Infection Of Adult Rats Research Articles

Evaluation of the Therapeutic Effect of Syzygium aromaticum Essential Oil in Wistar Rats Infected with Candida albicans - Biochemical and Hematological Study

The objective of this study, on the one hand, is to evaluate the impact of Candida Albicans infection (10 6 CFU per 0.2 ml of intravenous inoculum) on the biochemical and hematological approaches of adult Wistar rats, on the other hand, to test the efficacy of Syzygium aromaticum essential oil (CEO) in restoring or not the harmful effects of the studied yeast with a daily intraperitoneal injection of 0.1 ml CEO/kg. The extraction of the essential oil from S.aromaticum by hydro-distillation allowed us to obtain CEO with a yield of 10.18%. Infection of adult rats with Candida albicans by intravenous injection at a concentration of 106 CFU per 0.2 ml of inoculum increased hepatic and renal fungal load. The infection also revealed a disruption of various biochemical parameters, including liver (AST, ALT), kidney (urea, creatinine) biochemical assays, and hematological (white and red blood cells, platelets...); also, the results show a correction in the values of these parameters following the administration of CEO (by an intraperitoneal injection of 0.1 ml CEO/kg/day) compared to those of infected animals. CEO also corrected the shape of the affected blood cells after infection with C. albicans.

Antibacterial effect of Chromolaena odorata (Awolowo Leaf) aqueous leaf extract on Pseudomonas aeruginosa induced gastrointestinal tract infection in adult Wistar rat

The effect of Chromolaena odorata aqueous leaf extract on Pseudomonas aeruginosa induced gastrointestinal tract infection in adult rats was studied using thirty six (36) adult wistar rats, whose weights range from 72-100g. The rats were allowed to acclimatize for two weeks and checked for fitness through weight check and urinalysis. Twelve rats were used for toxicological study (LD50) while 24 rats were used to determine the antibacterial effects of Chromolaena odorata leaf extract. The 12 rats for LD50 were divided into three groups of four rats each while the other 24 rats were divided into four groups of six rats each. The antibacterial effect of Chromolaena odorata extract was significantly high in group Q after treatment (4.5±2.12 Cfu/ml) when compared with the mean value before treatment (20.0±4.24 Cfu/ml). The antibiotic effect of ciprofloxacin was higher in group R rats after treatment (0.00±0.00 Cfu/ml) when compared with the mean value before treatment (24.0±1.41 Cfu/ml). But in group S, the mean value of count after treatment was significantly higher (26.5±13.44 Cfu/ml) when compared with the mean value before treatment (14.5±4.95 Cfu/ml) and this is because this group was not treated with either leave extract or antibiotics. Conclusively, the leave extract of Chromolaena odorata could be adopted as an alternative treatment against gastrointestinal tract infections especially those due to Pseudomonas aeruginosa.

Comparison of Mucosal, Subcutaneous and Intraperitoneal Routes of Rat Leptospira Infection.

Leptospirosis is a zoonosis found worldwide that is caused by a spirochete. The main reservoirs of Leptospira, which presents an asymptomatic infection, are wild rodents, including the brown rat (Rattus norvegicus). Experimental studies of the mechanisms of its renal colonization in rats have previously used an intraperitoneal inoculation route. However, knowledge of rat-rat transmission requires the use of a natural route of inoculation, such as a mucosal or subcutaneous route. We investigated for the first time the effects of subcutaneous and mucosal inoculation routes compared to the reference intraperitoneal route during Leptospira infection in adult rats. Infection characteristics were studied using Leptospira renal isolation, serology, and molecular and histological analyses. Leptospira infection was asymptomatic using each inoculation route, and caused similar antibody production regardless of renal colonization. The observed renal colonization rates were 8 out of 8 rats, 5 out of 8 rats and 1 out of 8 rats for the intraperitoneal, mucosal and subcutaneous inoculation routes, respectively. Thus, among the natural infection routes studied, mucosal inoculation was more efficient for renal colonization associated with urinary excretion than the subcutaneous route and induced a slower-progressing infection than the intraperitoneal route. These results can facilitate understanding of the infection modalities in rats, unlike the epidemiological studies conducted in wild rats. Future studies of other natural inoculation routes in rat models will increase our knowledge of rat-rat disease transmission and allow the investigation of infection kinetics.

Viral interference with neuronal integrity: what can we learn from the Borna disease virus?

