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Microbiology and immunogenetics Flashcards

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1
Q

What is bacterial meningites mode of transmission?

A

Respiratory droplets

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2
Q

What is the most important virulence factor for all bacterial meningitis causes?

A

Polysaccharide capsule

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3
Q

What bacteria and aetiology does meningococcus cause?

A

Aetiology: Meningococcaemia and meningitis
Bacteria: Neisseria meningitides

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4
Q

What tpe of bacteria is Neisseria meningitides?

A

Gram-negative capsulated diplococci with adjacent sides flattened

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5
Q

What is the most important virulence factor of Neisseria meningitides?

A

Its polysacharide capsule with antiphagocytic action.

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6
Q

What are the most common serogroups causing meningitis?

A

A, B, C, Y, W135

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7
Q

What does it mean when we say Neisseria meningitides is gram -ve?

A

Its cell walls have lipopolysaccharide (endotoxin)

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8
Q

What are the clinical features of Neissera meninitides?

A

Endotoxin mediated vasculitis
Skin rash
(DIC) Disseminated intravascular coagulopathy

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9
Q

What is Neisseria meningitides mode of infection?

A

It enters the blood stream (meningococcaemia) and than localizes in the meninges to cause meningitis and cerebral oedema

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10
Q

what is pneumococci?

A

Streptococcus pneumoniae a gram positive diplcocci

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11
Q

What is streptococcus pneumoniae’s most important virulence factor?

A

its polysaccharide capsule which ic antophagocytic

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12
Q

Who are the individuals at risk of getting infected with streptococcus pneumoniae?

A

Post-splenectomy
Immunosuppressed
Infants
Enderly

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13
Q

Where is s.pneumoniae ussually found?

A

In the pharynx of 1/3 of adults mostly endogenous infection

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14
Q

Where is haemophilus influenzae found?

A

In the normal flora of the upper respiratory tract

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15
Q

What is the haemophilus influenzae bacteria?

A

causatie agent of influenza, Gram -ve capsulated bacilli

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16
Q

What is the most common anitgenic type to cause bacterial meningitis?

A

Haemophlus influenza b (Hib)

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17
Q

What are the clinical presentation of meningitis in adults?

A

Vomiting
Fever
Headache
Stiff neck
light aversion
Drowsiness
Joint pain
Fits

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18
Q

What is the mode of infection of neonatal meningitis?

A

vaginal delivery

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19
Q

What is the most common of neonatal meningitis?

A

Group B streptococcus (streptococcus agalactia)
E. coli
Listeria monocytogenes

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20
Q

What are the meningitis symptoms in babies?

A

Fever (hands &feet may also feel cold)
Refusing feeds or vomiting, diarrhoea
High pitched moaning cry or whimpering
Dislike of being handled fretful
Neck retraction with arching neck
Diffcult to wake, lethargic
Pale blottchy complexion
Blank & staring expression, bulging fontanelle

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21
Q

What are the CSF examination tests?

A

Appearance
Chemical analysis: glucose, protein
Microscopic examination
Gram stain
Culture and sensitvity
Microbial antigen tests e.g. Latex agglutination
PCR

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22
Q

What are the characteristics of bacterial (septic) meningitis?

A

physically : CSF is cloudy and under tension
Cytologically: High leucocytic count (200-20000ml) with predominant neutrophils
chemically: Reduced glucose level and elevated protein level

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23
Q

What is the CSF profile bacterial meningitis?

A

increased neutrophils, decreased glucose and increased protein

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24
Q

What is the CSF profile in viral meningitis?

