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At least 937 records · Page 52Linked to original sources
PubMed1995

Riluzole prevents MPTP-induced parkinsonism in the rhesus monkey: a pilot study.

Previous studies have shown that riluzole (2-amino-6-trifluoromethoxy-benzothiazole), a drug which interferes with glutamate neurotransmission, has a neuroprotective action in rodent models of global and focal cerebral ischemia. In this pilot study, the protective and palliative effects of riluzole have been examined using an animal model of Parkinson's disease. Two monkeys were rendered hemiparkinsonian by one intracarotid injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and motor signs were evaluated using clinical examination and electromyographic recordings. When riluzole (4 mg/kg) was administered before the injection of MPTP, parkinsonian motor symptoms, in particular bradykinesia and rigidity, were absent. When injected daily in one monkey which presented stable motor symptoms, bradykinesia and rigidity were significantly reduce d. Riluzole pretreatment induced a persistent increase in dopamine turnover when compared to MPTP alone. Thus, a possible neuroprotection and a facilitation of dopamine release may explain the behavioural effects reported with riluzole treatment. These preliminary results suggest that riluzole could possess neuroprotective and palliative effects in a primate model of Parkinson's disease.

Animals↗
PubMed2001

Sterilizing immunity against experimental Helicobacter pylori infection is challenge-strain dependent.

The development of a murine model of Helicobacter pylori infection through serial in vivo passage of candidate strains has enabled a quantitative assessment of vaccine efficacy. In this study we compare infection with and protection against challenge from both CagA(+) type I, and CagA(-) type II in vivo adapted isolates. In vivo passage of a type II H. pylori isolate resulted in a highly infectious strain (X47-2AL), capable of reproducibly infecting mice to high density (10(7) CFU/g of gastric tissue). Similarly adapted type I strains were found to colonize mice at a significantly lower level (10(4)-10(5) CFU/g tissue). Mucosal immunization with recombinant urease (rUre) significantly protected animals against both types. Protection against X47-2AL was characterized by a > or =100-fold (or 2 log) reduction in bacterial density. However, the presence of a residual infection highlighted the inability to achieve sterilizing immunity against this strain. The level of protection appeared independent of challenge dose, and was stable for up to 6 months, all animals exhibiting a low-level residual infection that did not recrudesce with time. Similarly immunized mice challenged with isolates representing the residual infection were also protected, confirming that they did not represent a sub-population of H. pylori that could escape immunity. Immunization and challenge studies with type I adapted-isolates, demonstrated a similar 2-3 log reduction in the bacterial burden, but that in this instance resulted in sterilizing immunity. These results suggest varied specificity for the murine host by different Helicobacter strains that can influence the outcome of both infection and immunity.

Administration, Oral↗
PubMed2001

Progressive pulmonary tuberculosis is not due to increasing numbers of viable bacilli in rabbits, mice and guinea pigs, but is due to a continuous host response to mycobacterial products.

Tuberculosis (TB) kills more people in the world today than any other infectious disease. A better vaccine to prevent clinical tuberculosis is greatly needed. Candidate vaccines are often evaluated by infecting rabbits, mice and guinea pigs by an aerosol of virulent tubercle bacilli and culturing their lungs for viable bacilli at various times thereafter. In all three species, however, the number of viable bacilli usually does not continuously increase until the host succumbs. The number of viable bacilli increases logarithmically for only about 3 weeks. Then, the host develops delayed-type hypersensitivity (DTH) and cell-mediated immunity (CMI), which keep the number of viable bacilli rather constant during the subsequent weeks. In the immunized host, DTH and CMI stop the logarithmic increase sooner than in the unimmunized controls, so that the stationary bacillary levels that follow are lower. This review analyzes host-parasite interactions in the lungs of rabbits, mice and guinea pigs. All three species cannot prevent inhaled fully virulent tubercle bacilli from establishing an infection, but they differ markedly in the type of the disease produced once it is established.

Animals↗
PubMed1998

Rhesus macaques infected with macrophage-tropic simian immunodeficiency virus (SIVmacR71/17E) exhibit extensive focal segmental and global glomerulosclerosis.

