Japan Monkey Research Articles

How to Chase a Monkey: Reforming the Oiharai Response to Crop-Feeding Macaques in Japan

Abstract This research is about the reform of the farmer’s chase response to crop-damaging monkeys in Japan. It focuses on a campaign to transform this chase response, known as oiharai, from a simple field-side act of expulsion into a collective, extended, and high-threat (but non-lethal) pursuit aimed at deterring future monkey visits. A number of problems with the reform are identified, including, most fundamentally, a shortage of residents in today’s depopulated, ageing villages able to do the chasing. In order to overcome this obstacle, attempts are made to boost this depleted chase capacity using (human and nonhuman) surrogate chasers.

High Prevalence of Hepatitis E Virus Infection in Imported Cynomolgus Monkeys in Japan.

Cynomolgus monkeys are important experimental animals for hepatitis E virus (HEV) infection. In Japan, cynomolgus monkeys are mainly imported from Asian countries for use at animal facilities and institutions. However, the status of HEV infection in cynomolgus monkeys remains unclear. Overall, 187 pairs of serum and fecal samples were collected from cynomolgus monkeys (Macaca fascicularis) imported from China and Cambodia to detect anti-HEV immunoglobulin (Ig) G and IgM antibodies, as well as HEV RNA. Based on an enzyme-linked immunosorbent assay using HEV-like particles derived from genotype 3 HEV as the antigen, 183 of 187 (97.9%) and 102 of 187 (54.5%) samples tested positive for anti-HEV IgG and IgM antibodies, respectively. In contrast, all 45 serum samples collected from cynomolgus monkeys bred and grown at the Tsukuba Primate Research Center, Japan tested negative for both antibodies. However, real-time quantitative reverse transcription polymerase chain reaction detected no HEV RNA in any of the 187 serum and fecal samples. These results strongly indicated that HEV infection is common in imported cynomolgus monkeys. A source of HEV-free monkeys for HEV studies is urgently needed.

Outbreak of toxoplasmosis in four squirrel monkeys (Saimiri sciureus) in Japan

Toxoplasma gondii is a protozoan parasite that causes fatal disease in New World monkeys. Several reports have described outbreaks of toxoplasmosis in squirrel monkeys. Here, we report the death of four squirrel monkeys in a captive colony from acute toxoplasmosis, one of which developed toxoplasmosis about 1 year after the initial outbreak. Serum anti–T. gondii antibody was detected by a latex agglutination test in the animals, and one presented seropositive before clinical signs were observed. Macroscopically, the lungs were severely affected and three animals showed pulmonary edema. Microscopically, interstitial pneumonia was observed in all animals. In the liver and heart, multifocal mononuclear cell infiltration with necrosis was detected. Parasite loading tended to be higher in the lungs, liver and heart than in the spleen, kidney and brain. The parasite was isolated from the brain of one animal and this isolate showed type II restriction patterns in the SAG1, SAG2, SAG3, BTUB, GRA6, c22-8, c29-2 and PK1 genes of T. gondii and type I restriction patterns in the L358 and Apico genes by PCR-Restriction Fragment Length Polymorphism analysis. The clinical signs were reduced in mice infected with this isolate compared with those infected with reference type II strain PLK in a bioassay. To our knowledge, this is the first report of isolation of the parasite from squirrel monkeys in Japan and offers the opportunity for genomic and pathogenic analyses to aid our understanding of acute toxoplasmosis.

Aberrant forms of Yersinia pseudotuberculosis as spheroplasts and filaments in yersiniosis in squirrel monkeys.

