This study was performed to observe histopathological changes and serological reactions in chronic anisakiasis of rabbits. Each rabbit was infected per os with 30 larvae of Anisakis type I. Their sera were collected chronologically and the rabbits were killed for histopathological examination, 3, 13, 20, 30, 60, 90 and 150 days after the infection. The results were summarized as below. 1. Most of the larvae were recovered from the stomach, but a few from the omentum, intestine, mesentery and abdominal wall. The recovery rates and distribution of worms by organ were not differed by duration of infection. 2. Histologically the lesion was abscess type on 13 days, i.e., the dead worms were surrounded by fibrinous exudate, histiocytes and thick zone of numerous inflammatory cells. After 30 days, histiocytes were found to invade the worms and the lesion was changing into abscessgranulomatous type. Also a calcified worm was found on the 30th day. After then the worms were observed to be dissolved slowly until 90 days. On 150 day, only one calcified worm was observed. 3. The levels of serum IgG antibody by ELISA reached their maximum 30 days after the infection. After then, it decreased slowly until 150 days after the infection. Above serological and histopathological findings indicated that antigenic stimulation from degenerating Anisakis larvae was the greatest during the first 30 days after infection. This period was corresponding with the beginning of worm resolution or calcification. Serologic test by ELISA would be a valuable tool for confirming chronic anisakiasis.
Background: Bronchial asthma is characterized by chronic eosinophilic inflammatory airway disease associated with bronchial hyperresponsiveness and reversible airway obstruction. Bronchial inflammation in asthma may depend in part on the activation of T helper lymphocytes that elaborate proinflammatory cytokines. T helper (Th) lymphocytes can be divided into two categories; Th1 lymphocytes, which secrete IL-2, IL-12 and IFN-$\gamma$, and Th2 lymphocytes, which secrete IL-4, IL-5, IL-6 and IL-10. Th2 lymphocytes appear to induce allergic responses, whereas Th1 lymphocytes induce delayed-type hypersensitivity response. Some infections, such as tuberculosis, cultivate a Th1 immunological environment and inhibit Th2 lymphocytes function. The presence of such infections might inhibit Th2 immune responses and thus protect development of atopic diseases. Method: 15 patients with allergic bronchial asthma, 10 patients with intrinsic bronchial asthma, and 10 healthy volunteers were studied. The serum concentrations of IFN-$\gamma$, IL-12, IL-4, IL-5, and IL-10 were measured by ELISA method and tuberculin skin test was estimated in different groups. Results: The positive response rates of tuberculin test were 46.7% in patients with allergic asthma, 100% in patients with intrinsic asthma and 60% in normal controls. The positive response rates were significantly lower in patients with allergic asthma than those of in patients with intrinsic asthma (p<0.05). Degree of responses to tuberculin test were $12.0{\pm}9.6mm$ in patients with allergic asthma, $18.4{\pm}4.5mm$ in patients with intrinsic asthma and $10.9{\pm}8.8mm$ in normal controls. The degree of responses were significantly reduced in patients with allergic asthma than those of patients with intrinsic asthma (p<0.05). The serum levels of IL-5 in patients with allergic asthma were significantly higher than in patients with intrinsic asthma and normal controls (p<0.05), although it was insignificant. the serum levels of IL-4 and IL-10 in patients with allergic asthma were higher than that of intrinsic asthma and normal controls. The serum levels of IL-12 and IFN-$\gamma$ in patients with allergic asthma and intrinsic asthma were significantly lower than those in normal controls(p<0.05). The serum levels of total immunoglobulin E (IgE) and peripheral blood eosinophile counts in patients with allergic asthma were significantly higher than those in normal controls. Peripheral blood esinophil counts had a significant correlation with the serum levels of total IgE, IL-5 and IL-10 in patients with allergic asthma (p<0.05). Conclusion: These results have showed that Th1 lymphocyte functions were lowered and Th2 lymphocyte functions were elevated in patients with allergic asthma than those in normal controls. Suppression of Th1 lymphocyte functions by activation of Th2 lymphocyte might be one of the important aspects of pathogenesis in allergic bronchial asthma.
