chylous ascites and enlarged abdominal lymph nodes, it was Davis (15), in 1939, who clearly asserted that chylous

D. E. Greydanus, T. F. Smith, G. B. Stickler: Acute Encephalopathy, Liver Dysfunction and Chylous Ascites

ascites could be the result of mesenteric lymphadenitis. In 1955, KuykendalI and Dederer (16) described a tenday-old infant who had chylous ascites. They discussed the mechanism of its production from obstructed lymphatic vessels. Sanchez et al. (13) injected Evans blue dye into an enlarged lymph node in a patient with chylous ascites and traced the course of the dye into the peritoneal cavity. Whittlesey et al. (17) and Volnohradsky (18) also have published descriptions of pediatric patients who had acute chylous ascites associated with obstructed abdominal lymphatic vessels. We assume that the enlarged mesenteric lymph nodes in our patient obstructed abdominal lymph flow, thus producing a transudation of lymph through the abdominal lymphatic wails and causing the abdominal distention. This loss of protein resulted in periorbital swelling and pedal edema. The presence of the hyperplastic nodes was demonstrated on the lymphangiogram. Although cytomegalovirus infection associated with chylous ascites in infancy has been rarely described (8, 9), our case is the only known one in which a specific viral cause has been suggested for acute chylous ascites in a child. When the abdominal distention was noticed, the cytomegalovirus complement-fixation titer had increased from less than 1 : 2 to 1 : 16. Two and a half weeks later, when the chylous ascites had subsided, the titer was 1 : 32, and the virus was isolated from the urine. The temporal association of increasing complement-fixation titers with the recovery of the virus indicated that the infection did not represent random cytomegalovirus excretion. Although possible, infection probably was not hospitalacquired. Whether or not our patient had a congenital weakness of the lymphatic walls, which contributed to the development of transudation under pressure from obstruction, is not known. Most children with mesenteric lymphadenitis do not develop acute chylous ascites, and a congenital weakness of the lymphatic walls, along with obstructed lymphatic flow, m a y be necessary for this unusual disorder to develop. Also, the protein loss may have been due to a proteinlosing gastroenteropathy, as reported in M~n~trier's disease (19, 20). Increasing cytomegalovirus titers have been noted in this very rare disease of childhood, but the virus has never been isolated (21). Contrast studies, gastric biopsy, or labeled protein studies were not done in our patient to rule out the possibility of this rare condition. Yet we believe that the enlarged lymph nodes were the main factor in the development of the ascitic fluid. In any event, the association of acute chylous ascites and cytomegalovirus infection seems more firmly established. We also do not believe that this was a traumatic condition. Although chylous pleural effusion has been associated with thoracic duct injury (22), there was no instrumentation in our patient that could have produced this condition. Transfusions were not given, and thus this was not a possible mode of viral transmission in this case.

