One of the factors on which the incidence of leptospirosis is dependent is the survival time of shed leptospires in surface water or soil water, and this time is in turn affected by the acidity or alkalinity of the water. The authors have therefore studied the survival of four leptospiral serotypes in buffered distilled water at pH's ranging from 5.3 to 8.0. All survived longer in alkaline than in acid water, and significant differences between the serotypes were found in response to pH. Survival at pH's under 7.0 ranged from 10 to 117 days and at pH's over 7.0 from 21 to 152 days. Survival was also studied in aqueous extracts of soil samples from different areas in Malaya; no correlation was found between pH and survival time.It was also noted that in a group of Malayan ricefields a low incidence of leptospirosis in man was accompanied by a high infection rate among rodents, and when it was found that this phenomenon could not be explained by pH or salinity, attention was turned to the soil. Bentonite clay, similar to the montmorrillonite clay of the ricefields, was found to adsorb about half the leptospires in suspension. The authors recommend that field study of this laboratory observation be undertaken.
Leptospirosis is recognised as one of the leading zoonotic diseases and rodents have been implicated as one of the natural reservoirs of the disease. The Malayan porcupines (Hystrix brachyura) which are also a rodent could possibly be a carrier of leptospiral organisms. This study was conducted to determine the serological prevalence of leptospiral infection among captive Malayan porcupines and to disclose the possibility of porcupines as a reservoir for leptospiral infection. Fifty serum samples were obtained from the Malayan porcupines kept in captivity at the Wildlife Conservation Centre, Sungai Dusun, Malaysia. The microscopic agglutination test (MAT) was performed on the serum samples to detect the presence of agglutinating antibodies to a panel of 16 Leptospira serovars (Australis, Autumnalis, Ballum, Bataviae, Canicola, Celledoni, Djasiman, Hardjobovis, Hardjopratjino, Hebdomadis, Hurstbridge, Icterohaemorrhagiae, Javanica, Pomona, Pyrogenes and Sejroe). From the serological test, 18% (n=9/50) of the Malayan porcupines tested had leptospiral antibodies to serovars Javanica (8%), Hurstbridge (4%), Ballum (2%), Celledoni (2%) and Hardjoprajitno (2%). It is seen that this study disclosed a high prevalence of leptospiral infection in the Malayan porcupines tested and indicated that the Malayan porcupines could possibly be a source of leptospirosis to other animals including humans and that they might play an important role in the epidemiology of leptospiral infection in the country.
Leptospirosis is caused by the spirochetal bacterium Leptospira of which rodents are considered the most important reservoir. This study aims to determine and characterize virulent Leptospira species among rodents and small mammals found in human settlements and recreational spots within the Hulu Langat and Gombak districts of Selangor, Malaysia; regions that frequently report probable human leptospirosis cases. Molecular analysis revealed an overall Leptospira detection rate of 14.3% among the 266 small mammals captured, and the human settlements were found to have the highest number of isolates (15.1%), followed by recreational sites (14.5%). The molecular characterization conducted based on the lipL32, secY genes and MLST revealed that the strains belonged to four different species, including; Leptospira interrogans (29; 76.3%; ST50, ST238, ST243), L. kirschneri (5; 13.15%; ST110), L. borgpetersenii (3; 8%; ST143) and L. weilii (1; 2.63%; ST242). The study revealed genotypes of circulating strains among small mammals in Malaysia, which include Leptospira locus ST110 L. kirschneri, ST 50 L. interrogans, ST143 L. borgpetersenii and ST242 L. weilii. Among the small mammals studied, 17/105 (16.2%) Rattus norvegicus, 7/59 (11.9%) of Rattus rattus, 5/24 (20.8%) of Maxomys whiteheadi, 4/18 (22.2%) of Sundamys muelleri, 2/22 (9%), Tupaia gliss, 2/16 (12.5%) Rattus tiomanicus and 1/4 (25%) of Suncus murinus carried pathogenic leptospires. The data from the present study may imply that, in addition to rodents, other small mammals also serve as maintenance hosts for Leptospira. Hence, much remains unknown about Leptospira maintenance hosts, and there is need for further investigation to ascertain the prevailing serovars of pathogenic Leptospira in Malaysia. This will assist in the development of efficient diagnostic assays with improved microscopic agglutination test (MAT) panels, and in the implementation of suitable prevention and control measures.
