effect of infection of the filarial parasite brugia malayi - Pondicherry ...

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the tegument by the release of their granules on the surface of the parasite (Ackerman et al., 1981). Initially it w& believed that the membrane basic proteins were the most powerful toxic component of eosinophils responsible for the killing of the parasite. But later, it was shown that the eosinophil cationic protein is more toxic than membrane basic proteins in vitro. The ability of eosinophils to kill the parasite 0. volvulus (Green et al., 1981) and B. malayi (Sim et al., 1982) in vitro had been well demonstrated. Batra et al. (1989) studied the status of superoxide dismutase, catalase, xanthine oxidase and lipid peroxidation in liver, lungs and spleen of M, natalensis during D. viteae infection. Xanthine oxidase and lipid peroxidatuion exhibited stimulation, while these antioxidant enzymes showed depression in liver and spleen. On the other band in lungs, the antioxidant enzymes were elevated and this lowered the lipid peroxidation. But no parallel study had so far been reported regarding B. malayi infection induced changes in M. natalensis, especially antioxidant enzymes and its relation to DEC treatment, membrane bound enzymes and their damage, testicular damage and the histopathological changes. 2.5 Chemotherapy The microfilaricidal efficacy of DEC was detected by Hewitt et al. (1947) in L. carinii infected cotton rats and D. immitis infected dogs and also for the treatment of human bancroftian filariasis (Santiago and Stevenson, 1947). Hawking et al. (1950) demonstrated that the drug had no direct action rn vitro on mf and adults of L. carinii. But when administered to cotton rats infected with the parasite, mf rapidly decreased from circulating blood and were trapped in the sinusoids of liver, where they were destroyed by phagocytosis, such an action of DEC was interpreted as 'Opsonin-like". Subsequent studies on DEC showed strong activity against microftlaria of 0. wlvulus, Loa loa, W. bancrofti and B. malayi in man (Zahner and Schaus. 1993). Significant lethal action against adults of B. malayi and B. pahangi in cats (Edeson and Buckley, 1959) and against Wuchereria and Brugia in man (Chen, 1964) was reported. Kume et al. (1964) and Tulloch et al. (1970) reported that daily adminstration of DEC prevented maturation of Dirofilnria immitis in dogs. Aubrey and Copeman (1972) reported that Dirojlaria imm? does not mature in dogs when adequate doses of DEC was given for 3 successive days ev@ 2 months. Ewert and
Emerson (1975) showed that DEC treatment of cats infected with B. malayi resulted in a reduction of living lakae at 2-10 mgkg body weight. Ewert et al. (1983) reported that weekly adminstration of DEC was the most effective in B. malayi infected cats. DEC has direct physiological effects on eosinophils (Mackenzie, 1980) and after DEC treatment eosinophils can be found degranulating on the surface of microfilaria (Gibson et al., 1976; Kephart, 1984; Racz, 1982). The mechanism by which filarial parasites are killed by DEC is not clearly understood. Most of the clearance occurs in the liver, spleen and lungs in association with a m~xed inflammatory cell reaction with large number of eosinophils surrounding the dying mf (Woodraff, 1951). Ackerman et al. (1981) had demonstrated eosinophilia and elevated levels of membrane basic proteins in banmttian filariasis after treatment with DEC. Lammler et al. (1975) reported that M. natalensis infected with L. cannii developed anaemia, an increased sedimentation rate and leucopenia. After treatment with DEC and a compound HOE 258V. there was a transient change towards normal in the peripheral blood values. Morikov el al. (1991) reported that the antioxidant propertla of drugs including DEC citrate in various microsoma1 lipid peroxidation models: NADPH, ascorbate and CC14 dependent. The most strong antioxidant of direct action turned out to be DEC citrate and dipyridamole. The dose most generally for treating banmftian filariasis is 6 mg of DEC per kg body weight per day orally for 12 days. For brugian filariasis, the recommended doses range h m 3 mg to 6 mg per kg of body weight per day upto a total dose of 36-72 mg of DEC per kg of body weight (WHO, 1992). The anthelminthic agents such as macwyclic lactone ivermectin, the amoscanate derivative CGP 6140 and the bemhazole derivative CGP 20376 were investigated for their invibo modulatory effects on eosinophilic effector cells by Tischendorf et al. (1993). The results indicated that the reactive oxygen metabolites were produced at an increased rate at low doses of ivermectin and CGP 6140. The toxic potential of eosinoplls includes the secretion of stored granular cationic proteins and the de novo generation of oxygen intermediates. The effect of the macrofilaricidal agent of 2, 2'dicarbomethoxylamine -5.5' dibmrimrhlyl ketone on the metabolism of reactive oxygen species in A. viteae and M. natalensis was studied by Batra el al. (1992). The host tissues i.e., subcutaneous and the adjoining muscle tissues exhibited elevated levels of antioxidants aih( GSH. It is shown that