This report describes atypical cases of yersiniosis in squirrel monkeys in which aberrant forms of Yersinia pseudotuberculosis were seen. There were 2 outbreaks due to yersiniosis in squirrel monkeys in Japan. The monkeys had systemic necrotizing and hemorrhagic lesions with Gram-negative rod-shaped bacilli and microthromboembolism in the kidneys. Some lesions contained filaments, globular bodies, and other pleomorphic forms of bacteria. All forms were usually seen in the same lesions, and those with pleomorphic morphology appeared to be an intermediate form between the rod-shaped bacteria and the filaments or globular bodies. In addition, they had strong immunolabeling for Y. pseudotuberculosis, as did the rod-shaped bacteria. Therefore, the globular bodies, filaments, and others are strongly suspected to be shape-changed bacilli of Y. pseudotuberculosis. These morphologically altered bacteria could cause errors in diagnosis since they resemble fungi or protozoa, and special staining techniques, including immunohistochemistry, can be helpful in establishing the correct diagnosis.

A Distinct Genetic Population ofGongylonema pulchrumfrom Water Buffaloes in Nepal

Whole-length esophagi of 111 Murrah cross water buffaloes (Bubalus bubalis) were collected in the Kathmandu and Chitwan districts of Nepal from December 2009 to February 2010. Gullet worms showing a typical epithelium-dwelling character were detected in 13 of 53 (24.5%) buffaloes in Kathmandu and in 5 of 58 (8.6%) buffaloes in Chitwan. The worms' morphology and measurements were identical to those of Gongylonema pulchrum Molin, 1857, except for the length of the left spicules relative to the body length. Scanning electron microscopy did not detect any further morphological differences regarding the collected specimen from Nepal compared with G. pulchrum . The ribosomal RNA gene (rDNA), including internal transcribed spacer (ITS) 1 and 2, and a partial region of the cytochrome c oxidase subunit I (COI) of mitochondrial DNA of the worms were characterized and compared with those of G. pulchrum collected from cattle, deer, wild boars, and monkeys in Japan and from cattle in Iran. The 18S, 5.8S, and 28S rDNA nucleotide sequences of the buffalo-collected worms had 99.8% (1,779/1,782), 100% (158/158), and 98.3-98.8% (3,494-3,507/3,551) identities, respectively, with those of G. pulchrum from the other host mammals. The ITS regions exhibited higher variations between the buffalo-collected worms and G. pulchrum from the other host mammals (85-88% identity for ITS1 and 56-80% identity for ITS2). The COI also showed lower identities (89.2-90.2%), although only a single amino acid substitution was noted compared with the majority of G. pulchrum samples collected in Japan. Based on these molecular genetic characters in the rDNA and COI mitochondrial DNA, together with a shorter left spicule length relative to body length, the gullet worms isolated from buffaloes in Nepal might belong to a distinct local or buffalo-preferring population of G. pulchrum, although its geographical distribution on the continent and host specificity remain to be clarified.

Lethal Canine Distemper Virus Outbreak in Cynomolgus Monkeys in Japan in 2008

Canine distemper virus (CDV) has recently expanded its host range to nonhuman primates. A large CDV outbreak occurred in rhesus monkeys at a breeding farm in Guangxi Province, China, in 2006, followed by another outbreak in rhesus monkeys at an animal center in Beijing in 2008. In 2008 in Japan, a CDV outbreak also occurred in cynomolgus monkeys imported from China. In that outbreak, 46 monkeys died from severe pneumonia during a quarantine period. A CDV strain (CYN07-dV) was isolated in Vero cells expressing dog signaling lymphocyte activation molecule (SLAM). Phylogenic analysis showed that CYN07-dV was closely related to the recent CDV outbreaks in China, suggesting continuing chains of CDV infection in monkeys. In vitro, CYN07-dV uses macaca SLAM and macaca nectin4 as receptors as efficiently as dog SLAM and dog nectin4, respectively. CYN07-dV showed high virulence in experimentally infected cynomolgus monkeys and excreted progeny viruses in oral fluid and feces. These data revealed that some of the CDV strains, like CYN07-dV, have the potential to cause acute systemic infection in monkeys.