The genus Ehrlichia is composed of tick-borne obligate intracellular gram-negative alphaproteobacteria of the family Anaplasmataceae. Ehrlichia includes important pathogens affecting canids (E. canis, E. chaffeensis, and E. ewingii), rodents (E. muris), and ruminants (E. ruminantium). Ehrlichiaminasensis, an Ehrlichia closely related to E. canis, was initially reported in Canada and Brazil. This bacterium has now been reported in Pakistan, Malaysia, China, Ethiopia, South Africa, and the Mediterranean island of Corsica, suggesting that E. minasensis has a wide geographical distribution. Previously, E. minasensis was found to cause clinical ehrlichiosis in an experimentally infected calf. The type strain E. minasensis UFMG-EV was successfully isolated from Rhipicephalus microplus ticks and propagated in the tick embryonic cell line of Ixodes scapularis (IDE8). However, the isolation and propagation of E. minasensis strains from cattle has remained elusive. In this study, the E. minasensis strain Cuiabá was isolated from an eight-month-old male calf of Holstein breed that was naturally infected with the bacterium. The calf presented clinical signs and hematological parameters of bovine ehrlichiosis. The in vitro culture of the agent was established in the canine cell line DH82. Ehrlichial morulae were observed using light and electron microscopy within DH82 cells. Total DNA was extracted, and the full genome of the E. minasensis strain Cuiabá was sequenced. A core-genome-based phylogenetic tree of Ehrlichia spp. and Anaplasma spp. confirmed that E. minasensis is a sister taxa of E. canis. A comparison of functional categories among Ehrlichia showed that E. minasensis has significantly less genes in the 'clustering-based subsystems' category, which includes functionally coupled genes for which the functional attributes are not well understood. Results strongly suggest that E. minasensis is a novel pathogen infecting cattle. The epidemiology of this Ehrlichia deserves further attention because these bacteria could be an overlooked cause of tick-borne bovine ehrlichiosis, with a wide distribution.
This data article presents on the ectoparasites infestation on small mammals in Peninsular Malaysia. The dataset on ectoparasites infestation is important because it raises a major medical concern regarding the spread of potentially zoonotic disease from wildlife to human. Tick and chigger are the primary ectoparasites as reservoirs of vector-borne diseases found on small mammals in Malaysia. These small mammals that are infested with ectoparasites occupy various types of habitats, including human settlements, could be of community health risks as the carriers of potentially zoonotic diseases. Field samplings were conducted from February 2015 to February 2016 in three different ecological habitats of mixed dipterocarp forest, coastal forest and insular forest, in Terengganu, Malaysia. A total of 35 and 22 species of bats and rodents respectively were captured and examined for ectoparasites. Twenty-three species of bats and 16 species of small mammal were recorded as hosts for at least one species of ectoparasites. These findings show that the highest ectoparasite infestation occurred on bat community.
Multiple alcohol use disorder (AUD)-related behavioral alterations are governed by protein kinase C epsilon (PKCε), particularly in the amygdala. Protein kinase C (PKC) is readily phosphorylated at Ser729 before activation by the mTORC2 protein complex. In keeping with this, the current study was conducted to assess the variations in mTORC2 and PKCε during different ethanol exposure stages. The following groups of rats were employed: control, acute, chronic, ethanol withdrawal (EW), and EW + ethanol (EtOH). Ethanol-containing and non-ethanol-containing modified liquid diets (MLDs) were administered for 27 days. On day 28, either saline or ethanol (2.5 g/kg, 20% v/v) was intraperitoneally administered, followed by bilateral amygdala extraction. PKCε mRNA levels were noticeably increased in the amygdala of the EW + EtOH and EW groups. Following chronic ethanol consumption, the stress-activated map kinase-interacting protein 1 (Sin1) gene expression was markedly decreased. In the EW, EW + EtOH, and chronic ethanol groups, there was a profound increase in the protein expression of mTOR, Sin1, PKCε, and phosphorylated PKCε (Ser729). The PKCε gene and protein expressions showed a statistically significant moderate association, according to a correlation analysis. Our results suggest that an elevated PKCε protein expression in the amygdala during EW and EW + EtOH occurred at the transcriptional level. However, an elevation in the PKCε protein expression, but not its mRNA, after chronic ethanol intake warrants further investigation to fully understand the signaling pathways during different episodes of AUD.