The neurotropic Borna disease virus (BDV) is unusual in that it can persistently infect neurons of the central nervous system (CNS) without causing general cell death, reflecting its favourable adaptation to the brain. The activity-dependent enhancement of neuronal network activity is however disturbed after BDV infection, possibly by its effect on the protein kinase C signalling pathway. The best model for studying BDV, which has a non-cytolytic replication strategy in primary neurons, is the rat. Infection of adult rats results in a fatal immune-mediated disease, whereas BDV establishes persistent infection of the brain in newborn rats resulting in progressive neuronal cell loss in defined regions of the CNS. Our recently developed system of BDV-infected hippocampal slice cultures has clearly shown that the onset of granule cell loss begins after the formation of the mossy fibre projection. Quantitative analysis has revealed a significant increase in synaptic density on identified remaining granule cell dendrites at 6weeks after infection, followed by a decline. Granule cells are the major target of entorhinal afferents. However, despite an almost complete loss of dentate granule cells during BDV infection, entorhinal axons persist in their correct layer, both in vivo and in slice cultures, possibly exploiting rewiring capabilities and thereby allowing new synapse formation with available targets. These morphological observations, together with electrophysiological and biochemical data, indicate that BDV is a suitable model virus for studying virus-induced morphological and functional changes of neurons and connectivity patterns.

Upregulation of chemokine receptor gene expression in brains of Borna disease virus (BDV)-infected rats in the absence and presence of inflammation.

Infection of adult rats with Borna disease virus (BDV) causes CD8 T cell-mediated meningoencephalitis. Previously, we described a complex pattern of chemokine gene expression in the central nervous system (CNS) of such rats. We now found that expression of chemokine receptor genes CXCR3, CCR5, CX(3)CR1, and CXCR4 was also upregulated, which is in agreement with the predominance in brains of adult infected rats of T cells and monocytes/macrophages that express these receptors. In contrast to these rats, neonatally infected rats (designated PTI-NB) develop a persistent CNS infection associated with neurodegenerative processes in the absence of inflammation. In brains of PTI-NB rats, sustained expression of chemokines also takes place. We therefore analyzed mRNA expression of selected chemokine receptor genes, as well as of the chemokine fractalkine in brains of PTI-NB rats. We observed a marked increase of CCR5 and CX(3)CR1 transcripts in brains of these rats. CX(3)CR1 expressing cells were predominantly microglia, and upregulation of CX(3)CR1 was mainly due to an increase in the number of CX(3)CR1 expressing microglia. Fractalkine gene expression was found to be reduced to similar extents in brains of adult and newborn infected rats. These findings might be of relevance with respect to the selective neuronal cell loss observed in brains of PTI-NB rats.

Cyclophosphamide-induced immunosuppression protects cardiac noradrenergic nerve terminals from damage by Trypanosoma cruzi infection in adult rats

Trypanosoma cruzi-infected juvenile rats develop severe cardiac sympathetic denervation in parallel with acute myocarditis. This aspect has not been studied in adult rats, thought to be resistant to this infection. The mechanism involved in T. cruzi-induced neuronal damage remains to be completely elucidated. In juvenile rats, the mortality during the acute phase depends on T. cruzi populations, ranging from 30% to 100%. Therefore, studies of mechanisms through hazardous procedures such as immunosuppression are restricted. The current paper shows that adult rats infected with T. cruzi (Y strain) develop severe acute myocarditis and cardiac sympathetic denervation, despite null mortality and virtual absence of patent parasitaemia followed by negative haemoculture. Recovery from the myocarditis and denervation occurred but PCR studies showed persistence of parasite DNA at least until day 111 post inoculation. Immunosuppression by cyclophosphamide treatment increased the parasitaemia, prevented the acute myocarditis and the sympathetic denervation without significant alteration of the myocardial parasitism. These results argue against a direct role for parasite-derived products and implicate the inflammatory cells in the denervation process. As previous studies in juvenile animals have discarded an essential role for radiosensitive cells, the macrophages remain as the possible effectors for the T. cruzi-induced neuronal damage.

Retrograde transynaptic pseudorabies virus infection of central autonomic circuits in neonatal rats

Pseudorabies virus (PRV) is widely used to map synaptically-linked neural circuits in adult animals. The present study sought to determine whether PRV has similar utility in neonatal rats, and whether central PRV infection in neonates elicits astrocytic and microglia/macrophage responses similar to those that contribute to specific transynaptic neuronal infection in adult rats. Retrograde transneuronal infection of autonomic circuits was examined 24–64 h after injection of an attenuated strain of PRV (PRV-Bartha) into the ventral stomach wall of 1-day-old rats. Brain and spinal cord sections were processed for immunocytochemical detection of PRV. Alternate sections were processed for immunolocalization of glial fibrillary acidic protein (GFAP) to identify fibrous astrocytes, or for an antigen associated with the complement C3bi receptor (OX42) to identify microglia. As in adult rats, the number and distribution of infected CNS neurons in neonatal rats increased progressively with advancing post-inoculation survival. Infected CNS neurons initially were restricted to the thoracic intermediolateral cell column and the dorsal motor nucleus of the vagus. Longer survival times led to retrograde transynaptic infection of additional neurons in the thoracic spinal cord, nucleus of the solitary tract, ventrolateral medulla, and caudal raphe nuclei. At the longest post-inoculation intervals, infected neurons also were observed in the area postrema and in certain autonomic-related regions of the rostral brainstem, hypothalamus, and amygdala. Quantitative analysis of immunolabeling in the dorsal vagal complex demonstrated that regions containing neurons at early stages of viral infection displayed increased astrocytic GFAP immunostaining; conversely, areas containing neurons at later stages of infection were characterized by a significant loss of GFAP staining and a parallel increase of OX42 microglia/macrophage immunolabeling. We conclude that PRV is effectively transported through synaptically-linked CNS circuits in neonatal rats, and that spatiotemporally-ordered responses by non-neuronal cells may contribute to the synaptic specificity of transneuronal viral transport.

