Abstract. Lesions induced in rhesus monkeys by different isolates of simian immunodeficiency virus (SIV)/ Delta were studied at necropsy. Four groups of monkeys were inoculated with SIV/Delta isolated from other experimentally infected rhesus monkeys, while one group was inoculated with SIV/Delta from an asymptomatic mangabey monkey. Three rhesus isolates and the mangabey isolate were virulent, killing 75-100% of infected monkeys. One rhesus isolate, which had been extensively passaged in vitro, was attenuated but was restored to virulence by single animal passage. Clinically, infected monkeys had lymphadenopathy, splenomegaly, diarrhea, and a rash. Most monkeys died of enteric disease. The following lesions were seen: weight loss, thymic atrophy, lymphoid atrophy, bone marrow hyperplasia, encephalitis, colitis, amyloidosis, hepatitis, glomerulosclerosis, and the presence of syncytial cells. One Rh Epstein-Barr virus (EBV)-related lymphoma occurred. Opportunistic agents were identified: cytomegalovirus, adenovirus, Cryptosporidia, and Pneumocystis. Shigella and Campylobacter often caused colitis.

Infection of the rhesus macaque (Macaca mulatta) with simian immunodeficiency virus (SIV) induces a disease similar to AIDS. We compared SIV-specific antibody and antigenemia with the progression of disease in monkeys experimentally infected with SIV/Delta isolates that varied in pathogenicity. Western blot, immunoprecipitation, and sandwich enzyme-linked immunosorbent assay of serial sera from macaques infected with attenuated virus revealed a persistent antibody response and no evidence of SIV antigenemia. Immunosuppressed macaques without central nervous system (CNS) infections responded similarly to initial infection, but antibody specific for gag or, less frequently, to gag and env determinants declined predictably before clinical disease. Monkeys with CNS infections, however, had little, if any, detectable antibody to either envelope or gag proteins, regardless of the duration of survival. SIV/Delta-specific antigenemia, evident only in immunodeficient monkeys, fluctuated reciprocally with antibody. Our data suggest that SIV/Delta-induced disease is dependent upon antigenemic episodes that, particularly in animals with CNS infection, appear coincident with diminished antibody.

Abstract. Necropsy materials from 5 7 cases of generalized amyloidosis in rhesus monkeys were reviewed. Clinically, animals with the disease were characterized by cachexia with muscle wasting, recurrent diarrhea, and arthritis. Gross lesions included hepatomegaly, splenomegaly, chronic/active colitis, fibrous strictures of the cecocolic junction, osteoarthritis, and generalized muscle atrophy. Histologic examination revealed minimal to severe deposits of amyloid in the small intestine (loo%), spleen (93%), large intestine (67%), liver (40%), lymph nodes (710/0), stomach and/or adrenal gland (32%). More amyloid was deposited in the spleen, liver, and small intestine than in other organs. Shigella sp. were isolated from feces in 23% of the cases and 84% had histologic evidence of colitis. Other findings indicated that 100% of the animals had lung mites, 25% had strictures of the cecocolic junction, and 40% had osteoarthritis. Thirty percent of the cases occurred in animals 10 months to 5 years of age, 10% in ages 6 to 10 years, and 60% in animals greater than 10 years old. Materials and MethodsApproximately 2,000 Macaca mulatta are maintained at the Delta Regional Primate Research Center (DRPRC), Covington, Louisiana. Most are housed outdoors in V 2 acre corrals as part of long-term breeding colonies. Complete necropsies are performed on all animals that die. Representative sections of all major tissues are fixed in 10% neutral buffered formalin, sectioned at 5 to 6 pm, and stained with hematoxylin and eosin. Sections suspected of containing amyloid are stained with Congo Red and Potassium PermanganateKongo Red. Necropsy records were examined from 1982 through 1985 and those animals with histologic evidence of generalized amyloidosis were identified. Fifty-seven consecutive cases over a 14 month period were selected from the 128 cases identified and were examined in detail, including clinical, gross and laboratory records, and histologic sections. Clinical laboratory tests included culture of tissues for bacteria when indicated by clinical or gross findings, complete blood counts, total protein, albumin, and globulin determinations, blood electrolyte levels, and blood urea nitrogen. All values were not obtained on every animal.The presence or absence of amyloid in each tissue section was recorded, and the amount deposited was subjectively evaluated as follows: 0 = none present, 1 = minimal, 2 = mild, 3 = moderate, and 4 = severe. The presence or absence of enteritis, colitis, pneumonia, chronic arthritis, and strictures of the cecocolic junction was recorded.

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Abstract. Naturally occurring deposition of calcium pyrophosphate has been identified in six rhesus monkeys following acute episodes of trauma and various septicemias. Scanning electron microscopy with energy-dispersive X-ray analytical system and single crystal electron diffraction studies were used to identify the crystals within the articular cartilage. The osteoarthritis grading system was used to determine the degree of cartilage degenerative changes.Calcium pyrophosphate deposition disease (CPDD) is a metabolic disease of articular cartilage associated with a degenerative arthropathy in man? Other crystalline structures have been identified as important etiologic factors of acute and chronic arthropathies such as: urate," hydroxyapatite, lo* and calcium hydrogen phosphate dihydrate3* crystals. One case of pyrophosphate crystal deposition in a dog synovial membrane has been reported.'A naturally occurring calcium pyrophosphate deposition arthropathy in a rhesus breeding colony has been identified. The acute form followed acute trauma-septicemias and primarily involved the knee and elbow joints; any joint may be affected, however. Generalized joint disease has been identified in adult animals. The chronic disease was evident in rhesus monkeys as joint rigidity, marked atrophy of the musculature, and a degenerative arthropathy. Preliminary attempts to determine the eti'ology '(mycoplasma, virus, rheumatoid) of the arthropathy were negative. Six naturally occurring cases of calcium pyrophosphate deposition disease in primates are reported and compared to pyrophosphate deposition disease in man. Materials and MethodsKnee joints fiom six rhesus monkeys of various ages were positive on scanning electron microscopy for pyrophosphate crystals and are included in this study. A positive sample had pyrophosphate crystals which projected from and integrally involved the articular cartilage. Pertinent clinical history is given in table I. All knees were opened and samples of synovial fluid were collected for bacteriologic aerobic and anaerobic culture. From each knee joint, samples of the synovial membrane, articular surface, and menisci were collected and fixed in 3% glutaraldehyde in cacodylate buffer, postfixed in 1% osmium tetroxide, dehydrated, and critical point dried and coated with gold for scanning electron microscopy. For light microscopy, the synovial membrane, and weight bearing and non-weight bearing articular surfaces were fixed in 3% glutaraldehyde in cacodylate buffer. Electron diffraction studies of each case were conducted after scraping critical point dried cartilage with a scalpel blade over formvar-coated grids. Electron diffraction patterns from known standards of hydroxyapatite, brushite and calcium pyrophosphate, (Sigma Chemical Company, St. Louis, MO.) then were compared to the patterns obtained from the unknown crystals.All articular surface sections for light microscopy were demineralized with decalcifying solution (American Scientific Products, McGraw Park, Ill.) overnight, washed in running ...