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

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Filariasis is one of the most debilitating diseases of the tropics. Mortality due to filariasis is negligible. Howevm, there is a high d e p of morbidity due to its acute and chronic manifestation. Filariasis has been the subject of cons~derable attention for long, but it is still poorly understood. Over two-thirds of the lymphatic filariasis cases of the world is contributed by India, China and Indonesia. It is an age old disease ncorded in India as early as in 6th century B.C. Both bancroftian and brugian lymphatic filariasis are prevalent in India. However, bancroftian filariasis is the commonest, accounting for 98% of the filarial infection. India alone accounts for 42.8% of the global problems due to Wuchereria bancrofti and 20.2% due to Brugia malayi. There are about 429 million people exposed to the risk of infection and 3 1.3 microfilaria (mf) carriers (Appavw et al., 1999). Lymphatic filariasis is caused by the lymphatic dwelling filarial nematodes such as I.Y bancrofti (Cobbold, 1877), B. malayi (Lichtenstein, 1927) and B. timori (David and Edeson, 1964). Three physiological races exist in W. bancroofii and B. malayi, depending on the microfilarial periodicity (Sasa and Tanaka, 1972; 1974). They are the nocturnally periodic, nocturnally subpenodic and diurnally subperiodic forms. In the Indlan sub continent both the parasites exist as nocturnally periodic forms. The vector of W bancrofri is Culer quinquefmciatu and vector ofB. malayi is Mansonoldes species. Recurrent fevers, inflammation of lymph nodes and vessels, sometimes accompanied by transient swelling of the limbs are the earliest s~gns of the disease. Later symptoms include scrota1 swelling and permanent swelling of the limbs caused by collection of fluid in cells, tissues or body cavihes. This may lead to the grossly swollen, thick-skinned limbs, a condition commonly called as elephanhasis. The general approach to control filariasis is to reduce morbidity and transmission. Diethylcarbamatine (DEC), is still considered the drug of choice for treating or suppressing lymphatic filarial infections (Hawking, 1979, Mak et al., 1991).
As stated earlier, the host immune mechanism and its role in the suppression or propsion of filarial disease is very poorly understood. Therefore, experiments were carried out using the animal model Mastomys natalensis and the filarial parasite, B. malayi to understand the influence of infection on the following parameten of the host. 1.1 Antioxidants and antioxidant enzymes Host immune effector cells such as phagocyks, macrophages, neutrophils and eosinophils release oxidants or free radicals such as superoxide dcal, hydroxyl radicals, singlet oxygen and hydrogen peroxide as defense mechanisms to kill the invading parasites (Bannister and Bannister, 1985; Callahan et al., 1988). In the host system, oxidants are also produced during normal cellular metabolic processes, and due to certain antiparasitic drugs. (Klebanoff, 1980; Klebanoff , 1982). The leucocytes can also secrete oxygen radicals from their outer membrane into the smundiigs (?-lathan and Root, 1977). This indiscriminate and self inflicting process of generation of oxygen radicals can contribute to the tissue damage in the host. Over recent years, there had been an increasing awareness that free radicals directed by the host to destroy the parasites can be an important cause of cellular injury and damaging membranes, proteins and nucleic acids. All l~ving tissues are protected from the damaging effects of free radicals by detoxifying them to harmless products by andoxidants and antioxidant enzymes. The process of generation of free radicals and antioxidant defense system may be same in the case of host defense against the invasion of filarial parasites. The host antioxidant defense mechanisms with respect to LPO and the enzymes SOD, catalase and xanthine oxidase had been reported in the case of animal filarial parasite, Diperalonema viteae, in Mastomys natalensis (Barn et a/.. 1989). However, the complete system of defense including various antioxidant enzymes such as SOD, catalase, GST, GPx, GR and G6PDH and antioxidants such as GSH, ascorbic acid and total thiol status and LPO are yet to be investigated especially in the case of a human filarial parasite. The mode of action of DEC, the drug of choice for the mtment of filariasis, is poorly understood. Cesbron et (11. (1987) had suggested that DEC activates the platelets to kill mf by free radicals. But so far, the role of antioxidant defense system after DEC treatment of filariasis has not yet been investigated. Henoe, the comfkte antioxidant system
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 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 18 and 19: the tegument by the release of thei
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
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Fig.49: Effect of B.malayi on Vit-C
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4.1.3 DISCUSSION 4.1 3.1.1 Toxic ox
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1973). The two major systems of LPO
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1981), and their increase in human
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1 0 Fig.58:Relationship between cha
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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
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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
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Jacob, H.S. and Lux, S.E. (1968). D
Page 151 and 152:
Linda, I. and Mayeda, B. (1974). Th
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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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