A total of 204 rodents comprising 14 host species from four different habitats were examined. Nine rodent species were trapped from the forest and another five species were trapped from the coastal, rice field and urban habitats. Rattus rattus diardii (67%) was the predominant rodent species examined. Fifty six (47.3%) rodents and shrews were found to be infested with at least one of the 20 species of ectoparasite recovered. Mites belonging to the family Trombiculidae were the predominant ectoparasite species recovered. Ticks belonging to the family Ixodidae were recovered mainly from the forest dwelling rodents. Polyplax spinulosa and Hoplopleura pacifica were the common lice species found infesting the urban rodents. Xenopsylla cheopis was the only flea species recovered. The following ecto-parasites have been incriminated as important vectors or as mechanical carriers for the transmission of zoonotic diseases: Ixodes granulatus, Dermacentor sp. Haemaphysalis sp., Amblyomma sp. Ascoschoengastia indica, Leptotrombidium deliense, Ornithonyssus bacoti, Laelaps nuttalli, H. pacifica, P. spinulosa and Xenopsylla cheopis. Urban and forest rodents were significantly higher in ecto-parasitic infestation, compared to rats from the other two habitats. However, there was no significant statistical association between male and female rodents infested with ectoparasites.
The rickettsial disease of man found only in Asia is mite-borne (scrub) typhus, caused by Rickettsia tsutsugamushi. Unique to southern Japan is a little-known human mononucleosis-like disease caused by Rickettsia sennetsu. In 1981 and 1982, there was a remarkable resurgence in the number of reported cases of mite-borne typhus in Japan after some years of virtual absence. Recent studies of R sennetsu have resulted in its reclassification to the genus Ehrlichia, members of which until now have been exclusively pathogens of animals. The historical background of ecologic investigations, in Malaysia and elsewhere, of these two developments suggest directions for future research.
An epidemiological study in a mature oil palm estate in Peninsular Malaysia has demonstrated a low prevalence of R. tsutsugamushi infection in small mammals. The direct fluorescent antibody technique for assaying infections in chiggers proved more sensitive than mouse inoculation. Most infections in both chiggers and rodents were caused by the Karp strain.
Here, we investigated an outbreak of leptospirosis among reserve military recruits that occurred following a survival exercise in the Hulu Perdik forest within the Hulu Langat district, Kuala Lumpur, Malaysia. Blood samples from the 12 patients that presented symptoms for febrile illness on clinical examination were subjected to laboratory investigation, comprising Lepto IgM rapid test, IgM ELISA, and microscopic agglutination test (MAT). All these patients were interviewed for possible risk factors for leptospirosis. Rodent trapping and environmental sampling for possible isolation of leptospires in the outbreak site was performed. The isolated leptospires were genetically characterized and investigated for the potential epidemiological link with human leptospirosis. Among the 12 patients, two (2/12; 16.6%) were confirmed positive for leptospirosis by microscopic agglutination test (MAT with titers 400-800; serovar autumnalis and hardjobovis). Two Leptospira species from rodents (L. interrogans and L. borgpetersenii) and two from the environment (L. kmetyi and L. wolffii) were identified. The possible epidemiological link between human serovars and animal Leptospira species indicates rodents as the potential reservoir while the environment (soil and water) serves as a transmission route. This investigation highlights the robust presence of pathogenic leptospires on Malaysian environment and rodents which may present the risk of infection, especially among high-risk individuals. Hence, occupational risk individuals are cautioned to observe appropriate preventive measures including prophylaxis and seek immediate medical attention for any illness following similar activities.
