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Biomedical subjects

R V Henrickson

Publications and source records attributed to R V Henrickson.

At least 19 recordsLinked to original sources
PubMed1987

Natural history of endemic type D retrovirus infection and acquired immune deficiency syndrome in group-housed rhesus monkeys.

A 2.5-year epidemiologic study of a breeding group of rhesus monkeys (Macaca mulatta), which is a focus of endemic simian acquired immunodeficiency syndrome (SAIDS), demonstrated a strong association between the occurrence of SAIDS and infection with a type D retrovirus, SAIDS retrovirus serotype 1 (SRV-1). Of 23 healthy "tracer" juvenile rhesus monkeys, 19 (83%) died with SAIDS within 9 months of introduction into the resident SAIDS-endemic population. In contrast, 21 healthy "sentinel" juvenile rhesus monkeys placed in the same outdoor enclosure but denied physical contact with the SAIDS-affected group by a 10-foot-wide "buffer zone" remained free of SRV-1, SRV-1 antibody, and disease for 2.5 years. The SAIDS-specific mortality rate was significantly higher in juveniles than in adults. In repeated serologic testing, the overall prevalence of SRV-1 antibody ranged from 68 to 85%. Antibody prevalence increased with age. Seroconversion was found to be a poor indicator of infection rate, as approximately 50% of virus-positive juvenile monkeys had no antibody detectable by enzyme-linked immunosorbent assay. Repeated viral isolations from all animals revealed 1) SRV-1 viremia with clinical SAIDS; 2) persistent viremia and viral shedding in apparently healthy animals; 3) transient viremia and clinical recovery; 4) intermittent viremia, suggesting activation of latent infections; and 5) viremia in a 1-day-old infant, suggesting transplacental transmission. The prevalence of SRV-1 antibody in SAIDS-free breeding groups of rhesus monkeys was 4%. The seroprevalence of antibodies against human T-cell leukemia virus type 1 (HTLV-1), human immunodeficiency virus (HIV), and simian immunodeficiency virus (SIV; formerly STLV-III) was uniformly low or absent in both SAIDS-free and SAIDS-affected groups of rhesus monkeys, demonstrating that these retroviruses are not etiologically linked to SAIDS at the California Primate Research Center.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Inapparent carriers of simian acquired immune deficiency syndrome type D retrovirus and disease transmission with saliva.

Simian acquired immune deficiency syndrome (SAIDS) type D retrovirus (SRV) was isolated from saliva, urine, and peripheral blood mononuclear cells of a 6-year-old healthy rhesus monkey (Macaca mulatta) seronegative for antibodies to human T-lymphotropic virus (HTLV) type I, HTLV type III, and simian T-lymphotropic virus type III (STLV-III), identified as an inapparent SAIDS carrier in retrospective epidemiologic studies. This animal was linked to 34 cases of SAIDS over a 3-year period. Two juvenile rhesus monkeys inoculated iv with the SRV-containing saliva from this carrier became persistently infected with the retrovirus and developed SAIDS after 4-6 weeks. Both animals seroconverted to SRV, but neither had detectable preinoculation or postinoculation antibodies against HTLV type I, HTLV type III, or STLV-III. One of these animals died of SAIDS with disseminated cytomegalovirus infection after 24 weeks, and the other remains alive with persistent SRV viremia, generalized lymphadenopathy, and splenomegaly after a transient immunosuppression. Major clinical and pathological features associated with the newly described STLV-III were not observed. SRV was subsequently identified in saliva of 2 additional healthy carriers as well as monkeys with SAIDS. The findings of a carrier state in SAIDS and evidence for saliva transmission of the probable causative virus further support the usefulness of this animal model of nononcogenic immunosuppressive retroviral disease.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immune defects in simian acquired immunodeficiency syndrome.

