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0answers
15 views

Direct spread of Parvovirus B19 from blood to Brain stem and CSF

Parvovirus can spread in blood (viremia) to bone marrow. It is detected in some stages of infection in Cerebrospinal fluid (CSF). However, I am thinking if it can spread directly with facilitated ...
0
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1answer
28 views

Can inhibition of lymphocytes migration be a direct cause of chronic inflammation?

Here is the original slide: I am thinking about the "cord factor" sentence in a more general case. Assume you inhibit Leucocytes migration. How does this lead to accumulation of macrophages in the ...
3
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3answers
82 views

Why do 6-8% of diphtheria patients do not develop natural immunity after being affected?

I am thinking of why some patients do not have natural immunity after exposure to the A-B toxin of diphthria. I think the A-B exotoxin is the key factor causing this disease and should trigger memory ...
1
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1answer
25 views

How host defends against S. pneumoniae capsule?

The host response involves at least phagocytosis and probably localised acute inflammatory response at least after the colonisation. I am thinking how the host can defend against pneumolysin which ...
0
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1answer
43 views

What does this sentence about toxemia and Clostridium tetani mean?

I know that Cl tetani is not invasive and strictly localised. I think toxemia means spread in the blood. I am thinking this sentence The volume of infected tissue is small, and the disease is ...
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0answers
36 views

Capsule and Antiphagocytosis as a pathogenesis factor

I am thinking the pathogenesis factor (capsule) of Pseudomonas aeruginose as an example: antiphagocytosis $\to$ anti antibodies (I think AB is antibodies) and complement; anbiotics ...
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1answer
14 views

Pathogenesis of Group B Streptococci and C5a

I am thinking the pathogenesis of the C5a in GBS. I think the pathogenesis happens like C5a-peptidase in acid environment (Sialic acid, capsule) $\to$ cleaves C'-derived Neu chemoattractant C5a ...