Oral administration of human T-cell leukemia virus type 1 induces immune unresponsiveness with persistent infection in adult rats.

The major route of human T-cell leukemia virus type 1 (HTLV-1) infection is mother-to-child transmission caused by breast-feeding. We investigated the host immune responses to orally established persistent HTLV-1 infection in adult rats. HTLV-1-producing MT-2 cells were inoculated into immunocompetent adult rats either orally, intravenously, or intraperitoneally. HTLV-1 proviruses were detected in the peripheral blood and several organs for at least 12 weeks. Transmission of HTLV-1 to these animals was confirmed by analysis of HTLV-1 flanking regions. Despite persistent HTLV-1 presence, none of the orally inoculated rats produced detectable levels of anti-HTLV-1 antibodies, whereas all intravenously or intraperitoneally inoculated rats showed significant anti-HTLV-1 antibody responses. T-cell proliferative responses against HTLV-1 were also absent in orally inoculated rats. Our findings suggest that gastrointestinal exposure of adult rats to HTLV-1-infected cells induces persistent HTLV-1 infection in the absence of both humoral and cellular immune responses against HTLV-1. This immune unresponsiveness at primary infection may subsequently affect the host defense ability against HTLV-1.

Axonal transport of Borna disease virus along olfactory pathways in spontaneously and experimentally infected rats

In this study it has been shown that infection of mother rats by Borna disease virus (BDV) from infected newborns led to a fatal disease. This differed both in clinical symptoms and in histological alterations from the form of the disease which occurred after intracerebral (i.c.) infection. Both parameters were, however, similar to those seen after experimental intranasal (i.n.) infection of adult rats. Detailed immunohistological studies showed clearly that after experimental i.n. infection, the infecting virus migrates intraaxonally from the neuroreceptors in the olfactory epithelium into the brain. It is therefore suggested that i.n. transmission is an important route of natural BDV infection.

Naturally occurring lethal parvovirus infection of juvenile and young-adult rats.

A lethal disease characterized by hemorrhage and necrosis of the brain, testes, and epididymides developed in young adult rats housed in specific pathogen free quarters. Morphological, virological, and serological investigations of the outbreak indicated that the probable causative agent was rat virus (Kilham), a common parvovirus of rats that usually induces persistent, asymptomatic infection in adult rats.

T and B cell population changes in young and in adult rats infected with Plasmodium berghei.

Malaria infection in young rats is characterized by high parasitemia, severe anemia, and death. Parasitemia is lower in older rats, and the rats usually survive. This study was designed to investigate the immunological basis of this difference. T cell numbers in the thymuses and spleens of young (4 weeks old) and in adult (18 weeks old) infected and control rats were determined by killing with anti-theta serum and complement. The number of complement receptor lymphocytes (B cells) in spleens was determined after these cells had formed rosettes with sensitized, complement-coated sheep erythrocytes. Infection in young rats was characterized by progressive and severe thymic involution and by decreasing numbers of T and B cells in the spleen. In 18-week-old rats, T cell numbers in the spleen were slightly below those of controls early in infection but exceeded normal values by day 15. Progressive thymic involution was not a feature of infection in adult rats. The number of complement receptor lymphocytes in the spleens of adult rats decreased dramatically early in infection but were nearly normal by day 15. Severity of malarial infection in young rats is related to the inability of their lymphocytes to respond to Plasmodium berghei antigens early in infection in a way that leads to immunity.

Enteric transmission of parvoviruses: pathogenesis of rat virus infection in adult rats.

Lipton, H. (Northwestern Univ. Medical School, Chicago, Ill. 60611), N. Nathanson and J. Hodous. Enteric transmission of parvoviruses: pathogenesis of rat virus infection in adult rats. Am J Epidemiol 96: 443–446, 1972.—To explore the hypothesis that rat virus (RV) is transmitted as an enteric infection in its natural host, an attempt was made to infect adult rats by several routes. Gastric infections produced regular viremia with virus excretion in feces but not in urine, and minimal levels of replication in the gut and other tissues. Furthermore, virus spread readily from gastrically infected rats to cage contacts and to environmental contacts housed in cages previously occupied by infected animals. The data support the view that RV is transmitted as an enteric infection and the published literature suggests a similar mode of transmission for several other parvoviruses.