We recently reported a Simian Acquired Immunodeficiency Syndrome (SAIDS) in rhesus macaques at the California Primate Research Center. Here, we studied in vitro lymphocyte response to the mitogens Concanavalin A (Con A), phytohemagglutinin (PHA) and pokeweed mitogen (PWM) with and without interleukin 2 (IL-2). Immunoglobulin (IgG and IgM) and complement (C3 and C4) concentrations were determined by radial immunodiffusion. T helper and T suppressor lymphocytes were identified with the monoclonal antibodies OKT4 and OKT8. Concentrations of IgG and IgM were significantly (p less than .05) decreased. Complement component C3 did not change but C4 was increased. The absolute lymphocyte count decreased but the OKT4:OKT8 ratio was unchanged from controls. A decreased lymphocyte response to all mitogens occurred early and became more severely depressed near death. IL-2 caused a complete or partial restoration of the response to the mitogens CON A and PHA. Both the humoral and cell mediated immune responses are affected in SAIDS. The role of IL-2 in this immune defect must be studied further.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Isolation of a new serotype of simian acquired immune deficiency syndrome type D retrovirus from Celebes black macaques (Macaca nigra) with immune deficiency and retroperitoneal fibromatosis.

A new serotype of simian acquired immune deficiency syndrome (SAIDS) retrovirus (type 2) belonging to the D genus of retroviruses is associated with a SAIDS occurring spontaneously in a colony of Celebes macaques (Macaca nigra) and rhesus macaques (Macaca mulatta) at the Oregon Regional Primate Research Center. This syndrome resembles SAIDS in M. mulatta at the California Primate Research Center, which is associated with a similar type D retrovirus (type 1). However, at the Oregon Center, SAIDS is distinguished by the occurrence of retroperitoneal fibromatosis in some of the affected monkeys. Type 2 virus was isolated from seven of seven macaques with SAIDS, retroperitoneal fibromatosis, or both and from one of six healthy macaques. The new strain is closely related to SAIDS retrovirus type 1 and Mason-Pfizer monkey virus but can be distinguished by competitive radioimmunoassay for minor core (p10) antigen and by genomic restriction endonuclease cleavage patterns. Neutralization tests indicate that type 1 and type 2 SAIDS retroviruses are distinct serotypes. Therefore, separate vaccines may be necessary to control these infections in colonies of captive macaques.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Simian AIDS: isolation of a type D retrovirus and transmission of the disease.

A type D retrovirus related to but distinct from Mason-Pfizer monkey virus was isolated in vitro from the blood of two rhesus monkeys (Macaca mulatta) with simian acquired immunodeficiency syndrome (SAIDS). Three juvenile rhesus monkeys that were injected intravenously with tissue culture fluids containing this virus developed SAIDS after 2 to 4 weeks.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Transmission of simian acquired immunodeficiency syndrome (SAIDS) with blood or filtered plasma.

Simian acquired immunodeficiency syndrome (SAIDS), a disease clinically and pathologically similar to acquired immunodeficiency syndrome in humans, was transmitted from diseased rhesus monkeys (Macaca mulatta) to normal monkeys by inoculation with heparinized whole blood or plasma that had been passed through filters of 0.45 micrometer pore size. This suggests that the causative agent is small and most probably a virus. No viruses, however, were isolated by standard cell culture techniques from the blood or filtered plasma which caused SAIDS. Both cellular and humoral immunity were markedly depressed in animals with advanced SAIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Rapid death of infant rhesus monkeys injected with Clostridium difficile toxins A and B: physiologic and pathologic basis.

Clostridium botulinum can colonize and produce botulinal toxin in the human infant intestine, which the toxin then permeates to cause generalized flaccid paralysis, and occasionally, sudden death. This study was undertaken to test the hypothesis that toxins produced by other intestinal clostridia, e.g., C. difficile, might also cause systemic illness and sometimes death in infants (J Pediatr 100:568, 1982). Because this hypothesis could not be evaluated clinically until the systemic manifestations of C. difficile toxins in primates were known, infant rhesus monkeys were given 6 to 11 micrograms/kg of the recently purified C. difficile toxins A or B, either intravenously or intraperitoneally. The animals showed no abnormalities for several hours, but then developed lethargy, hypotonia, hypothermia, and, shortly before death, sudden elevation of serum concentrations of potassium, magnesium, and phosphorus and of enzymes that derived mainly from skeletal muscle, heart and brain. Five of six animals died quietly 3.5 to 8.0 hours after onset of symptoms. Death appeared to result from cessation of breathing, after which the sinus tachycardia then deteriorated to a flat ECG. Necropsy findings were insufficient to explain the cause of death. It appears that in infant monkeys microgram amounts of C. difficile toxins A and B can produce a rapid quiet death, the cause of which is undetectable at necropsy, a situation pathologically reminiscent of crib death in human infants, although the possible clinical identity of these two conditions has yet to be established.