We previously showed that inoculation of rhesus macaques with molecularly cloned lymphocytetropic simian immunodeficiency virus (SIVmac239) results in SIV-associated nephropathy (SIVAN) and that the glomerulosclerotic lesions were associated with the selection of macrophagetropic (M-tropic) variants (V. H. Gattone et al., AIDS Res. Hum. Retroviruses 14:1163-1180, 1998). In the present study, seven rhesus macaques were inoculated with M-tropic SIVmacR71/17E, and the renal pathology was examined at necropsy. All SIVmacR71/17E-infected macaques developed AIDS, and most developed other systemic complications, including SIV-induced encephalitis and lentivirus interstitial pneumonia. There was no correlation between the length of infection (42 to 97 days), circulating CD4(+) T-cell counts, and renal disease. Of the seven macaques inoculated with SIVmacR71/17E, five developed significant mesangial hyperplasia and expansion of matrix and four were clearly azotemic (serum urea nitrogen concentration of 40 to 112 mg/dl). These same five macaques developed focal segmental to global glomerulosclerotic lesions. Increased numbers of glomerular CD68(+) cells (monocytes/macrophages) were found in glomeruli but not the tubulointerstitium of the macaques inoculated with SIVmacR71/17E. All macaques had glomerular deposits of immunoglobulin G (IgG), IgM, and tubuloreticular inclusions, and six of seven had IgA deposition. However, there was no correlation between the presence of circulating anti-SIVmac antibodies, immunoglobulin deposition, and glomerular disease. Tubulointerstitial infiltrates were mild, with little or no correlation to azotemia, while microcystic tubules were evident in those with glomerulosclerosis or azotemia. The four most severely affected macaques were positive for diffuse glomerular immunostaining for viral core p27 antigen, and there was intense staining in the glomeruli of the two macaques with the most severe glomerulosclerosis. Viral sequences were isolated from glomerular and tubulointerstitial fractions from macaques with severe glomerulosclerosis but only from the tubulointerstitial compartment of those that did not develop glomerulosclerosis. Interviral recombinant viruses generated with env sequences isolated from glomeruli confirmed the M-tropic nature of the virus found in the glomeruli. The correlation between the increased number of CD68(+) cells (monocytes/macrophages) in the glomeruli, the localization of p27 antigen in the glomeruli, and the glomerular pathology confirms and extends our previous observations of an association between glomerular infection and infiltration by M-tropic virus and SIVAN.

AIDS-Associated Nephropathy↗
PubMed1992

Evidence for a lentiviral etiology in an epizootic of immune deficiency and lymphoma in stump-tailed macaques (Macaca arctoides).

A retrospective study determined that an epizootic of immune suppression and lymphoma in stump-tailed macaques (Macaca arctoides) that began in 1976 was associated with a horizontally spread lentivirus infection. This conclusion was based on serology, epidemiology, pathology, and virus isolation. The lesions found in the stump-tailed macaques were more compatible with lesions seen in SIV-infected rhesus than those seen in rhesus macaques infected with type D retroviruses. A lentivirus, isolated from a rhesus inoculated with lymph node homogenate from a stump-tailed macaque, was designed SIVstm and was pathogenic for rhesus macaques. The isolate was antigenically related to other SIVs as well as to HIV-1 and HIV-2. Two surviving stump-tailed macaques sent to another colony carried SIVstm latently for at least 7 years and disseminated it throughout that colony.

Animals↗
PubMed1999

Clinical outcome of a protocol to produce immunosuppression in rhesus monkeys (Macaca mulatta): application to infectious disease and gene therapy studies.

Induced immunosuppression is required for a number of studies using rhesus monkeys (Macaca mulatta). This report describes the clinical outcome and safety of a dose-finding experiment that determined doses of cyclophosphamide and prednisone that could be used to induce a state of immunosuppression in rhesus monkeys. After determining the optimum dose of immunosuppressive agents, the protocol was then used on animals participating in infectious disease and gene therapy studies. Splenectomy was performed in some animals to increase the severity of immunosuppression. The onset, duration, and severity of lymphopenia and leukopenia were consistent in all animals. In most animals, physical examination findings and clinical serum chemistry profiles demonstrated only transient abnormalities. With proper clinical monitoring, combination treatment with cyclophosphamide and prednisone is an effective and safe method for inducing immunosuppression in rhesus monkeys.

Animals↗
PubMed1998

Rapid diagnosis of simian varicella using the polymerase chain reaction.

Simian varicella virus (SVV) causes sporadic epizootics of a varicella-like disease in nonhuman primates. Rapid diagnosis of simian varicella is critical in controlling epizootics. A polymerase chain reaction (PCR)-based diagnostic assay for detection of SVV DNA in cell culture and clinical samples from SVV-infected monkeys was developed. The assay is rapid, specific, and highly sensitive. The SVV DNA is readily detected in skin rash specimens and in peripheral blood lymphocytes of infected monkeys during the early stages of clinical varicella. In addition to providing an important diagnostic tool, the SVV PCR assay is also useful for investigating the epidemiology and pathogenesis of simian varicella.

Animals↗
PubMed1977

Respiratory pathogens in non-human primates with special reference to Corynebacterium ulcerans.