Page 1 and 2: EFFECT OF INFECTION OF THE FILARIAL
Page 4 and 5: I wish to express my deep sense of
Page 6: 1. INTRODUCTlON 2. REVIEW OF LlTERA
Page 9 and 10: As stated earlier, the host immune
Page 11 and 12: 13 Testicular changes Testosterone
Page 14 and 15: 2. REVIEW OF LITERATURE Filariasis
Page 16 and 17: 2.2 Clinical signs Inflammalation o
Page 20 and 21: the compound kills the filarial wor
Page 22: 3. MATERIALS AND METHODS COLONY MAI
Page 25 and 26: Ragenb 1. Tris-HCI buffer . : 0.1 M
Page 27 and 28: 3. Reduced glutathione : 30 mM To I
Page 29 and 30: 4.1.1.6 Glucose-6-phosphate dehydro
Page 31 and 32: absorbance of the clear supernatant
Page 33 and 34: -eats I. Lowry's reagent :Solution
Page 35 and 36: 4.1.2.1 Changes in antioxidant enzy
Page 37 and 38: Fig.3: Effect of B.malayi on SOD in
Page 39 and 40: Fig.9: Effect of B.rnalayi on GST i
Page 41 and 42: Fig.12: Effect of 6.rnalayi on GPx
Page 43 and 44: Fig. 18: Effect of B.malayi on G6PD
Page 45 and 46: 12- 3 m- 15- lor, Fig.21: Effect of
Page 47 and 48: Fig.27: Effect of B.malayi on Ascor
Page 49 and 50: 4.1.2.3 Change in the antioxidant e
Page 51 and 52: Fig.35: Effect of B.malayi on CAT i
Page 53 and 54: m 20 0) - 15 9 g 10 il! 5 0 Fig.39:
Page 55 and 56: 30 25 8 - a 20 2 15 C I 10 I 5 0 35
Page 57 and 58: Fig.45: Effect of B.maiayi on GSH i
Page 59 and 60: Fig.49: Effect of B.malayi on Vit-C
Page 61 and 62: 4.1.3 DISCUSSION 4.1 3.1.1 Toxic ox
Page 63 and 64: 1973). The two major systems of LPO
Page 65 and 66: 1981), and their increase in human
Page 67 and 68: 1 0 Fig.58:Relationship between cha
Page 69 and 70:
1 - 0- ' 1 5 - 6 - 7 - Fig.63:Relat
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Catalase had been reported to be re
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- Fig.68:Relationship between chang
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esults in its reduced activity (Con
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g 20- :I-. F1g.70:Relationship betw
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12, - I 0 U) Q 4 2 0 - + - Fig.75:R
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$ Fig.80:Relationship between chang
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Fig.85:Relationship between change
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V) (3 :; - Fig.9O:Relationship betw
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A reduction in the total thiol cont
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2 5- Fig.98:Relationship between ch
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Fig. 103:Relationship between chang
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4.2.1.1 N ay ATPase Reagents Nay AT
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Reagents 1. Acetylcholine bromide :
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To 1.5 ml of carbonate buffer, 1.5
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4.2.1.10 Differential leucocyte cou
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increase in the control animals (Fi
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- Fig.110: Effect of 6. malayi on H
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efflux and thereby alter the membra
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with i n d lymphocytes and decrease
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Tubes were labeled for calibrators,
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Fig.114: Effect of B, malayi on GTP
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433 DISCUSSION Testosterone is a se
Page 115 and 116:
CHAPTER 4.4 HISTOPATHOLOGICAL CHANG
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Platc 2 Plate 3 Plate 4 Plate 5 Pla
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Platc X Plate 9 Plate 10 Plate 11 P
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Plate w: Section of Testes of norma
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4.4.2.1.5 Brain The control animals
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Plate ICt Section of Kidney of infe
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4.4.2.2 Histopathological changes i
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Plate 32
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The mf could not be seen in spleen
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ain, it decreased from 0 day itself
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inflammatory nature indicative of c
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BIBLIOGRAPHY Ackerman, S.J., Gleich
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Case, T., Leis, B., Witte, M., Way,
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Drabkin, D.L.R. and Austin, J.H. (1
Page 147 and 148:
Fukuota, M., Zhou, Y. and Tanaka.(l
Page 149 and 150:
Jacob, H.S. and Lux, S.E. (1968). D
Page 151 and 152:
Linda, I. and Mayeda, B. (1974). Th
Page 153 and 154:
Murray, H.W. (1981). Susceptibility
Page 155 and 156:
Santiago- Stevenson, D., Oliver-Gon
Page 157 and 158:
Tate, S.S., Thomson, G.A. and Meist
Page 159 and 160:
Zaini, M., Ramachandran, C.P. and E
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