Animals↗
PubMed1984

Clinical features of simian acquired immunodeficiency syndrome (SAIDS) in rhesus monkeys.

A syndrome of acquired immunodeficiency has been identified in a group of rhesus monkeys (Macaca mulatta) which died at the California Primate Research Center. Clinical evaluation of these animals revealed that 50% or more had lymphadenopathy, weight loss, and diarrhea. At least 30% had splenomegaly, fever, cutaneous abscesses and/or arthritis/myositis. Two animals had fibrosarcomas. Anemia was seen in 19 animals, lymphopenia in 14, granulocytopenia in four and thrombocytopenia in three. Hepatitis was diagnosed histopathologically in 13. Electrophoresis revealed hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. Numerous bacterial, protozoal, and viral agents were identified including cytomegalovirus and leukocyte-associated herpesvirus. Pathologic lesions included severe post-reactive depletion of lymphocytes in germinal centers and paracortical regions of lymph nodes. Clinical and pathologic changes indicate an acquired immunodeficiency syndrome which has some similarities to AIDS in humans. This disease in monkeys may provide a model for studying that disease.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Treatment of pulmonary acariasis in rhesus macaques with ivermectin.

Rhesus monkeys were treated for pulmonary acariasis with single injections of ivermectin (200 micrograms/kg). Monkeys were killed and complete necropsies performed. Control monkeys had numerous live mites, while treated monkeys had only dead, frequently fragmented mites. Histopathologically, inflammatory lesions were most severe in control monkeys and monkeys killed one week after treatment. Inflammatory changes progressively decreased with increasing time post treatment.

Animals↗
PubMed1984

The pathology of an epizootic of acquired immunodeficiency in rhesus macaques.

A syndrome of acquired immunodeficiency within a group of outdoor-housed rhesus macaques (Macaca mulatta) with unusually high mortality has been identified at the California Primate Research Center. The cause of death for most of the affected animals included septicemia and/or chronic diarrhea with wasting, often complicated by other problems. In many cases, multiple or unusual infectious agents were isolated or recognized, including cytomegalovirus, Cryptosporidium spp., and Candida albicans. Septicemias due to usually innocuous agents such as Staphylococcus epidermidis and Alcaligenes faecalis were seen. Two animals developed cutaneous fibrosarcomas. Affected animals had generalized lymphadenopathy and splenomegaly, with depletion of T-cell populations, initially follicular hyperplasia followed by depletion, and absence of plasma cells. This spontaneous disease syndrome in nonhuman primates has similarities to acquired immune deficiency syndrome (AIDS) in humans, providing an animal model for the study of the complex factors modulating the immune system.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Epidemiologic aspects of an outbreak of acquired immunodeficiency in rhesus monkeys (Macaca mulatta).

Since August 25, 1981, an outbreak of simian acquired immunodeficiency syndrome ( SAIDS ) has been recognized in a single outdoor corral housing 77 rhesus monkeys (Macaca mulatta) over a 16-month period. The etiology of this syndrome is unknown but epidemiologic evidence suggests an infectious agent. Thirty-two cases of SAIDS have been identified (31 female, 1 male), and 27 of these animals have died (case fatality rate = 84%). Three of these deaths occurred among 13 infants born in the corral . All 27 deaths were females. For animals in the original cohort, sex was not a statistically significant risk factor. For animals born in the corral females were at greater risk (p = 0.0489; Fisher's Exact Test). SAIDS mortality rates were highest for animals entering the corral at less than 30 months of age (4.4 deaths per 100 monkey months of follow-up) and for animals born into the cage (3.3 deaths per 100 monkey-months of follow-up). The mortality rate was lowest for animals entering the corral at greater than 30 months of age, (0.32 deaths per 100 monkey-months of follow-up). No significant associations were found for the factors weaning history, cage-move history, parentage, generation, and medical history, including history of bite-wound trauma. Nine of the original 64 animals entering the corral on August 25, 1981, were previously associated with a group of 110 rhesus monkeys occupying this same corral from September 1976 to August 1981. Though less dramatic, a similar pattern of morbidity and high mortality was recognized retrospectively in this group.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1983

Experimental transmission of simian acquired immunodeficiency syndrome (SAIDS) and Kaposi-like skin lesions.