The resource plants of the Mt. Geonji was listed 354 taxa; 92 families, 242 genera, 303 species, 48 varieties and 3 forms. 354 taxa listed consists of 205 taxa of edible plants(57.1%),234 taxa of medicinal plants(65.2%), 167 taxa of ornamental plants(46.5%) and 218 taxa of the others(60.7%). Specific plant species by floral region were total 22 taxa; Trapella sinensis var. antennifera in class IV, Iris ensata var. spontanea in Class II, 16 taxa(Salix glandulosa, Alnus hirsuta, Chrysosplenium flagelliferum, Mallotus japonicus, Ilex macropoda, Grewia biloba var. parviflora, Vaccinium oldhami, Lysimachia barystachys, Fraxinus mandshurica, etc.) in class I. The naturalized plants in this site were 12 families, 23 genera, 28 species, 2 varieties, 30 taxa(Bromus unioloides, Phytolacca americana, Oenothera erythrosepala, Ipomoea hederacea var. hederacea, Aster pilosus, Erechtites hieracifolia) and naturalization rate was 8.5% of all 354 taxa vascular plants. Wild plants disturbing ecosystem like Solanum carolinense and Ambrosia artemisiifolia var. elatior have been increasing. So, it needs continuing control and conservation measures on the plant ecosystem.
The purpose of this observation was to investigate the natural killer cell activities in mice Infected with pathogenic free-living amoeba, Naegleria fowleri and Acanthomoeba culbertsoni according to the infection doses, and infected with non-pathogenic free-living amoeba, Naegleria fowleri. The natural killer cell activity was examined by means of target binding capacity, active NK cell and maximum recycling capacity of the mice after inoculating free-living amoebae with low and high doses. The mice infected with 1 103, 1 105 A. culbertsoni trophozoites showed mortality rates of 6.9% and 65.5%, respectively. The mice infected with 1 104, 1 105 N.fowleri trophozoites showed mortality rates of 5.9% and 72.2%, respectively. The NK cell activities in all experimental groups increased significantly on day 1 after infection as compared with control group, and then remarkably declined thereafter, there was no difference of the cytotoxic activity of the NK cells In mice among inoculation doses of pathogenic free-living amoebae. The target binding capacities of NK cells and percentages of activated NK cells in mice Infected with pathogenic free-living amoebae were slgrlificantly Increased a day after Infection, as compared Uth control group. There was no difference of the maximal recycling capacities of NK cells in all experimental groups as compared Uth control group. There was significant difference in the cytotoxic activity and single cell cytotoxlcity of NK cells between the experimental groups infected with pathogenic free-living amoebae and that infected with non-pathogenic free-living amoebae.
Protective effects of monoclonal antibodies against n. fowleri were comparatively studied. nALB/c mice were treated with two types of monoclonal antibodies, Nf 2 and Nf 154, before and after the infection with N. fowleri. The mortality and mean survival times were then compared. Also, direct effect of the monoclonal antibodies on the N. fewleri trophozoites in vitro were observed. In vitro protective effects of the monoclonal antibodies were also studied in cells infected with N. fowleri. The observed results are summarized as follows: 1. Among mice pretreated twice before the infection with monoclonal antibody Nf 2 (McAb Nf 2), only 15.8% were killed, and the mean survival time was 17, 7 days. This was not much different from the mice pretreated once, as the mortality and mean survival time were 16.7% and 17 days. Those effects were compatible with monoclonal antibody Nf 154 (McAb Nf 154). The above findings contrast with the mortality and mean survival time of the control mice, which were 22.7% and 14.6 days respectively. 2. Mice which received twice the McAb Nf 2 following N. fowleri infection incurred a 19.4% mortality rate with 13.6 days survival time; 17.9% and 15.8 days with on time administration, in contrast to the 25% and 14.6 days in the control group. 3. Marked agglutination effect of McAb Nf 2 or McAb Nf 154 were observed on n. fowkwi, trophogoites. 4. When N, fowleri trophozoites were treated with McAb Nf 2 or McAb Mf 154 combined with comments, the proliferation rate was more significantly suppressed than in that the control, 5. N. fowleri trophozoites treated with McAb Nf 2 or McAb Nf 154 showed an increased number of swollen mitochondria, disfigured cisternal, lipid droplets, and osmiophilic granules in the cytoplasm. 6. A remarkable protective effect of monoclonal antibodies was noticed in CHO cells infected with N. fowleri. More than 90.6% of the infected CHO cells survived, contrasted with 27% of untreated cells. The overall results in this study suggest that N. fewleri treated with monoclonal antibodies against N. fowleri reduce the mortality and prolong the survivial time of the mice when the antibodies are administered before the infection. The protective effect of the monoclonal antibodies is surmised being caused by agglutination of the trophozoites.