Epidemiological Findings on Yersiniosis in Nonhuman Primates in Zoological Gardens in Japan

Yersiniosis, which is caused by pathogenic Yersinia enterocolitica or Yersinia pseudotuberculosis, poses a serious problem for zoological gardens engaged in breeding nonhuman primates. In Japan, Y. pseudotuberculosis in particular frequently causes fatal infection, and affected nonhuman primates may die unexpectedly or after a very short illness. Our epidemiological study in 17 zoological gardens in Japan suggested that Yersinia pseudotuberculosis-derived mitogen (YPM), which is a kind of super-antigenic toxin, might be the cause of, or at least the most important factor in, the high mortality of breeding nonhuman primates infected by Y. pseudotuberculosis in Japan. Furthermore, seroepidemiological study proved that pathogenic Yersinia is highly prevalent among breeding squirrel monkeys in Japan. It is likely that the monkeys that are pathogenic Yersinia positive have been inapparently or mildly infected by low pathogenic strains of Yersinia, not highly pathogenic strains of Yersinia, such as YPM-producing Y. pseudotuberculosis. In this review, we will describe the epidemiology of yersiniosis in breeding nonhuman primates in Japan.

Seroepidemiological Survey of Pathogenic Yersinia in Breeding Squirrel Monkeys in Japan

To investigate the prevalence of antibodies to pathogenic Yersinia in breeding squirrel monkeys, the serum samples of 252 squirrel monkeys from 9 zoological gardens in Japan were tested by ELISA using plasmid-encoded Yersinia outer membrane protein (Yops) as the antigen. The cutoff value was calculated by using the serum samples of the squirrel monkeys from Suriname, where no prevalence of pathogenic Yersinia have been reported. According to the cutoff value, 164 of 252 (65.1%) squirrel monkeys were considered positive against pathogenic Yersinia. These positive monkeys belonged to 8 of the 9 zoological gardens, and the percentage of the seropositive monkeys ranged from 22.2 to 89.4%. Furthermore, in one zoological garden, the positive rate of the squirrel monkeys which were over 1 year old (95.7%) was significantly higher than those which were under 1 year old (23.3%). These results suggested that pathogenic Yersinia is highly prevalent among breeding monkeys in Japan.

細胞レベルの霊長類脳機能研究４０年

In 1966, Edward Evarts reported the neuronal activities of mortar cortex of behaving monkeys. That was the first report of the cellular level research using behaving monkeys. The Primate Research Institute (PRI) was established in Kyoto University, next year in 1967. To start a new research project in the new institute using primates, research on cellular level of brain functions, especially the functions of the frontal association cortex was selected. This topic was selected since the higher brain functions are the well-developed functions in the primates. Later, in 1970, Edward Evarts was invited to come to Japan. He stayed PRI for 4 months and brought his new techniques to PRI. Thus the cellular level of study on functions of the association corteces started using behaving monkeys in Japan. Since then, the cellular basis of the integrative brain functions, such as, perceptual decision making, emotional decision making, planning of complex behavior or complex motor control were revealed based on the analyses of the correlations of behavior and neuronal activities while monkeys are performing behavioral tasks. To investigate correlations, it was important to segregate behavioral events in the time sequence of the single task or in the multiple tasks. In addition to this, the effect of the lesion and the effect of electrical stimulation of the target brain area were helped to understand the behavioral role of the neuronal activities. Although this field of research revealed higher brain functions of monkeys in the single neuronal level, the understanding of the brain mechanisms of higher brain functions is still in the primitive phenomenal level. In future, it is necessary to reveal the role of each neuronal activity in the neural circuit of the brain.