A disease that is similar to human AIDS may occur in monkeys. Simian AIDS (SAIDS) was experimentally transmitted from 2 rhesus monkeys dying of the disease to 4 cytomegalovirus (CMV) antibody-negative rhesus monkeys. The inocula consisted of the supernatant fluid from 10% homogenates of various tissues with or without buffy-coat cells from blood. Lymphadenopathy, splenomegaly, neutropenia, polymyositis, and other signs of the disease appeared in recipients within a few weeks after inoculation. Two animals developed Kaposi-like "patch" and "plaque" skin lesions and one died of sepsis and profound lymphoid depletion. A second animal also died with lymphoid depletion. All animals became infected with CMV but antibody levels were low in two animals, appeared and then disappeared in one, and never developed in the second monkey which died.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Epidemic of acquired immunodeficiency in rhesus monkeys.

A syndrome closely resembling acquired immunodeficiency syndrome (AIDS) in man has been identified in a group of 64 rhesus monkeys (Macaca mulatta) maintained outdoors at the California Primate Research Center. The syndrome is characterised by generalised lymphadenopathy, severe opportunistic infections including cytomegalovirus, chronic wasting, and high mortality. In 1 animal a multifocal cutaneous fibrosarcoma developed. This syndrome in monkeys may provide an animal model for human AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Neonatal deaths in bonnet monkeys born to dams with rudimentary papillae mammae.

Deaths due to dehydration and starvation occurred in the early neonatal period in bonnet monkey (Macaca radiata) infants housed with their dams in an outdoor half-acre corral. Dams were found to have small, rudimentary papillae mammae of insufficient size to permit suckling. Both papillary and breast tissue of affected dams were histologically normal; the nipples differed macroscopically from those of normal females only in size. This abnormality accounted for half of the neonatal mortality experienced in this breeding colony over a 5-year period.

Animals↗
PubMed1982

Nontuberculous mycobacterial disease in rhesus monkeys.

In a colony of rhesus monkeys (Macaca mulatta), 42 cases of nontuberculous mycobacterial-related disease were identified from 1970 to 1978. The disease affected young and old colony-born and wild-caught monkeys of both sexes. Serotypes 1, 2, 4, 8, and 18 of the Mycobacterium avium-intracellulare group were isolated from different monkeys. The lesions were primarily intestinal in 36 monkeys. Lesions of the large intestine, small intestine, and mesenteric lymph nodes were characterized by diffuse accumulations of large macrophages containing many acid-fast bacteria. Acid-fast bacteria could not be identified histologically in four monkeys with typical histories of diarrhea and weight loss, positive skin reactions to the tuberculin test with M. avium tuberculin, and isolation of the organism from tissues on one or more occasions. Two monkeys had histologically positive lesions limited to the lungs, although chronic colitis of undetermined cause was present.

Animals↗
PubMed1982

Nontuberculous mycobacterial disease in rhesus monkeys.

In a colony of rhesus monkeys (Macaca mulatta), 42 cases of nontuberculous mycobacterial-related disease were identified from 1970 to 1978. The disease affected young and old colony-born and wild-caught monkeys of both sexes. Serotypes 1, 2, 4, 8, and 18 of the Mycobacterium avium-intracellulare group were isolated from different monkeys. The lesions were primarily intestinal in 36 monkeys. Lesions of the large intestine, small intestine, and mesenteric lymph nodes were characterized by diffuse accumulations of large macrophages containing many acid-fast bacteria. Acid-fast bacteria could not be identified histologically in four monkeys with typical histories of diarrhea and weight loss, positive skin reactions to the tuberculin test with M. avium tuberculin, and isolation of the organism from tissues on one or more occasions. Two monkeys had histologically positive lesions limited to the lungs, although chronic colitis of undetermined cause was present.

Animals↗