Medwayella traubiana n. sp., M. pfeifferi n. sp. and M. sabahae n. sp. (Pygiopsyllidae) are described from Sabah (north of Borneo island), the first two on Tupaia tana (Scandentia), the last on Sundasciurus lowii (Rodentia). Sex male is only identified, because these fleas have been collected in sympatry, or even in syntopy. Their determination is based on segment IX and aedeagus. If M. traubiana and M. pfeifferi are related to some known species, M. sabahae is clearly distinct from other Medwayella.
Cyclic AMP (cAMP) inducible transcription factor cAMP responsive element binding protein 3 like 1 (Creb3l1) is strongly activated in the hypothalamus in response to hyperosmotic cues such as dehydration (DH). We have recently shown that Creb3l1 expression is upregulated by cAMP pathways in vitro, however the exact mechanisms are not known. Here we show that increasing Creb3l1 transcription by raising cAMP levels in mouse pituitary AtT20 cells automatically initiates cleavage of Creb3l1, leading to a greater abundance of the transcriptionally active N-terminal portion. Inhibiting protein synthesis indicated that de novo protein synthesis of an intermediary transcription factor was required for Creb3l1 induction. Strategic mining of our microarray data from dehydrated rodent hypothalamus revealed four candidates, reduced to two by analysis of acute hyperosmotic-induced transcriptional activation profiles in the hypothalamus, and one, orphan nuclear receptor Nr4a1, by direct shRNA mediated silencing in AtT20 cells. We show that activation of Creb3l1 transcription by Nr4a1 involves interaction with a single NBRE site in the promoter region. The ability to activate Creb3l1 transcription by this pathway in vitro is dictated by the level of methylation of a CpG island within the proximal promoter/5'UTR of this gene. We thus identify a novel cAMP-Nr4a1-Creb3l1 transcriptional pathway in AtT20 cells and also, our evidence would suggest, in the hypothalamus.
Isoflavones are dietary phytoestrogens commonly found in soy-based products. The widespread presence of isoflavones in soy infant formula and breast milk may have long-lasting effects on the development of sex hormone-sensitive organs like the skeleton. Animal early-life programming models are suitable for testing the skeletal effects of pre- and neonatal exposure of soy isoflavones. This review aims to collate the impacts of early-life exposure of soy isoflavones as evidenced in animal models. The isoflavones previously studied include daidzein, genistein, or a combination of both. They were administered to rodent pups during the first few days postnatal, but prolonged exposure had also been studied. The skeletal effects were observed when the animals reached sexual maturity or after castration to induce bone loss. In general, neonatal exposure to soy isoflavones exerted beneficial effects on the skeletal system of female rodents, but the effects on male rodents seem to depend on the time of exposure and require further examinations. It might also protect the animals against bone loss due to ovariectomy at adulthood but not upon orchidectomy. The potential benefits of isoflavones on the skeletal system should be interpreted together with its non-skeletal effects in the assessment of its safety and impacts.
The progressive loss of structure and functions of neurons, including neuronal death, is one of the main factors leading to poor quality of life. Promotion of functional recovery of neuron after injury is a great challenge in neuroregenerative studies. Melatonin, a hormone is secreted by pineal gland and has antioxidative, anti-inflammatory, and anti-apoptotic properties. Besides that, melatonin has high cell permeability and is able to cross the blood-brain barrier. Apart from that, there are no reported side effects associated with long-term usage of melatonin at both physiological and pharmacological doses. Thus, in this review article, we summarize the pharmacological effects of melatonin as neuroprotectant in central nervous system injury, ischemic-reperfusion injury, optic nerve injury, peripheral nerve injury, neurotmesis, axonotmesis, scar formation, cell degeneration, and apoptosis in rodent models.
