Gram Negative Bacteria: Neisseria meningitidis — Transcript

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1. 0:02Assalamu alaikom everyone, and welcome to a new ATP video. Today we'll be talking
2. 0:07about the gram-negative bacteria that have a Diploccocus arrangement, probably
3. 0:13the only pathogenic bacteria that have this arrangement is: Neisseria! Neisseria
4. 0:17has two main important species: the first one is Neisseria meningitidis,
5. 0:21and the second one is Neisseria gonorrhea. In this video we'll talk about
6. 0:25the first one, Neisseria meningitidis. But first let's start with the shared
7. 0:30features between these two species. First of all they're both gram-negative
8. 0:35diplococci, and second of all, they are both oxidase positive. For the lab stuff,
9. 0:42Neisseria species grow on chocolate agar, but what is that? Do we actually use
10. 0:48chocolate? No not really :D Neisseria species can't grow on blood agar because
11. 0:54it's inhibited by some of the elements in the blood agar. However when we heat
12. 0:58the blood agar these inhibitory elements become inactive, and thus, Neisseria can
13. 1:03grow. This heated blood is in fact the famous chocolate agar! The other medium
14. 1:09that we use for Neisseria growth is Thayer-Martin agar, which is selective
15. 1:13agar that only allows Neisseria species to grow while inhibiting other organisms
16. 1:18from growing. This is also known as VCN agar, referring to the antibiotics used
17. 1:24to inhibit the other organisms which are: vancomycin, colistin, and nystatin.
18. 1:29Now let's move to the shared virulence factors. First we have pili which allows
19. 1:35attachment to mucosal surfaces. These pili also display antigenic variation,
20. 1:39which makes it difficult for our immune system to target, because as you know
21. 1:44they always change, they "camouflage". Then we have IgA protease which will cleave
22. 1:49IgA antibodies at its hinge point. This facilitates Neisseria survival
23. 1:55along the mucosal surfaces. Because if you remember, IgA antibodies are found
24. 2:00predominantly at the mucosal surfaces. Since Neisseria meningitidis is a
25. 2:04gram-negative bacterium, he has the ability of producing endotoxin, but be
26. 2:09aware the Neisseria endotoxin is a little different than the original one
27. 2:14that we already know about. It has a
28. 2:17lipo-oligosaccharide instead of the lipopolysaccharide in the previous
29. 2:21examples. You can think of it as an alternative version of the
30. 2:25lipopolysaccharide found in other gram-negative bacteria. Lastly you need
31. 2:30to know that patients with C5 - C9 deficiency, also known as terminal
32. 2:34complement deficiency, are more susceptible to Neisseria infection,
33. 2:38because these particular complement proteins are essential to form the MAC,
34. 2:42or also known as membrane attack complex, that is usually used to cause bacterial
35. 2:47lysis. So when these proteins are deficient the MAC won't be produced
36. 2:51enough, and that will cause them to be more prone to infections. Now let's talk
37. 2:58about our main topic today: Neisseria meningitidis. The first unique feature
38. 3:02that distinguished Neisseria meningitidis from other Neisseria
39. 3:05species is that it's the only one that ferments maltose in addition to glucose,
40. 3:11while other Neisseria species ferment glucose only. You can remember that from
41. 3:15the M letter in its name. Another differentiating feature is that it has a
42. 3:20polysaccharide capsule. This capsule inhibits phagocytosis, and thus, it's a
43. 3:25very important virulence factor for this particular species, in addition to the
44. 3:29other valence factors that it has. A quick note here is that patients with
45. 3:34sickle cell disease or asplenic patients, asplenic means they don't have
46. 3:38a spleen, are more susceptible to gain Neisseria meningitidis
47. 3:42infection or any other infection with encapsulated organisms. Now let's discuss
48. 3:48the pathogenesis of Neisseria meningitidis infection. First it spreads by
49. 3:52respiratory secretions like respiratory droplets that come from sneezing,
50. 3:56coughing, or kissing; thus, it spreads more easily in crowds and between people in
51. 4:03close quarters like college dorm residence or military recruits. Neisseria
52. 4:09meningitidis colonizes the nasopharynx first, and he uses the pili to
53. 4:13attach to the nasopharynx mucosal surface, and then it will use the IgA protease to
54. 4:18escape IgA antibody, then he uses the blood to spread through the entire body,
55. 4:23and we call this the hematogenous spreading.
