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

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4.4.2.1.2 Heart The heart of the control animals did not show any other significant change. However, in the infected animals, a few mononuclear inflammatory cells were seen in the connective tissue and in the myocardium around the parasite. In the epicardium, moderate to severe infiltration of mononuclear cells was observed (Plate I I). Some of the muscle fibres in the myocardium had a few fat vacuoles. Microfilariae were seen in the myocardium (Plate 12), in the capillaries and in interstitial connective tissues. Presence of some erythrocytes in the vicinity of the mf indicated haemorrhage (Plate 13). 4.4.2.1.3 Testes The testes of the control group had seminiferous tubules with normal spermatogenesis. The lumina of the tubules were filled with many sperms (Plate 14). The interstitial tissue had normal number of leydig cells. In this group, no circulatory or degenerative change was noticed. In the infected animals, though some of the tubules appeared normal, many of them did not have multilayered spermatogenic cells. The lumina contained only a few developed sperms (Plate IS). When compared to the control, the testicular damage was marked. A few tubules showed initial stages of calcification. In some areas, the interstitial cell of leydig was normal, but in the areas of tubular damage, these cells also became degenerated and atrophied. 4.4.2.1.4 Liver The liver of the control animals did not have any significant change. In the infected group, vacuolation of hepatocytes was more pronounced and in addition, some of the hcpatocytes showed fatty changes and necrosis (Plate 16). Portal veins showed hyperaemia. Nuclear hyperchromacia and presence of twin nuclei in some hepatocytes suggested an ongoing regenerative process (Plate 17). A few small foci of mononuclear cellular infiltration particularly in the areas of hepatic degeneration were also recorded (Platel8). Microfilaria was mainly in the sinusoids (Plate 19).
Plate w: Section of Testes of normal group showing seminifmus tubules with normal spermatogenesis (Haematoxylin and Eosin 400X). Plate 19 Section of Testes of infected group showing moderate reduction in spermatogenesis indicating testicular degeneration (Haematoxy tin and Eosin 400x1. Plate Y: Won of Liver of infected group showing hydropic degeneration of fatty changes in the perilobular areas (Hamatoxylin and Eosin 100X). Plate IT Section of Liver of infected group showing hyperchromatic binucleated hepatocytes indicating regenerative prwm (Haematoxylin and =n 400X). Plate 18: Section of Liver of infected group showing hepatic degeneration with moderate mononuclear cellular infiltration (Haematoxylin and Eosin 2SOX). Plate 19: Section of Liver of infected group showing microfilaria in hepatic sinusoids (Hacmatoxylin and Eosin 400X).
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EFFECT OF INFECTION OF THE FILARIAL
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I wish to express my deep sense of
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1. INTRODUCTlON 2. REVIEW OF LlTERA
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As stated earlier, the host immune
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13 Testicular changes Testosterone
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2. REVIEW OF LITERATURE Filariasis
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2.2 Clinical signs Inflammalation o
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the tegument by the release of thei
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the compound kills the filarial wor
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3. MATERIALS AND METHODS COLONY MAI
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Ragenb 1. Tris-HCI buffer . : 0.1 M
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3. Reduced glutathione : 30 mM To I
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4.1.1.6 Glucose-6-phosphate dehydro
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absorbance of the clear supernatant
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-eats I. Lowry's reagent :Solution
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4.1.2.1 Changes in antioxidant enzy
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Fig.3: Effect of B.malayi on SOD in
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Fig.9: Effect of B.rnalayi on GST i
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Fig.12: Effect of 6.rnalayi on GPx
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Fig. 18: Effect of B.malayi on G6PD
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12- 3 m- 15- lor, Fig.21: Effect of
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Fig.27: Effect of B.malayi on Ascor
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4.1.2.3 Change in the antioxidant e
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Fig.35: Effect of B.malayi on CAT i
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m 20 0) - 15 9 g 10 il! 5 0 Fig.39:
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30 25 8 - a 20 2 15 C I 10 I 5 0 35
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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
Page 69 and 70: 1 - 0- ' 1 5 - 6 - 7 - Fig.63:Relat
Page 71 and 72: Catalase had been reported to be re
Page 73 and 74: - Fig.68:Relationship between chang
Page 75 and 76: esults in its reduced activity (Con
Page 77 and 78: g 20- :I-. F1g.70:Relationship betw
Page 79 and 80: 12, - I 0 U) Q 4 2 0 - + - Fig.75:R
Page 81 and 82: $ Fig.80:Relationship between chang
Page 83 and 84: Fig.85:Relationship between change
Page 85 and 86: V) (3 :; - Fig.9O:Relationship betw
Page 87 and 88: A reduction in the total thiol cont
Page 89 and 90: 2 5- Fig.98:Relationship between ch
Page 91 and 92: Fig. 103:Relationship between chang
Page 93 and 94: 4.2.1.1 N ay ATPase Reagents Nay AT
Page 95 and 96: Reagents 1. Acetylcholine bromide :
Page 97 and 98: To 1.5 ml of carbonate buffer, 1.5
Page 99 and 100: 4.2.1.10 Differential leucocyte cou
Page 101 and 102: increase in the control animals (Fi
Page 103 and 104: - Fig.110: Effect of 6. malayi on H
Page 105 and 106: efflux and thereby alter the membra
Page 107 and 108: with i n d lymphocytes and decrease
Page 109 and 110: Tubes were labeled for calibrators,
Page 111 and 112: Fig.114: Effect of B, malayi on GTP
Page 113 and 114: 433 DISCUSSION Testosterone is a se
Page 115 and 116: CHAPTER 4.4 HISTOPATHOLOGICAL CHANG
Page 117 and 118: Platc 2 Plate 3 Plate 4 Plate 5 Pla
Page 119: Platc X Plate 9 Plate 10 Plate 11 P
Page 123 and 124: 4.4.2.1.5 Brain The control animals
Page 126 and 127: Plate ICt Section of Kidney of infe
Page 128 and 129: 4.4.2.2 Histopathological changes i
Page 130 and 131: Plate 32
Page 132: The mf could not be seen in spleen
Page 135 and 136: ain, it decreased from 0 day itself
Page 137: inflammatory nature indicative of c
Page 141 and 142: BIBLIOGRAPHY Ackerman, S.J., Gleich
Page 143 and 144: Case, T., Leis, B., Witte, M., Way,
Page 145 and 146: 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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