The prognosis in acute chylous ascites not associated with trauma or congenital anomalies is excellent (23). The course is self-limited. The diagnosis rarely can be made before paracentesis. A lymphangiogram may demonstrate enlarged lymph nodes, but lymphangiography probably is not warranted in small children because general anesthesia is required. A radionuclide lymphangiogram might be done in these cases (24). The need for laparotomy is determined by the underlying cause and clinical course. Generally, because the condition is benign, surgery should not be done when there is associated mesenteric lymphadenitis. Conservative treatment is recommended, and this includes a high-protein, low-fat diet, supplemented with medium-chain triglycerides. Intravenous hyperalimentation m a y be necessary. Sanchez et al. (13) have outlined the indications for surgery in the presence of chylous ascites. Literature 1. Johnson, G. M., Scurletis, T. D., Carroll, N. B.: A study of sixteen fatal cases of encephalitis-like disease in North Carolina children. N. Carolina Med. J. 24 (1963) 464-473. 2. Haller, J. S.: The enigmatic encephalopathy of Reye's sy~adrome. Hosp. Pract. 10 (1975) 91-99. 3. Hanshaw, J. B.: Cytomegalovirus infection and cerebral dysfunction. Hosp. Pract. 5 (1970) 111-120. 4. Carter, A. R.: Cytomegalovirus disease presenting as hepatitis. Brit. reed. J. 3 (1968) 786. 5. Hanshaw, J. B., Betts, R. F., Simon, G., Boynton, R. C.: Acquired cytomegalovirus infection: Association with hepatomegaly and abnormal liver-function tests. N. Engl. J. Med. 272 (1965) 602-609. 6. Weller, T. H.: The cytomegaloviruses: Ubiquitous agents with protean clinical manifestations: Parts I and II. N. Engl. J. Med. 285 (1971) 203-214; 267-274. 7. Lamb, S. G., Stern, H.: Cytomegalovirus mononucleosis with jaundice as presenting sign. Lancet 2 (1966) 1003-1006. 8. Frank, D. J., DeVaux, IV. D., Perkins, J. R., Perrin, E. V.: Fetal ascites and cytomegalic inclusion disease. Amer. J. Dis. Child. 112 (1966) 604-607. 9. Andersen, F. U.: KylCs ascites hosbcirn: Et tilfaelde hos et spaedbarn reed lever og miltsvulst, mesenterialadenit og samtidig cytomegalovirus-infektion. Ugeskr. Laeger 132 (1970) 1391-1393. 10. Kelley, M. L., Butt, H. R.: ChyIous ascites: An analysis of its etioIogy. Gastroenterology 39 (1960) 161-170. 11. Vasko, J. S., Tapper, R. I.: The surgical significance of chylous ascites. Arch. Surg. 95 (1967) 355-368. 12. Boysen, B. E.: Chylous ascites: Manifestation of the battered child syndrome. Amer. J. Dis. Child. 129 (1975) 1338-1339. 13. Sanchez, R. E., Mahour, G. H., Brennan, L. P., Woolley, M. M.: Chylous ascites in children. Surgery 69 (1971) 183-188. 14. Huber, F., Silver, H. M.: A case of acute chylous ascites (non-fatty, pseudochylous, lactescent or milky type) in a boy eight years old. Amer. J. Dis. Child. 8 (1914) 50-57. 15. Davis, N. P.: Chyle ascites and other disturbances of the chyle system. Pa. Med. J. 43 (1939) 142-144. 16. Kuykendall, S. J., Dederer, A.: Acute chylous ascites in infancy: Report of case in which the cause was mesenteric lymphadenitis. Surgery 38 (1955) 738-740.

Infection 5 (1977) Nr. 4

257

D. E. Greydanus, T. F. Smith, G. B. Stickler: Acute Encephalopathy, Liver Dysfunction and Chylous Ascites 17. Whittlesey, R. H., lngram, P. R., Riker, W. L.: Chylous ascites in childhood: Report of five cases. Ann. Surg. 142 (1955) 1013-1020. 18. Volnohradskj, R. T.: Akute chyl6se Peritonitis in Verbindung mit der Lymphadenitis mesenterialis. Bruns. Beitr. klin. Chir. 221 (1974) 531-534. 19. Pittman, F. E., Harris, R. C., Barker, H. G.: Transient edema and hypoproteinemia: Possible Menetrier's disease. Amer. J. Dis. Child. 108 (1964) 189-197. 20. Sandberg, D. H.: Hypertrophic gastropathy (Menetrier's disease) in childhood. J. Pediatr. 78 (1971) 866-868.