56. 4:27At the same time it will utilize the polysaccharide capsule it has to protect
57. 4:31it from phagocytosis, like we mentioned before. Then Neisseria meningitidis will cause
58. 4:36two main diseases: meningitis also known as meningococcal meningitis and/or
59. 4:42disseminated meningococcemia. Let's begin with meningitis. Once inside the
60. 4:47bloodstream, Neisseria meningitidis preferentially travels to the brain, then
61. 4:52it crosses the blood CSF barrier and enters the cerebrospinal fluid or CSF
62. 4:58where it replicates and causes inflammation of the surrounding meninges.
63. 5:03Meningitis patient presents with symptoms like headache, fever, neck
64. 5:08stiffness, photophobia, photo means: light in greek and phobia: comes from Phobos or
65. 5:15fear, and it means feeling of discomfort in the presence of light, and lastly
66. 5:21phonophobia, phono: comes from sound in Greek and it means feeling of discomfort
67. 5:27in the presence of loud sounds. Now let's talk about disseminated meningococcemia.
68. 5:34when Neisseria meningitidis spreads through the blood all over the body, it
69. 5:38will release the endotoxin lipooligosaccharide and this will result in
70. 5:43massive inflammation response that were result in increased capillary
71. 5:46permeability, and activation of coagulation. When there's extensive
72. 5:51coagulation inside the blood vessel throughout the body we call this
73. 5:54condition: disseminated intravascular coagulation, intra means inside and
74. 5:59vascular means blood vessel, so inside the vessels. This disseminated
75. 6:04coagulation will consume the platelets and results in thrombocytopenia.
76. 6:09The thrombocytopenia will result in increased tendency of bleeding, because
77. 6:13you don't have platelets and that will happen throughout the body,
78. 6:16and will present as petechial rash, especially over the trunk and lower
79. 6:21extremities. Lastly when there is damage to endothelial cells and increased
80. 6:26capillary permeability subsequently, this will lead to leakage of blood to the
81. 6:31interstitial space and this will ultimately result in generalised
82. 6:34hypovolemia, and clinicians call this: hypovolemic shock, hypo means less and
83. 6:41volemic from volume. Now we'll talk about Waterhouse Frederickson
84. 6:45syndrome. When the inflammatory response happens in the small blood vessels of
85. 6:49the adrenal gland, it will result in endothelial damage and rupture of the
86. 6:53blood vessels. The DIC condition will make it harder to form clot properly,
87. 6:57because we're using the platelets somewhere else, and this will lead to
88. 7:02leakage of blood into the interstitial space of the adrenal gland. This along
89. 7:07with the generalized hypoperfusion will result in ischemia and necrosis of the
90. 7:11adrenal glands, which eventually leads to acute adrenal insufficiency, also known
91. 7:17Adissonian crisis. Okay I know it's a lot, so let's do a quick
92. 7:22recap. Neisseria meningitidis infects a patient through the respiratory
93. 7:25secretions. Then Neisseria meningitidis will colonize the nasopharynx, then it
94. 7:30will disseminate hematogeneously and release the endotoxin
95. 7:34lipooligosaccharide, which will result in massive inflammatory response throughout
96. 7:38the entire body. This will lead to increased capillary permeability and
97. 7:42activation of coagulation inside the blood vessels, and this will lead to DIC,
98. 7:48which will consume the platelets and lead to thrombocytopenia, and petechial
99. 7:52rash, in addition to that, the increased capillary permeability will lead to the
100. 7:56blood leakage throughout the body, and lead to generalized hypoperfusion or
101. 8:01shock. When all that happens and results in ischemia necrosis of the adrenal
102. 8:06gland, we will have adrenal insufficiency, or acute adrenal insufficiency, and we
103. 8:12call this condition what? Waterhouse Frederickson syndrome.
104. 8:18For treatment we use a third-generation cephalosporin: ceftriaxone and for the
105. 8:23close contact of the affected patient we use rifampin as prophylaxis. For
106. 8:29prevention we have a vaccine for certain strains, and these are: Group A and C. The
107. 8:36vaccine we use is a purified capsular polysaccharide which is immunogenic
108. 8:41from these strains. Immunogenic means it induces an immune response from the body.
109. 8:47However we don't have a vaccine yet for Group B, because type B strain capsule is
110. 8:54not immunogenic. So most of the infections all around the
111. 8:58world are caused by type B strain usually. That is all you need to know
112. 9:03about Neisseria meningitidis. We hope you enjoyed the video! Please give us
113. 9:07your feedback so we can improve in the next videos. And don't forget to Like,
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