• Journal of fish pathology
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• v.30 no.1
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• pp.11-24
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• 2017

The current investigation dealing with the causative agent of mass mortalities in cultured Oreochromis niloticus. The diseased fish showed external hemorrhage, unilateral and bilateral eye opacity, ended by blindness and fish death. The postmortem lesions revealed congested friable kidney and spleen, and liver has yellow nodules. Obtained isolates were identified as Aeromonas hydrophila (the causative agent of Motile Aeromonas Septicemia) and found to be highly pathogenic as they contained hemolysin virulence gene causing mortality reached to 100 and 70% in intraperitoneal and intramuscular infection. The prevalence of MAS was 80% among the surveyed O. niloticus. Blood and serum were collected from naturally diseased, intraperitoneal and intramuscular injected O. niloticus for hematological and biochemical examination. Similarly, gills, musculature, kidney, liver and spleen were collected for histopathological evaluation, and micropathomorphological analysis of spleen was done. Macrocytic hypochromic anemia was recorded in the intraperitoneal infection. Serum protein, albumin and globulin were decrease only in naturally diseased fish. Leucocytosis with heterophilia and lymphocytosis were observed in naturally diseased and intraperitoneal infected fish. There were severe degenerative changes and hemorrhagic necrosis in the examined tissues which were more obvious in intraperitoneal than intramuscular infection. Activation and proliferation of melanocytes macrophages centers with severe hemosiderosis were recorded in spleen of naturally diseased and experimentally infected fish.

• IMMUNE NETWORK
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• v.12 no.5
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• pp.196-206
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• 2012

Besides their role as building blocks of protein, there are growing evidences that some amino acids have roles in regulating key metabolic pathways that are necessary for maintenance, growth, reproduction, and immunity. Here, we evaluated the modulatory functions of several amino acids in protective immunity against mucosal infection of herpes simplex virus type 1 (HSV-1). We found that glutamine (Gln) and leucine (Leu) showed enhanced protective immunity to HSV-1 mucosal infection when two administration of Gln and single administration of Leu per day, but not when administered in combinations. Ameliorated clinical signs of HSV-1 challenged mice by the intraperitoneal administration of Gln and Leu were closely associated with viral burden and IFN-${\gamma}$ production in the vaginal tract at 2 and 4 days post-infection. In addition, the enhanced production of vaginal IFN-${\gamma}$ appeared to be caused by NK and HSV-1 antigen-specific Th1-type CD4+ T cells recruited into vaginal tract of mice treated with Gln and Leu, which indicates that IFN-${\gamma}$, produced by NK and Th1-type CD4+ T cells, may be critical to control the outcome of diseases caused by HSV-1 mucosal infection. Collectively, our results indicate that intraperitoneal administration of Gln and Leu following HSV-1 mucosal infection could provide beneficial effects for the modulation of protective immunity, but dosage and frequency of administration should be carefully considered, because higher frequency and overdose of Gln and Leu, or their combined treatment, showed detrimental effects to protective immunity.

• The Journal of the Korean Society for Microbiology
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• v.7 no.1
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• pp.29-41
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• 1972

To grow Myocbacterium leprae in cultured mouse peritoneal macrophages, studies were made with trypsin-purified Myco. laprae on 1) the dynamics of infection of mouse peritonal macrophages in vivo with Myco. leprae by intraperitoneal inoculation, 2) growth experiment of Myco. leprae in cultured mouse peritoneal macrophages by in vivo infection and in vitro cultivation and 3) the observation of pathological changes in spleens of mice induced by intraperitoneal inoculation of Myco. leprae. Results are summarized as follows; 1. Continuing and significant decreases were observed in the numbers of both acid-fast bacilli in cultured macrophage and of macrophages harboring.acid-fast bacilli by the length of inter vats between the time of intraperitoneal inoculation of Myco. leprae and the time of initiation of macrophage culture. 2. No evidence of multiplication of Myco. leprae in the peritoneal macrophages in vivo was found up to 5 months after intraperitoneal inoculation. 3. With cultures of macrophages made 24 hours and 1 week after intraperitoneal inoculation of Myco. leprae and maintained in vitro up to 2 to 3 months, microscopic examination of the stained preparations of cultured macrophages indicated that an apparent increase in the number of acid-fast bacilli in the macrophages did occur. 4. Quantitative experiment with in vivo infected-in vitro cultured macrophages revealed certain features of increase in the number of total acid-fast bacilli in the cultured macrophages 7 and 9 weeks after initiation of the cultures. 5. Pathological changes in the spleens mice inoculated with Myco. leprae were of mainly degenerative nature in the red pulp. No multiplication of Myco. leprae was observed in the spleens of mice up to 5 months after intraperitoneal inoculation.

• Korean Journal of Veterinary Research
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• v.40 no.1
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• pp.145-152
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• 2000

This study was performed to study the sequential clinical and pathologic changes of Korean isolate KBA-2 of Neospora caninum in SCID mice following intraperitoneal infection. Also the results of PCR and in vitro isolation was compared during the study. The infection appears to be disseminated hematogenously, when the infection was chased every 3days up to 21 days following infection. The PCR method was determined to be more effective than in vitro isolation regarding early detection of the organism follwing infection.

• YAKHAK HOEJI
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• v.47 no.3
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• pp.190-194
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• 2003

As previously reported, an immunoglobulin M (IgM) monoclonal antibody (MAb) B6.1, specific for a cell wall B-l,2-mannotriose, was protective against vaginal infection due to Candida albicans when mice were treated with the antibody. In this study, the role of neutrophil was examined in the protective effect of MAb B6.1 against vaginal infection. To deplete neutrophils, mice were given intravenously rat anti-mouse neutrophile MAb RB6-8C5 prior to intraperitoneal administration of MAb B6.1 to these mice. The mice were examined for antibody in their reproductive tract. By an ELISA, MAb B6.1 was found in the vaginal homogenates, but no antibody was detected in vaginal lavage materials. The neutropenia was induced by a single dose of the anti-neutrophil antibody, but lymphocytes were also partially depleted. The protective effect of MAb B6.1 was decreased when mice pretreated with MAb RB6-8C5 were given the anti-Candida antibody before challenge with C. albicans yeast cells intravaginally. These results show that neutrophils are involved in the MAb B6.1 protection against Candida vaginal infection.

