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

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2.2 Clinical signs Inflammalation of lymph nodes (adenolymphangitis) and lymphatic vessels particularly of the extremities is the main clinical feature of brugian filariasis. Pitting odema and finally leading to elephantiasis are the clinical hallmarks of the chronic stage (WHO, 1992). Other manifestations of the disease include the asymptomatic microfilaraemia, obstructive consequences like lymphoedema, hydrocoele, occult infection called TPE and acute episodes of adenolyphangitis (ADL) (Ottesen and Nutman, 1992). 2.3 Experimental fdariasis Efforts to combat the widespread parasitic diseases have benefitted from the availabilty of the animal models. The ideal animal model for human parasitosis was aptly described as the one faithfully recapitulating the parasitic, immunologic and pathologic attributes of the disease, making available large quantities of parasitic material and leading to the detailed immunological analysis (Philip et al., 1988). The only filarial parasite naturally occurring in man and easily transmissible to animals is the subperiodic form of 8. malayi. The use of Brugia species in experimental studies are of special significance since they are the same as or closely related to those found naturally infecting in man (Sasa, 1976). Edeson et al. (1960) succeeded in transmitting B. pahangi from cats to cats and other animals. He reported that the prepatent period was 59 days in cats and 57 to 84 days in jirds (Meriones unguiculatu). Among the rodents, male Meriones unguiculatus and male M, natalensis were susceptible to B. malayi infection. Zaini et a]. (1962) reported worms in the heart of hamsters infected with B. pahangi. Ramachandran and Pacheco (1965) found that in the early developmental stages B. pahangi worms were mainly in the skin, subcutaneous tissues and the caracass of cotton rats, whereas after maturity they were only in the heart and pulmonary artery. Ahmed (1967) reported B. malayi and B, phangi worms mainly from lymph glands and testes of spleenectomized rats and cotton rats. Dissanaike and Paramananthan (1961) reported that B, buckleyi inhabits the heart and pulmonary arteries of the Ceylon Hare. Vincent 4 al. (1976) studied the *
development of B. malayi, B.pahangi and B. patei in Menones unguiculatus and they showed a characteristid tendency to localize within the heart and pulmonary arteries. Ash and Riley (1970a,b) succeeded in transmitting both 5. pahangi and B. malayi in the Mongolian jird from cats and dogs. The adult worn were found in heart, lungs and testes and more numbers were present in the latter than the former. The mode of distribution of mature B. malayi was investigated in cats by Ewert, 1971 and In rhesus monkeys and jirds by ElBihari and Ewert (1971). He found that the majority of worms remained in the lymph vessels distal to the popliteal node for approximately 6 weeks and thereafter, they moved to the heart and lungs. McCall et 41. (1973) reported that intraperitoneal infection of Meriones unguiculatus with B. pahangi lead to a high percent recovery of developing larvae or adult filariae and about 90- 100°/o of the filariae that was recovered were located in the peritoneal cavity. Pabanyi et al. (1975) found that in M. natalensis infected by 5. malayi, 47% of female worms were found in lymphatic system and the prepatent period was 128.8 days. Whereas Sanger et al. (1981) had observed a prepatent period of 107 days and recovered majority of adult worms from heart and lungs and less number from the testes and lymphatics. Murthy et 41. (1997) showed that the peritoneal environment of M. natalensis is not conducive to the development of B. malayi, which is due to its high macrophage activity in the peritoneum compared to that in the jirds, where large ~x.unber of worms were recovered through intra peritoneal infection (Mak et al., 1994). Tyagi et 01. (1998) reported that 5. malayi in immunosuppressed (cortisone) M, coucha showed prepatent period of 90.7 days and the adult worm recovery was also higher as compared to the controls. 2.4 Changes in host physiology in relation to parasitic infection The last few decades have seen great advances in the parasite response and host defence, especially on the free radical and the antioxidant defence mechanisms. Mamphages, neutrophils and eosinophils nlease supemxide radicals as a host defense mechanism to kill the invading parasites (Bannister and Bannister, 1985). Electron 4 microscopic and phase contrast microscopic studies have shown th& eosinophils damaged
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 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
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
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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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