Virulence characteristics of Yersinia pseudotuberculosis isolated from breeding monkeys in Japan

Between April 2001 and 2007, 18 Yersinia pseudotuberculosis outbreaks occurred in breeding monkeys at 12 zoological gardens in Japan, and 28 monkeys of 8 species died. A total of 18 Y. pseudotuberculosis strains from the dead monkeys, comprising one strain per outbreak, were examined for serotype and the presence of the virulence genes virF, inv, ypm ( ypmA, ypmB and ypmC) and irp2. Of the 18 Y. pseudotuberculosis strains, 7 (38.9%) were serotype 4b, 7 (38.9%) were serotype 1b, and there was one each of serotypes 2b, 3, 6 and 7. All the 18 strains examined harbored virF and inv. Sixteen (88.9%) strains, including the strain of serotype 7, harbored ypmA. However, no strain harbored ypmB, ypmC and irp2. This study demonstrated that among other pathogenic factors, almost all the Y. pseudotuberculosis isolated from the outbreaks had the ypm gene encoding the superantigenic toxin, YPM. As most of the monkeys who died in those outbreaks originated from South America and other regions, where the presence of the ypm gene have not been reported, YPM might be the cause, or at least the most important factor for, the high mortality of the breeding monkeys infected by Y. pseudotuberculosis in Japan. This is also the first report of a fatal case due to Y. pseudotuberculosis serotype 7 infection in the world.

Genotyping of Giardia intestinalis from domestic and wild animals in Japan using glutamete dehydrogenase gene sequencing

To determine the genotypes of Giardia intestinalis from domestic and wild animals in Japan, Giardia isolates obtained from feces of 24 dogs kept in households and breeding kennels, three companion cats, five dairy calves and three wild monkeys, Macaca fuscata, were genotyped using the 177 bp sequence of the glutamete dehydrogenase gene (gdh). The genotypes were assemblages A, C, D or A/D for dog isolates, Assemblage F for cat isolates, assemblages A or E for calf isolates and assemblage B for monkey isolates. This is the first report on the genotypes of Giardia isolates from cats, calves and wild monkeys in Japan.

Uptake of phthalate esters, di(n-butyl)phthalate and di(2-ethylhexyl)phthalate, as environmental chemicals in monkeys in Japan.

K. Asaoka, K. Hagihara, H. Kabaya, Y. Sakamoto, H. Katayama, K. Yano 1 Department of Cellular and Molecular Biology, Primate Research Institute, Kyoto University, Inuyama, Aichi 484-8506, Japan 2 Minegami Station, Boso Monkey Research Center, 327 Utobara, Futtsu, Chiba 299-1732, Japan 3 University Forest in Chichibu, Faculty of Agriculture, The University of Tokyo, Chichibu, Saitama 368-0034, Japan 4 Laboratory of Biomedical Research, Saitama Medical School, 38 Morohongo, Moroyama, Iruma-gun, Saitama 350-0495, Japan 5 Saitama Medical Collage, 38 Morohongo, Moroyama, Iruma-gun, Saitama 350-0495, Japan 6 Department of Chemistry, Saitama Medical School, 981 Kawakado, Moroyama, Iruma-gun, Saitama 350-0496, Japan

Prevalence of antibodies to five selected zoonosis agents in monkeys.

The prevalence of antibodies against 5 zoonosis agents was determined in serum samples of 443 breeding monkeys. Of the monkeys, 296 were bred or kept for a long time at R institute, and the remaining 147 were newly imported from the Philippines and kept at S institute for quarantine. Antibodies to simian virus 40 were highly prevalent at 89.1% among monkeys of R institute, whereas no antibody could be detected in those of S institute. Antibodies to Chlamydia psittaci and Yersinia pseudotuberculosis were detected in 14.4 and 11.6% at R institute, and in 9.0 and 3.5% at S institute, respectively, evidencing a significant difference (P less than 0.05) between those of the two institutes for both agents. Antibodies to Toxoplasma gondii and Leptospira interrogans were found in 3.6 and 2.9% of the overall, respectively, showing no difference in positive rates in relation to breeding place. Even in cases positive to the latter 4 zoonosis agents, the antibody titers were low. The results obtained suggest that all zoonoses tested do not seem to be so serious diseases among monkeys at the present time except simian virus 40 infection, which is highly prevalent among breeding monkeys in Japan.

Hyperargininemia in man and monkeys in Japan

Hyperargininemia in man and monkeys in Japan