The worm development and egg laying pattern of Echinostoma hortense (Trematoda; Echinosto-matidae) were studied in albino rats and the brief clinical course was observed in human volunteers. A total of 21 rats were infected with 20~69 metacercariae each and two humans were with 7 and 27 metacercariae, which were collected from the loaches. For recovery of worms, the rats were sacrificed at irregular intervals from the 6th to 150th day after infection and the human volunteers were treated with praziquantel and purged with magnesium salt on the 26~27th day. The stools of the rats and humans were examined for the eggs. The results were as follows: 1. The worm recovery rate from the rats was not affected by the increase of infection time but varied individually; 9.1~50.0% (31.1 % in average). From humans, 14.3% and 37.0% (32.4% in average) of challenged were recovered. 2. In the rats, it was revealed that the worms rapidly grew for the first 14 days to become 7.59mm in average length and 1.17mm in average width but the growth became much slower thereafter until the 150th day; 7.95mm in length on the 21 th day, 9.04mm on the 28th day, 10.21mm on the 49th day and 12. 62mm on the 150th day. During the early stage of infection, the growth of genital organs (male or female) was expressed as sigmoid curves whereas non-genital organs (such as suckers) was simply as straight lines. 3. The prepatent period of this fluke was 10~12 days in the rats and 16~17 days in men. After the start of oviposition, the egg production by the worms remarkably increased, reached maximum on the 32~33th day, followed by decrease thereafter. The maximum value of E.P.G./worm was 390. 4. The major subjective symptoms in human volunteers were abdominal pain and diarrhea during the early stage of infection. The results show that human is as susceptible as the rats to E. hortense infection and the amount of egg production in the rats is greatly affected by the age of worms.
This study was performed to observe the role of Pneumocystis carinii as an etiologic agent of interstitial pneumonia in immunocompromised hosts. Total 90 male Sprague-Dawley rats, approxi. mately 150-180 g, were used. Fifteen of them were used as control group and remaining 75 (5 groups) were as immunosuppression groups; group 1 received prednisolone (25 mg/kg twice weekly) only; group 2 Prednisolone and tetracycline (75 mk/kg/day) ; group 3 Prednisolone, tetracycline and trimethoprim-sulfamethoxasole (50~250 mg/kg/day) : group 4 prednisolone and trimethoprim-sulfamethoxasole; and group 5 prednisolone and griseofulvin (300 mg/kg/day) until death. The survival days of each group rat were calculated, and upon death their lungs were removed immediately and then stamp smears were prepared and stained by Giemsa or toluidine blue O. For histopathologic observation, lungs were fixed in 10% formalin, cut into sections and stained with Gomori's methenamine silvei, hematoxylin-rosin, and Brovkn & Brenn stain. The results obtained were as follows: 1. The mean survival time of each group rat was 19.3$\pm$5.2 days (group 1), 41.1$\pm$14.0 days (group 2), 50.5$\pm$18.4 days (group 3), 43.0$\pm$22.9 days (group 4) or 21.8$\pm$5.1 days (group 5). Significant differences were noted between group 1 and group 2(p<0.01), group 1 and group 3 (p<0.01), and group 1 and group 4 (p<0.01), which represented bacterial infections were most fatal in immunocompromised rats. Group 5 revealed no difference in the survival day from group 1, while significant differences were noted between group 2 and group 5(P<0.01), group 3 and group 5(p<0.01), and group 4 and group 5(p<0, 01), which represented little importance of fungal infection as the cause of death of the rats. 2. The first fatality due to p. carinii pneumonia occurred 17 days after the beginning of the immunosuppression. The occurrence rate of P. carinii pneumonia in the decreasing order was 92.9% (group 3), 80.0% (group 2 and group 5), 78.6% (group 4) and 33.3% (group 1). With regard to the pathological stage of P. carinii pneumonia, the stage 1 was 11.3%, the stage 2, 28.3%, and the stage 3, 60.4%. 3. Viewing from the duration of immunosuppression, bacterial pneumonia chieay appeared in 1 month, mixed infections (P. carinii and bacteria, or p. carinii and fungi) in 1~2 months, and pure P. carinii pneumonia after 2 months. The present study revealed that P. carinii pneumonia was the most important cause of death of immunocompromised rats later than 1 month after the start of immunosuppression.
In order to determine the susceptible age of Enterobius vermicular is to anthelmintics and to observe the chronologie growth of female E. vermicularis in man, experimental infections were done. About 500 eggs were challenged to 19 volunteers. After 4, 8, 16, 20, 24, 28, 32 and 35 days of infection, each case was treated by either mebendazole or pyrantel pamoate. On the 40th day of infection all cases including control were treated again to terminate the experimental infection and to evaluate the effect of previous treatment. Each case collected 3-day stools to harvest the expelled worms. The results could be summarized as follows: 1. The infection rates of females were in range of 0.6~13.1 % in control cases. Because the collected worms showed comparable growth and development by day, the worms were concluded to be derived from experimental infection. 2. Cases that were treated with mebendazole on 4, 8 and 16 days after infection expelled 37.5%, 2.5% and 67.5% of the number expelled by a control case on the 40th day. Cases treated thereafter expelled no worms on the 40th day. 3. Cases that were treated with pyrantcl pamoates on 4, 8, 16, 24, 28, 32 and 35 days, expelled 90.7%, 25%, 45.3%, 8%, 2.7%, 5% and 29.3% of the number collected from control cases in respect. 4. All the worms collected were females. The total body length increased consistently and comparably from the 20th day of infection. Those collected on the 20th day were 2.5~3.0 mm long with vagina, sac-like structure and strands of ovaries; 24 day-old worms may have short uterus, 28 day-old worms had long uterus without eggs, 32 day-old worms began to produce eggs, 35 day-old worms showed wide variations in egg deposit in uterus, and 40 day-old worms had uterus filled with eggs from vulva to anal levels. From the above results, it was inferred that the life span of female Enterobius vermicularis was longer than 40 days, and the developmental stages of worms younger than 16 days resisted considerably to both mebendazole and pyrantel pamoate.