• Korean Journal of Veterinary Research
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• v.20 no.1
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• pp.33-38
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• 1980

1. In adult ICR-SLC mice, significant increase in the occurrence of the Tyzzer's disease was noted when the reticuloendothelial system was blockaded with the carbon particles. The most suitable bloakading time was 2 hours before inoculating Tyzzer's organisms, the route was intraperitoneal and the dose was 3mg/body. 2. Survival rate of the experimental group ICR-SLC suckling mice receiving BCG ($3{\times}10^8$) 6 days prior to intraperitoneal inoculation of Tyzzer's organisms was 80 percent, but the control group was 17%. 3. In comparing the survival rate of the nude/nude mice with the nude/+ mice, the former congenitally thymus deficient mice are 11 percent, but the latter are 67 percent.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.2
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• pp.276-279
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• 2001

The effect of helminthiasis on zinc metabolism was monitored using endogenous $^{65}Zn$ after intraperitoneal injection of 1 g of $^{65}Zn$ as zinc chloride. In the first experiment zinc turnover was investigated in 18 male weanling rats, which were randomly divided into 3 groups. One group was infected with 73 third stage larvae of Nippostrongylus brasiliensis per gram body weight ; the other groups were the pair-fed and ad lib-fed controls. The route of loss of zinc was investigated in the second experiment with the same design using 18 animals with a lower dose of infection (33 larvae per gram body weight). The biological half life of endogenous $^{65}Zn$ was lower (p<0.05) in the infected group as compared to the controls. In the later phase of infection (9th to 16th day) there was reduced retention of $^{65}Zn$ and increased loss (p<0.05) of $^{65}Zn$ from the body though urine and faeces. It was concluded that infection of N. brasiliensis was accompanied by increased loss of endogenous Zn through faeces and urine.

• Journal of Korean Neurosurgical Society
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• v.56 no.4
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• pp.361-363
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• 2014

Percutaneous endoscopic gastrostomy tube placement is often performed in patients with a ventriculoperitoneal shunt and it has been accepted as a safe procedure. The authors report a case of a 50-year-old male who developed acute exacerbation of the hydrocephalus immediately after the percutaneous endoscopic gastrostomy tube placement without any signs of shunt infection, which has not been reported until now. After revision of the intraperitoneal shunt catheter, the sizes of the intracranial ventricles were normalized.

• Parasites, Hosts and Diseases
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• v.48 no.4
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• pp.325-329
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• 2010

Toxoplasma gondii KI-1, a recent new isolate from Korea, shows similar pathogenicity and infectivity to mice compared to the virulent RH strain. To understand characteristics of host immunity, including immune enhancement or suppression, we investigated proliferative responses and phenotypes of spleen cells. In addition, kinetics of IFN-${\gamma}$, a Th1 cytokine, was examined in BALB/c mice up to day 6 post-infection (PI). Intraperitoneal injection of mice with $10^3$ KI-1 tachyzoites induced significant decreases (P < 0.05) in proliferative responses of spleen cells. This occurred at days 2-6 PI even when concanavalin A (con A) was added and when stimulated with KI-1 antigen, suggesting suppression of the immunity. $CD4^+$ T-cells decreased markedly at day 2 PI (P < 0.05), whereas $CD8^+$ T-cells, NK cells, and macrophages did not show significant changes, except a slight, but significant, increase of $CD8^+$ T-cells at day 6 PI. The capacity of splenocytes to produce IFN-${\gamma}$ by con A stimulation dropped significantly at days 2-6 PI. These results demonstrate that intraperitoneal injection of KI-1 tachyzoites can induce immunosuppression during the early stage of infection, as revealed by the decrease of $CD4^+$ T-cells and IFN-${\gamma}$.

• Parasites, Hosts and Diseases
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• v.57 no.2
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• pp.117-125
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• 2019

Malarial infection induces tissue hypoxia in the host through destruction of red blood cells. Tissue hypoxia in malarial infection may increase the activity of $HIF1{\alpha}$ through an intracellular oxygen-sensing pathway. Activation of $HIF1{\alpha}$ may also induce vascular endothelial growth factor (VEGF) to trigger angiogenesis. To investigate whether malarial infection actually generates hypoxia-induced angiogenesis, we analyzed severity of hypoxia, the expression of hypoxia-related angiogenic factors, and numbers of blood vessels in various tissues infected with Plasmodium berghei. Infection in mice was performed by intraperitoneal injection of $2{\times}10^6$ parasitized red blood cells. After infection, we studied parasitemia and survival. We analyzed hypoxia, numbers of blood vessels, and expression of hypoxia-related angiogenic factors including VEGF and $HIF1{\alpha}$. We used Western blot, immunofluorescence, and immunohistochemistry to analyze various tissues from Plasmodium berghei-infected mice. In malaria-infected mice, parasitemia was increased over the duration of infection and directly associated with mortality rate. Expression of VEGF and $HIF1{\alpha}$ increased with the parasitemia in various tissues. Additionally, numbers of blood vessels significantly increased in each tissue type of the malaria-infected group compared to the uninfected control group. These results suggest that malarial infection in mice activates hypoxiainduced angiogenesis by stimulation of $HIF1{\alpha}$ and VEGF in various tissues.