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A 60-year-old Native American diabetic female patient had a history of nine episodes of peritonitis (both relapsing and persistent) during the year that she was treated with continuous ambulatory peritoneal dialysis (CAPD). At the start of CAPD the patient had an inverted CD4 to CD8 ratio that decreased from 0.97 to 0.50 in 1 year. This finding was due to a decrease in CD4+ cells and an increase in CD8+ cells that were also positive for CD57 (Leu-7) and HLA-DR (Ia) antigen, suggesting a state of activation. The serology indicated a cytomegalovirus immunoglobulin G titer of 1:2,048. The patient also had significantly increased natural killer cells. These alterations suggest the presence of a chronic viral infection that may have caused the patient to be immunosuppressed, thereby predisposing her to repeated episodes of peritonitis.

Features helpful in diagnosis and associated with death were evaluated in 26 episodes of peritonitis associated with intra-abdominal pathology (IAP) in continuous ambulatory peritoneal dialysis (CAPD) patients. Culture of multiple enteric pathogens, or of a single unusual enteric pathogen, from the dialysate was useful for diagnosis in 22/26 instances. Other diagnostic features (fecal material in dialysate, diarrhea containing dialysate, increasing free air in the abdominal cavity) were infrequently found. A comparison of patients who died (n = 11, 42%) and those who survived revealed that death was associated with bowel gangrene (5/6 died), recovery of bacteroides from the dialysate, more frequent and severe comorbid conditions (bacteremia, pneumonia, intra-abdominal and intracerebral bleeding, septic shock, hepatic failure), the development of severe malnutrition and thrombocytopenia during infection, and multiple surgical procedures until the diagnosis was established. Peritonitis associated with intra-abdominal pathology in CAPD patients is a severe infection with considerable diagnostic difficulty and high mortality. Early exploratory laparotomy upon suspicion of the nature of the peritonitis, usually raised by the recovery of enteric pathogens from the dialysate, may improve mortality.

In June, 36 lizards (males and females) were injected with 0.01, 0.1, 1.0, 10.0, or 100 mg/kg of MIF-I, or the diluent vehicle, and placed in a cage for ten minutes. Tonic immobility (TI) was then induced on an open lab table. All doses of MIF-I significantly reduced TI duration as compared to the duration with the diluent alone. In subsequent experiments lizards were injected with 0.1 mg/kg of MIF-I, 0.1 mg/kg of naloxone, or the diluent vehicle, and placed in small aquaria for ten minutes. TI was then induced in the small aquaria. In July, using 60 females, MIF-I and naloxone slightly reduced the duration of TI, but not significantly, and overall TI durations were reduced as compared with the first experiment possibly because the lizards could escape from the view of the experimenter in the corners of the aquaria. A third experiment was done in late September and early October with 120 males and 120 females. No drug effect was seen, but there was a significant difference between the TI durations of males and females, the females having longer durations. A relationship between the difference in response to MIF-I and the breeding seasons of the lizards could not be determined due to the possibility that the change in experimental design after the June experiments may alone have accounted for the loss of the significant response to MIF-I.

A 61-year-old man developed clinical lupus syndrome with positive antinuclear antibody, positive lupus erythematosus (LE) cell preparation, and diffuse proliferative glomerulonephritis following 26 months of procainamide therapy. He was treated sequentially with prednisone and azathioprine (2 weeks), decreasing doses of prednisone alone (21 months), and no immunosuppressive drugs (10 months). Coincidental with this treatment, the immunopathology of the glomerulonephritis improved dramatically, dramatically, renal function returned almost to normal, and both antinuclear antibody and LE cell preparation became negative. The course of this patient's renal disease contrasts sharply with diffuse proliferative glomerulonephritis of idiopathic systemic lupus, and suggests that this rare complication of procainamide therapy may have a favorable course.

Nine of 81 members of two families were found to have renal problems. Three patients in one family had renal-retinal dysplasia with probable recessive inheritance. Of the 6 patients in the second family, one received a kidney transplant from his brother who initially had no detectable renal abnormality but later developed renal failure. In this family, the mode of inheritance seems to be dominant. Hereditary renal-retinal dysplasia differs from medullary cystic disease and nephronophthisis in its pattern of uniformly recessive inheritance and its accompaniment by retinitis pigmentosa. Because genetic considerations have important implications in selection of donors for renal transplant, these entities should be considered distinct despite the similarities in their clinical and pathologic features.

Serum protein electrophoresis revealed a monoclonal gammopathy in three patients who presented with glomerulonephritis. Other features of myeloma were not found. Clinical manifestations of glomerulonephritis included marked proteinuria and significant hematuria. Rate of progression of renal failure was variable. Morphologically, glomerulonephritis was characterized by diffuse proliferative lesion with predominant mesangial involvement. Immunoglobulins and complement were found deposited in the mesangium. Immunoglobulins deposited in the glomeruli were found to consist exclusively of the circulating monoclonal IgG in one patient. Immunoglobulins eluted from the glomeruli of another patient consisted of immunoglobulin (IgM) which had electrophoretic mobility similar to that of the monoclonal spike in the serum. Selective deposition of monoclonal immunoglobulins in the glomeruli indicated that an active process was involved in their glomerular localization and that the monoclonal immunoglobulins may have had a role in the pathogenesis of glomerulonephritis in these patients.

When uniform histologic criteria are applied to staging schistosome egg and granuloma development in the hamster liver, the evolution of the egg foci is shown to be monophasic, albeit with considerable variation of the individual cell response. Both real and artifactual egg-granuloma asynchrony are demonstrable. Alternate granuloma stages occur simultaneously within the same single organ, so that necrosis or fibrous scarring may result in some lesions but not in others. The granulomas of Schistosoma japonicum, S mansoni and S haematobium show both shared and distinctive features. Thus, oviposition is serial in S mansoni but clustered in the other two species. Neutrophils are common in S japonicum granulomas but are rare in the others. The differential features, listed in detail, will usually permit histologic identification of species during the early stages of infection; subsequently, the species-specific features and the overall intensity of host reaction tend to decline. At comparable egg loads and time spans, the liver pathology of S japonicum is the most severe. This is not related to granuloma size, but rather to more exudation and necrosis in early S japonicum granulomas, their tendency to encroach on adjacent liver tissue and to more extensive diffuse inflammatory infiltration. Hoeppli phenomena occur around S japonicum eggs both in stellate form, and as intraovular "reverse" precipitates. Plasma cells and amyloid deposition are frequent. Conversely, S haematobium lesions are less destructive than those of S mansoni. These findings can be correlated, to some extent, with current knowledge of the biology of schistosomes and of the antigenic components of their eggs, but several key problems concerning the immunologic host response remain to be solved.