The author studied on the bionomics of Oriental moth. Cnidocampa flavescens WALKER, damaging to the persimmon tree n the southern part of Korea from 1964 to 1965. The results can be summarized as follows; 1. Emergence peak period of Oriental moth was mid-June in Taegu district and eggs are deposited on the opposite side of persimmon tree leaf. Specially most of eggs are deposited on the terminal part of opposite side and peak period s also mid-June. 2. Hatched Percentage of eggs was $84.4\%$ in 1964 while $96.1\%$ in 1965 at the rearing room. Mean egg Period was $5.984\pm0.162$ in 1964 while $6.262\pm0.094$ days in 1965. Thus during two years, the egg period was about 6 days. 3. In the growth ratio of Oriental moth fed on various host plants persimmon tree, Acer negund, Hazel-wood and Platanus, the best growth ratio was shown on the leaf of Hazel-wood from 1st till 3rd instar, but, on the contrary, persimmon tree was the best from 4th till the last instar. The growth ratio of head width was also the same tendency as the body length above mentioned. Individuals fed on the leaf of platanus were dead after 20 days. 4. Oriental moth has one generation a year and molts 6 times. The first molting occurred in 5 hours after hatched, and the other moltings were done at f days intervals. After 3 days since the last molting, larvae made the non for over-winter in it. 5. As the bristles on the process of larval body are different from each position and instar, judgement of instars are possible by the counting of bristles on the body according to the Table 8. Specially the bristle of L. 2., D. 2, 3 ,8. 10. and L. 1, 3, 4, 5, 6, 7, are perfectly different from each instar. From these bristles, instars can be recognized easily. 6. Pupation of larvae in the over-wintered cocoon on the stem of persimmon tree was done in mid-May and continued will early June when emergence will take place. 7. Mean number of eggs in the ovary was $1325.5\pm2.7182$
Observations were made on the differences of cell-mediated responses in mice of three infectiorl groups di여erently scheduled in their severity with pathogenic Acanthamoeba culbertseni. Infections were done by dropping $5{\;}{\mu}l$ saline suspension containing $3{\times}10^3,{\;}1{\times}10^4,{\;}or{\;}1{\times}10^5$ trophosoites, respectively. Amoebae were cultured anenically in CGV medium and inoculated into the right nasal cavity of CSH/HeJ mice aging around 6∼8 weeks, under the anesthesia by intraperitoneal injection of secobarbital. Delayed type hypersensitivity (DTH) responses in footpad and blastogenlc responses of mouse spleen cells using ($^3H$)-thymidine and the serum antibody titer were measured up to day 14 after infection, and natural killer cell activities were measured up to day, i after infection. The results obtained in this study were as follows: 1. The mice infected with $3{\times}10^3$ trophosoites showed mortality rate of 17%, and 345 in the mice infected with $1{\times}10^4$ trophozoites and 65% with $1{\times}10^5$ trophozoites. 2. In regard to DTH responses in all experimental groups, the level increased on day 7 and declined on day 14 after infection, but their differences could not be noted between infected and control groups. 3. The blastogenic responses of splenocytes treated with amoeba Iysates and lipopolysaccharides (LPS) showed no difference from the control group. The blastogenic responses of splenocytes treated with concanavalin A were declined significantly in the experimental group as compared with the control group, but the blastogenic responses of splenocytes treated with polyinosinic acid were not different from the control group. There was also no difference among three infected groups. 4. The cytotoxic activity of the natural killer cells was activated on day 1 after infection and declined to the level of control group on day 2 in all experimental groups. On day 5 after infection, the natural killer cell cytotoxicity was significantly suppressed as compared with the control groups. 5. The serum antibody titers of the infected mice increased after day 7, but there was no statistical difference between the three infected groups. In summary of the results, there was no difference in cell-mediated immune responses of three experimental groups scheduled with different infection intensities. But there was a significant difference in cell$.$mediated immune responses between infected and control mice. It is considered that cell-mediated immune responses should be involved in murine model infected with A. culbertsoni.
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