Neisseria meningitidis pathogenesis — Transcript

Full transcript

1. 0:00[music]
2. 0:04So far we have talked about the
3. 0:05structure and infective properties about
4. 0:07the narium men andis. Now in this video
5. 0:09we'll be talking about the pathogenesis.
6. 0:11So we'll be talking about
7. 0:14pathogenesis.
8. 0:17Pathogenesis.
9. 0:19Now for the pathogenesis part what we
10. 0:21know about the pathogenesis for all the
11. 0:23different kinds of bacteria. In
12. 0:25pathogenesis bacteria always adopt two
13. 0:27different situations. one is to evade or
14. 0:30escape the host immune system. So this
15. 0:32is the first one. So escaping escaping
16. 0:37escaping host
17. 0:40host immune system
18. 0:44host immunity or host immune system and
19. 0:46the second important components for this
20. 0:48pathogenesis is a virulence factor
21. 0:51destruction. Right? So destruction
22. 0:55destruction of
23. 0:57host cells right. So these are the two
24. 1:02important steps that are carried out by
25. 1:03all the bacterias to provide the
26. 1:05pathogenesis. Now for the escaping of
27. 1:08the host immunity for this nizerium
28. 1:10meningitis they are having two different
29. 1:11approaches for that. Now one approach
30. 1:14for that is simply uh simply the
31. 1:17presence of capsule
32. 1:19presence of capsule on the outer layer.
33. 1:22So the outer layer consists of
34. 1:26capsules as we all know because if you
35. 1:29imagine the structure of this miseria
36. 1:32menitis you can find this half bean like
37. 1:35structure and and in the outside what we
38. 1:37are having a slimy layer. Now this slimy
39. 1:40layer is the capsule layer. So it is
40. 1:42helping them to evade or escape the
41. 1:44immune system. So this is the first
42. 1:46thing that is helping them. Now the
43. 1:47second important thing that is also
44. 1:48helping them to escape this immune
45. 1:50system is the py or the cytoplasmic
46. 1:52extension which is coming out. Now this
47. 1:54py
48. 1:56so this py is helping them again uh to
49. 2:00escape the immune system because it is
50. 2:01the cytoplasmic extension. So let me
51. 2:03write it is called the cytoplasmic
52. 2:08cytoplasmic
53. 2:10extension.
54. 2:13Right? It's called the cytoplasmic
55. 2:14extension. So py is not only helping
56. 2:17them to escape the immunity of host
57. 2:19system but it also helps them to adhere
58. 2:22to the host cell and then penetrate and
59. 2:24finally go to the host cell. And this
60. 2:26pely is also act can also act as this
61. 2:29pely can also act as an antigen right it
62. 2:32is anti- sorry it's antigen and and and
63. 2:35it instigates immune system to develop
64. 2:37antibodies. So it's also called
65. 2:39antigenic.
66. 2:41So antigenic right. So the pill is very
67. 2:44very important villance factor above all
68. 2:46in niseria menitis. Obviously capsule is
69. 2:48helping them to escape and obviously
70. 2:50they are having another important
71. 2:52mechanisms which is a kind of unique to
72. 2:53niseria meningitis. If we can't find it
73. 2:56in case of news area but we find it for
74. 2:58menis and that property is the third
75. 3:01thing I'm going to write and that
76. 3:03property is uh simply uh it is it is uh
77. 3:08the IgA proteas or immunoglobuline a
78. 3:12proteas. Now we all know that
79. 3:16imunoglobulins or antibodies are simple
80. 3:18protein constructions. Now this IG
81. 3:20proteas is an enzyme that will degrade
82. 3:23imunoglobuline A. Now what it will do it
83. 3:25will degrade imunoglobinia right? So IgA
84. 3:28if we write IGA so it will degrade this
85. 3:31IgA
86. 3:35degradation. Now degradation of IG will
87. 3:38help them to reduce the activity against
88. 3:41this particular pathogen. Right? So this
89. 3:42this this is another way of escaping or
90. 3:45evading immune system of host. And now
91. 3:48let us talk about the destruction of the
92. 3:50host cell. And the destruction of the
93. 3:51host cell is largely brought about using
94. 3:54the endotoxin.
95. 3:56The endotoxin. Now the endotoxin part we
96. 3:59know for nizarium meniterase is simply
97. 4:02lipoaccharide layer. So let me write the
98. 4:05full term here. Lipoaccharide
99. 4:08lipoaccharide and this
100. 4:09lipoligosaccharides are having small but
101. 4:13highly highly branched structure in the
102. 4:16O antigen region. The polyosaccharide
103. 4:20saccharide they are having very very
104. 4:22branched highly branched. So let me
105. 4:24write highly branched.
106. 4:27Highly branched
107. 4:30but short
108. 4:33but short
109. 4:36O antigen.
110. 4:38Right? So that is the important fact.
111. 4:40They're having highly branched but short
112. 4:42O antigen region here. [snorts] But this
113. 4:44lipolycharide is helping them to degrade
114. 4:47the host cell. and how it helps to
115. 4:48destruct uh in the destruction of the
116. 4:50host cell. Actually this this endotoxin
117. 4:53is attached to the cell membrane. So
118. 4:55it's a part of the cell membrane of gram
119. 4:57negative bacteria and we all know that.
120. 4:59So let us talk about if this is the
121. 5:00bacterial cell and lipopolyaccharide a
122. 5:03lipolyosaccharide layer is attached to
123. 5:05this this bacterial cell like that. Now
124. 5:08usually this won't be acting as a
125. 5:11endotoxin if until and unless the cell
126. 5:14is degrading itself. So self-destruction
127. 5:16or self degradation of its own cell is
128. 5:19required for the release of this
129. 5:22lipolyosaccharide layer as endotoxin.
130. 5:25Now as it is degrading itself as it is
131. 5:27degrading itself after the degrade what
132. 5:28we get we get the fragmented sections
133. 5:31like like this we get the smaller
134. 5:33fragments like that. Now as we getting
135. 5:34the smaller fragments out the degraded
136. 5:37section out now this degraded form. So
137. 5:40this is degraded
138. 5:44degraded form and this is sorry and this
139. 5:46is the degraded form and this is called
140. 5:48the endotoxin. This is a active
141. 5:51active
142. 5:55endotoxin.
143. 5:56This form is called the active
144. 5:58endotoxin. Right? So all of these are
145. 6:00called the active endotoxin and they can
146. 6:02act and kill the host cell. Not only can
147. 6:05kill the host cell but form different
148. 6:06kind of necrosis right. So we all know
149. 6:08that they can form the tissue tissue
150. 6:10damage or necrosis there. So necrosis
151. 6:14will set in this case. Okay. So these
152. 6:18are the different effects of the
153. 6:19destruction of the host cell using this
154. 6:22uh endotoxin. Okay. So that's the
155. 6:25pathogenicity and I hope that's helpful.
156. 6:28Thank you.