Leptin, a 16 kDa protein and a product of the ob/ob gene, has a tertiary structure similar to that
of a cytokine. It is primarily secreted by white adipose tissue and its levels in the blood correlate
positively with percentage body fat. Leptin was first identified in 1994 as a major factor that
regulated food intake and energy balance. Leptin in the circulation exists either as a free
monomeric hormone or bound to its soluble receptor. Its serum levels usually range from 0.5 to
37.7 ng/ml in males and 2.0 to 45.2 ng/ml in females. The half-life of leptin is between 20 - 30
minutes and it is eliminated mainly by the kidneys. However, research over the last 25 years
has revealed numerous other physiological roles for leptin, including roles in inflammation,
immune function, neuro-endocrine function, bone metabolism, blood pressure regulation and
sexual maturation. Most of these roles have been identified from studies on leptin deficient
rodents. Apart from energy balance and sexual maturation, where its role is direct and obvious,
its actions on the rest of the other systems are permissive. Actions of leptin are both centrally
and peripherally mediated involving receptors that are widely distributed in the body. Six leptin
receptor isoforms, belonging to the class 1 cytokine receptor family, have been identified.
These receptors are products of the OBR gene. The cellular actions of leptin are mediated
through any one of five different signalling pathways that include the JAK-STAT, PI3K, MAPK,
AMPK, and the mTOR signalling pathways.
Chronic isoleucine supplementation prevents diet-induced weight gain in rodents. Acute-isoleucine administration improves glucose tolerance in rodents and reduces postprandial glucose levels in humans. However, the effect of chronic-isoleucine supplementation on body weight and glucose tolerance in obesity is unknown. This study aimed to investigate the impact of chronic isoleucine on body weight gain and glucose tolerance in lean and high-fat-diet (HFD) induced-obese mice. Male C57BL/6-mice, fed a standard-laboratory-diet (SLD) or HFD for 12 weeks, were randomly allocated to: (1) Control: Drinking water; (2) Acute: Drinking water with a gavage of isoleucine (300 mg/kg) prior to the oral-glucose-tolerance-test (OGTT) or gastric-emptying-breath-test (GEBT); (3) Chronic: Drinking water with 1.5% isoleucine, for a further six weeks. At 16 weeks, an OGTT and GEBT was performed and at 17 weeks metabolic monitoring. In SLD- and HFD-mice, there was no difference in body weight, fat mass, and plasma lipid profiles between isoleucine treatment groups. Acute-isoleucine did not improve glucose tolerance in SLD- or HFD-mice. Chronic-isoleucine impaired glucose tolerance in SLD-mice. There was no difference in gastric emptying between any groups. Chronic-isoleucine did not alter energy intake, energy expenditure, or respiratory quotient in SLD- or HFD-mice. In conclusion, chronic isoleucine supplementation may not be an effective treatment for obesity or glucose intolerance.
Introduction: Polymetabolic syndrome is a malady encompassing centralized accumulation of lipids and subsequent resistance to insulin leading towards diabesity. Currently, this condition is perilous threat to public health and also, creating perplexity for medical scientists. There is an intensive need for the development of obese rodent model having close resemblance with human metabolic syndrome (MetS); so that intricate molecular and/or therapeutic
targets can be elucidated. The resultant simulations will be beneficial to explicate not only pathogenesis but also secret conversation of signaling pathways in inducing MetS related complications in other organs. Methods: Currently, there are different methods for the development of rodent models of MetS, for instance, utilizing high lipogenic diet, genetic alterations, induction by chemicals or by combination of high fat diet and few others. In general, combination of cafeteria or western diet and low dose of streptozotocin (STZ) is a fine example of diet induced experimental model. In this model animals are allowed free access to highly palatable, energy dense, unhealthy human food for 12-18 weeks which promotes voluntary hyperphagia resulting in weight gain, increased fat mass and insulin resistance. At the end of feeding period 30mg/kg STZ is given intraperitoneally to mimic human type 2 diabetic condition.
Conclusion: Consumption of cafeteria diet with low dose STZ is considered to be the robust model of diabesity offering an exceptional stage to investigate the genomic, molecular, biochemical and cellular mechanisms of obesity and type 2 diabetes.