A cell wall complex has been isolated by gentle methods from both the medium supernatant fluid and whole organisms of Neissieria meningitidis cultures. The two types of preparations have been shown to be essentially identical on the basis of chemical composition, electron microscopy, and polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate (SDS-PAGE). Four major components were identified in the complex: group-specific polysaccharide (4 to 10%), protein (45 to 65%), lipopolysaccharide (10 to 25O), and lipid (15 to 30%). The whole complex was found to be immunogenic in rabbits and to elicit production of antibody directed against the protein, the group-specific polysaccharide, and the lipopolysaccharide components. The isolated protein component was also found to be immunogenic in rabbits and to elicit production of serotype-specific antibody. The protein component was found to produce a band pattern in SDS-PAGE that is simple, reproducible, and strain dependent. The lipopolysaccharide component was found to have chemical and biological properties characteristic of bacterial endotoxin. We propose that this complex is representative of the outer trilaminar membrane of the meningococcal cell envelope in its native state.

An electron microscopic study was conducted to explore the interaction between normal guinea pig peritoneal macrophages and phase I and II Coxeilla burnetii previously treated with either normal or immune serum. A comparison was made on the efficiency of phagocytosis and subsequent killing of rickettsiae by macrophages. Both phases of rickettsiae previously treated with normal serum multiplied within phagosomes after phagocytosis with resultant destruction of macrophages. In contrast, suspending rickettsiae in immune serum rendered them more susceptible to phagocytosis and potentiated their destruction within macrophages.

The interaction between Coxiella burnetii and peritoneal macrophages obtained from immune guinea pigs was studied by transmission electron microscopy. Phagocytosis and subsequent fate of ingested phase I and II rickettsiae were compared. Phase I rickettsiae were more resistant to phagocytosis than were phase II organisms. Macrophages from phase Iand II-immunized animals were equally capable of phagocytizing rickettsiae. Phase I and II rickettsiae previously treated with normal serum multiplied and destroyed macrophages from guinea pigs that had been immunized with phase II rickettsiae. Phase II organisms were initially suppressed in macrophages from phase I-immunized animals, but eventually multiplied in these cells. In contrast, only phase I organims were destroyed by macrophages from phase I-immunized animals. Treatment of rickettsiae with immune serum enhanced ingestion by macrophages and potentiated the destruction of organisms by both types of macrophages. The macrophage migration inhibition assay was performed on peritoneal exudate cells from immune animals. Migration of peritoneal macrophages from phase I-immunized guinea pigs was inhibited, whereas macrophages from phase II-immunized animals migrated when cells were cultured in the presence of killed, intact phase I or II C. burnetii. MATERIALS AND METHODSPreparation of rickettsial stock suspension. The third egg passage of the Henzerling strain of C. burnetii in phase I and the 88th egg passage of the 601 on July 16, 2020 by guest http://iai.asm.org/ Downloaded from

A patient with acute myelomonocytic leukemia and multiple myeloma occurring simultaneously prior to initiation of chemotherapy is described. Possible mechanisms for this occurrence are discussed.Cancer 41:1381-1386, 1978. EVERAL INVESTIGATORS HAVE DESCRIBED T H ES development of acute myelomonocytic leukemia in patients with multiple myeloma.8~9~'0~'9 I n general, these have been patients w h o have undergone long-term chemotherapy with alkylating agents prior t o t h e development of t h e leukemia. It h a s been postulated i n these cases that chemotherapy h a d a leukemogenic effect or acted a s an immunosuppressant allowing t h e establishment of a malignant clone of cells. R a r e cases of t h e simultaneous occurrence of t h e two diseases have been reported. 1 6 3 2 0~2 3 W e describe a patient in w h o m well-documented acute myelomonocytic leukemia a n d multiple myeloma were simultaneously present prior t o the initiation of Chemotherapy. Included are electron microscopic and chromosomal findings. Postulated mechanisms of this simultaneous occurrence are discussed. CASE REPORTMSL, a 64-year-old white male first seen in May 1976, related a one-month history of increasing fatigue, low-grade fever, and anorexia, but no adenopathy or bleeding. Five years previously he had a partial gastrectomy for peptic ulcer disease. O n examination, there was no lymphadenopathy or hepatosplenomegaly. tion was evident on the peripheral smear. The platelet count was 208,000. Examination of the bone marrow smear showed a marked increase in cellularity with slight decrease in megakaryocytes. There was myeloid and myelomonocytoid hyperplasia with 25 percent blast forms. There was an increase in plasma cells of five to ten percent, some of which were primitive, multinucleated and in clusters (Figs. 1, 2). A diagnosis of myelomonocytic leukemia was made. Because the platelet and peripheral granulocyte counts were adequate, no treatment was initiated.Ten weeks later, with increasing symptomatology, increasing white-cell count to 105,000, and a decreasing platelet count of 46,000, the patient was admitted for initiation of chemotherapy with cystosine-arabinside by continuous infusion for seven days and daunomycin iv push for three days. The only positive physical finding at that time was a liver palpable two centimeters below the right costal margin. The serum muramidase was 117 mg/ml (normal 7-15 mg/ml), and the urine muramidase was 31 mg/ml (normal less than 2 mg/ml). Serum protein electrophoresis revealed the following: total protein 6.6, albumin 2.95, alpha-1 globulin 0.25, alpha-2 globulin 0.61, beta globulin 2.15, and gamma globulin 0.63, with a monoclonal spike in the beta region. Quantitative immunoglobulin levels showed IgG 720, IgA 2,550, IgM 22. There was an abnormal preciptin arc for IgA kappa paraprotein in both serum and urine. The urine was negative for Bence Jones protein. A bone marrow smear one week following chemotherapy showed normal cellularity with a marked decrease in megakaryocyte and erythroid activity. ...