An investigation of 272 non-human primates (75 Macacca cynomolgus, 97 Macacca mulatta and 100 Cercopithecus aethiops) revealed a high incidence of respiratory disease caused by Corynebacterium ulcerans, Staphylococci, Diplococci and Streptococci. Escherichia coli was also found as a secondary invader. Most of the infections occurred during winter in Macaca cynomolgus and were caused by Corynebacterium ulcerans and Diplococcus pneumoniae. The C. ulcerans strains were phage type VI G. A phage type III C strain was isolated from a Macacca mulatta. The high incidence of C. ulcerans suggests that this organism plays a significant role in the pathology of respiratory disease in the non-human primate.

Animals↗
PubMed1978

Tuberculosis in laboratory animals.

Tuberculosis can cause great losses in captive colonies of various animal species. In South Africa the culprit is the human type of tubercle bacillus. Interspecific transmission of tuberculosis infection amongst laboratory animals, notably primates, is known to occur, and often handlers and caretakers act as the source of infection. The need for preventive measures in laboratory colonies and procedures for case finding and treatment of tuberculous animals are discussed. Indiscriminate destruction of diseased animals is opposed. The South African situation as revealed by questionnaire survey is described.

Animals↗
PubMed1997

Proteinuric hypertension in a pregnant baboon: was this pre-eclampsia?

We report the results of investigating a pregnant baboon that developed hypertension, proteinuria, and oedema in late gestation. Although the clinical presentation suggested a diagnosis of pre-eclampsia, the evolution of her clinical signs and results of a renal biopsy performed 3 weeks after delivery suggested that glomerulonephritis was the underlying disease.

Aged↗
PubMed1975

Erysipelas in a black and red tamarin.

Erysipelothrix rhusiopathiae was isolated in large numbers from the kidneys and was visualized histologically in the kidneys, heart muscle, skeletal muscle, selected lymph nodes, and the submandibular salivary glands of a black and red tamarin (Saguinus nigricollis) following an acute fatal illness. Sites (heart valves, joints) usually associated with disease mediated by E rhusiopathiae appeared uninvolved.

Animals↗
PubMed1976

Changes in blood serum constituents and hematologic values in Macaca mulatta with Rocky Mountain spotted fever.

Forty-seven male Macaca mulatta, 3 to 4 kg weight, were inoculated intravenously or subcutaneously with various doses of yolk sac-grown Rickettsia rickettsii. Thirty-four macaques became febrile and exhibited signs of infection ranging from transient illness with a few days of fever to severe illness with subsequent death. The rash appeared more frequently in the macaques inoculated subcutaneously. Febrile macaques that survived had leukocytosis, with concomitant neutrophilia. Febrile macaques that died had, in addition, marked terminal leukopenia and thrombocytopenia. Packed cell volume of all febrile macaques decreased. In almost all of the febrile macaques, there were increased serum urea nitrogen, glutamic-oxaloacetic transaminase, and lactate dehydrogenase and decreased total serum protein and amylase concentrations. A few febrile macaques had increased bilirubin values and decreased sodium, chloride, phosphorus, and alkaline phosphatase concentrations. Changes did not occur in serum glucose, potassium, calcium, and glutamic-pyruvic transaminase values. The experimental form of Rocky Mountain spotted fever in the macaque provides a subhuman primate model for studying the pathophysiology of this disease.

Amylases↗
PubMed1981

Nephritis and hemolytic anemia in owl monkeys (Aotus trivirgatus).

The two most common diseases of captive owl monkeys (Aotus trivirgatus) are hemolytic anemia and glomerulonephritis. The anemia is characterized by total red blood cell counts between 0.45 and 3.44 x 10(6) microliters, hemoglobin values as low as 1.0 g/dl, and many circulating nucleated red blood cells. Centrilobular necrosis in the liver, extramedullary hematopoiesis in liver and spleen, and hemoglobin casts in kidney tubules are prominent histologic features. Hemosiderin and lipofuscin often are found in liver, spleen, kidney and lymph nodes. Microthrombi and microinfarcts sometimes are scattered throughout the brain. Glomerular lesions in Aotus have been described previously and are characterized by increased numbers of mesangial cells and matrix, glomerulosclerosis and electron dense deposits in basement membranes. Lymphocytes, plasma cells and eosinophils frequently are present in the interstitium. In the early stages the cellular infiltrate is periglomerular. The foci then grow to encompass adjacent glomeruli and tubules. Finally, large portions of the kidney are affected and connective tissue proliferates. The incidence of extramedullary hematopoiesis in the liver correlated significantly with that of interstitial nephritis (0.001 less than p less than 0.01) but not with glomerular lesions. The two kidney lesions, glomerulonephritis and interstitial nephritis correlated strongly in incidence. They also found with equal frequency in 87 monkeys with clinical evidence of anemia. This analysis indicates that there may be no common pathogenesis of the hematologic and renal abnormalities as seen in certain autoimmune diseases. However, there could be complex interactions between two or more disease mechanisms that account for the various manifestations of disease.

Anemia, Hemolytic↗