21. Leonidas, J. C., Beatty, E. C., Wenner, H. A.: M6n6trier disease and cytomegalovirus infection in childhood. Amer. J. Dis. Child. 126 (1973) 806-808. 22. Khalil, K. G., Parker, F. B., Jr., Mukher]ee, N., Webb, W. R.: Thoracic duct injury: A complication of jugular vein catheterization J. Amer. reed. Ass. 221 (1972) 908-909. 23. Dreznik, Z., Dinbar, A., Wolfstein, L, Tulcinsky, D. B.: Acute chylous peritonitis: A case report with a review of the literature. Isr. J. Med. Sci. 9 (1973) 89-91. 24. Gates, G. F., Dore, E. K., Kanchanapoom, V.: Thoracic duct leakage in neonatal chytothorax visualized by *98Au lymphangiography. Radiology 105 (1972) 619-620.

impressum SchriftIeitung: Prof. Dr. med. Walter Marget (Editor-in-Chief), Prof. Dr. reed. Werner Lang (Editor), Daryl Elder (Editorial Assistant) Universitiits-Kinderklinik, Lindwurmstrage 4, D-8000 Miinchen 2, Telefon O 89) 53 47 33. Herausgeber: R. Ackermann, K6tn, BRD • Alexander, Berlin, BRD • E. Holzer, Miinchen, BRD - G. MSssner, Freiburg, BRD • H. Stickl, Miinchen, BRD. Europiiischer Beirat: L. Binder, Budapest, U n g a r n • J. Bc~e, Bergen, Norwegen - W. Brumfitt, London, G B . G. R. Burgio, Pavia, Italien • F. Daschner, Freiburg, BRD . F. Deinhardt, Miinchen, BRD • J. Drews, Wien, Osterreich - M. Duniewicz, Prag, Tschechoslowakei • D. Frommel, Bic~tre, Frankreich • R. van Furth, Leiden, Niederlande • E. Haefliger, Wald, Schweiz • M. yon Hattingberg, GiefSen, BRD • H. Hirsch, Tiibingen, BRD • F. O. H/Srig, Berlin, BRD . M. Just, Basel, Schweiz • B. Kassur, Warschau, Polen • W. Knapp, Erlangen, B R D . H. Knothe, Frankfurt, BRD • G. Linzenmeier, Essen., BRD • T. Luthardt, Freiburg, BRD • G. Marinescu, Bukarest, Rum:in i e n . H. yon Oldershausen, Friedrichshafeu, B R D . H. Pohle, Berlin, BRD - D. S. Reeves, Bristol, G B . G. Regamey, Genf, Schweiz • R. A. Shooter, London, GB • W. Siegenthaler, Ztirich, Schweiz • R. Skalova, Zagreb, Jugoslawien . D. Tyrrell, Harrow, GB • O. Vivell, Karlsruhe, BRD • T. Wegmann, St. Gallen, Schweiz • I. D. Williams, London, GB . E. Yourassowsky, Brfissel, Belgien. (Ibersee-Beirat: M. Barza, Boston, Mass., USA • P. S. Brachmann, Atlanta, Ga., USA - W. A. Craig, Madison, Wisc., USA • R. Deibel, Albany, N.Y., USA • L. Falk, Chicago, Ill., U S A . S. Finegold, Los Angeles, Calif., USA • M. Finland, Boston, Mass., USA • S. P. Gotoff, Chicago, Ill., USA • A. yon Graevenitz, New Haven, Conn., USA • K. Hummeler, Philadelphia, Pa., U S A - G. G. Jackson, Chicago, Ill., USA • E.H. Kass, Boston,, Mass., USA • R. Kretschmer, Chicago, Ill., U S A • E. H. Lennette, Berkeley, Calif., U S A - P. O. Madsen, Wise., USA - W. McCabe, Boston, Mass., U S A • E. Neter, Buffalo, N.Y., USA • H. C. Neu, New York, N.Y. U S A • P. G. Quie, Minneapolis, Minn., USA . L. D. Sabath, Minneapolis, Minn., USA - G. M. Savage, Tuckahoe, N.Y., U S A . M. F. Sl:affer, Newark, N. J., USA • A Todd Davis, Chicago, Itl., U S A . M. Turck, Seattle, Wash., USA.

Anzeigenverwaltung: Deutscher 14~zte-Verlag G m b H , Postfach 400 440, Dieselstr. 2, 5000 KSln 40, Tel. (0 22 34) 70 11-2 17, Telex 889 168. 7_, Z. gilt Anzeigenpreisliste Nr. 4a. AnzeigenschluB: 4 Wochen vor Erscheinen. Anzeigenleiter: Eugen Volkert. Verantwortlich ftir den Anzeigenteil: Olaf Borchert.

Abonnement: Bestellung beim Verlag, bei ]edem Postamt, beim Buch- und Zeitschriftenhandel. Bezugszeit: Das Abonnement gilt zun:ichst fiir das laufende Kalenderjahr. Es verl:ingert sich u m jeweils ein Kalenderjahr, wenn eine Ktindigung nicht bis 30. September im Verlag vorliegt. A u f n a h m e in Lesezirkel nur mit Zustimmung des Verlages. Bei h f h e r e r Gewalt besteht kein Anspruch auf Ersatz.

Erscheinungsweise: I N F E C T I O N erscheint vorerst vierteljahrlich. Vier Hefte bilden einen Band. Supplementhefte (erscheinen unregelm~il3ig) sind im A b o n n e m e n t enthalten. Bezugspreise: Einzelheft D M 39,- q- Porto. Jahresbezugspreis D M 125,- q- Porto; Vorzugspreis ]iir Mitglieder yon Gesellschaften, deren offizielles Organ die Zeitschrift ist, D M 100,+ Porto. Versandkosten Inland D M 9,-, Ausland D M 12,-. Luftpostzuschlag extra. Einbanddecke D M 15,-. Konten: Postscheck-Konto Miinehen 4134-805 und Bayer. Hypotheken- und Wechsel-Bank, Miinchen, Konto 3180088775. Druck: Gebr. Parcus KG, Buchdruckerei und Verlagsanstalt, Postfach 92, 8000 Mtinchen 34. Gerichtsstand und Erfiillungsort: M/inchen. Der Verlag behiilt sich das ausschliel31iche Recht der Verbreitung, 13bersetzung und jeglicher Wiedergabe auch yon Teilen dieser Zeitschrift durch Naehdruek, Fotokopie, Mikroverfahren USW. v o r .

Blumenstrage 48, 8000 Miinchen 2, Telefon: (0 89) 2 60 40 88. VerantwortIich fiir den InhaIt: Professor Dr. med. Walter Marget u n d Professor Dr. reed. Werner Lung, beide Miinchen.

Fiir unverlangt eingesandte Manuskripte wird keine Gewiihr iibernommen. Mit Namen, Initialen oder Pseudonym gezeichnete Artikel steUen die Meinung des Verfassers, nicht aber in jedem Fall die der Redaktion dar. Das Fotokopieren aus ,,Infection" ist n u t mit ausdriicklicher Genehmigung des VerIages gestattet. Sie gilt als erteilt, wenu jedes Fotokopierblatt mit einer 50-Pf-Wertmarke versehen wird, die yon tier Inkassostelle ftir Fotokopiergebiihren, GroBer Hirschgraben 17-19, 6000 Frankfurt/M. 1, zu beziehen ist. Sonstige MiSglichkeiten ergeben sich aus dem R a h m e n a b k o m m e n zwischen dem Btirsenverein des Deutschen Buchhandels und dem Bundesverband der Deutschen Industrie vom 14. 6. 1958. Mit der Einsendung yon Beitfggen iibertr:igt der Verfasser dem Verlag auch das Recht, die Genehmigung zum Fotokopieren gem:ig diesem R a h m e n a b k o m m e n zu erteilen.

Inhaber und Beteiligungsverhiiltnisse: Pers6nlich haftender Gesellschafter Dr. Ulrich Wechsler und Bertelsmann-Thomson Fachverlag GmbH.

,,Infection" ist offizieltes Organ der Paul-Ehrlich-Gesellschaft, Frankfurt/M. und der Deutschen GeselIschaft fiir InfektioIogie, Miinchen.

Verlag: Verlagsgeseltschaft Otto Spatz OHG, Postfach 20 23 40,

258

Infection 5 (1977) Nr, 4