A

Increased lympohcytes, No glucose, no or increases protein

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25
What is the CSF cryptococcal meningitis?
cells and biochemistry often normal
26
What are immediate empirical?
Third-generation cephalosprins eg; Ceftriaxone injection
27
What are the chemoprophylaxis recommended?
The antibiotic recommended is either rifampin for 2 days orally or 1 ceftriaxone injection
28
What are the available meningitis vaccine?
Conjugate Hib polysaccharide capsular vaccine Conjugate pneumococcal polysaccharide vaccine Meningococcal polysacchride vaccine (A,C,Y,W135)
29
When are children given the meningitis vaccine?
2, 4, 6
30
When are children given the meningitis vaccine?
2, 4, 6 months
31
What is an immune priviliged site?
Tissues evolved to be protected to a variable degree from immune respones
32
How is cns considered to be an immune privilged site?
Lacks classical lymphatic drainage Scarcity of dendritic cells DElivery of immune cells and inflammatory mediators into the brain is impaired by the BBB Lymphoid cells are normally excluded from the brain, spinal cord and peripheral nerves
33
What proinflammatory cytokines do microglias secrete?
IL-6, IL-1 or TNF-a
34
How can immunecells enter the CNS?
Across the BBB into the brain Across the spinal cord barrier into spinal cord parenchyma (BSpCB) Across choroid plexus into the CSF-filled entricles (BCSFB)
35
What are the steps of priming of immune responses to CNS antigens in MS?
(A) Neural antigens are released into the lymph nodes, where they are presented to B and T cells (such as dendritic cells) (B) T and B cells with high affinity receptors for these antigens are expanded and releases from the lymph nodes. The cells migrate through the body and accumulate at sites where they re-encounter their priming antigen (C) On reactivation, these cells recruit effector functions
36
what are targeted myelin sheath antigens in MS?
MAG: Myelin-associated glycoprotein MBP: Myelin basic protein MOG: Myelin oligodendrocyte glycoprotein PLP:Proteolipid protein
37
What is the immune response in MS?
1. Antigens are released from the CNS or cross reactive antigens presented via dendritic cells (APCs) prime T and B cells in the peripheral lymphoid tissue 2. After colonal expansion, t and b cells infiltrate the CNS. This is aided via focal changes in the BBB permeanility or focal increase in expression of cell adhesion molecules that are necessary for the disease activity 3.Clonally expanded B cells re-encounter their specific antgens, mature to plasma cells and release large amounts of igG antibodies.MS patients have elevated CSF levels of IgG 4.Clonally expanded CD8 positive T cels (cytotoxic T lymphocytes) invade the cNS where i encounters specific peptide ligand, presented by glial or neuronal cells in association with class I MHC molecules inducing direct cell damage 5.CD4 positive t cells (T helper cells) migrate to cNS, encounter antigens presented by microglial cells in association with class II MHC molecules leading to hightend production of inflammatory cytokines 6.Cytokines released by myelin reactive CD4 Th1 cells cause upregulation of mHC class II molevules and costimulatory molecules (B7-1) on astrocytes and microglia in cNS (Activated macrophages contribute to inflammation and tissue damage through the release of injurious immune mediators and direct phagocytic attack on the meylin sheath)
38
What is the role of Th17 cells in MS?
EXpression of iL-17 and IL-22 receptors on BBB endothelial cell in MS disrupt BBB tight junctions, Th17 lymphocytes transmigrate efficiently across BBB-ECs, highly express granzyme B, kill human neurons and promote CNS inflammatio through CD4+ lymphocyte recruitment
39
what is the charcteristic findings of MS in CSF?
Mild pleocytosis Elevated IgG synthesis levels HIgh IgG synthesis levels HIgh IgG index (0.7 or greater) Oligoclonal banding on electrophoresis Myelin basic protein is normally <1ng/ml but increases in 80% of acute MS relapses
40
What are some diagnostic tests than can be used for MS?
Evoked potential testing (Visual evoked potentials can establish evidence of optic nerve damage) CSF MRI
41
What is a common presenting symptom of MS?
Include visual/occulomotor problems
42
What are the types of MS and how are they classified?
Spinal MS variant, Cerebellar MS variant, Cognitive MS variant they are classified according to the most affected neurologic subsystem
43
What are the classification of MS?
(RRMS) Relapsing remitting MS most common and is charcterized by relapses and remissions of neurologic diasbility over years to decades (SPMS) Secondary progressive MS follows an initiial relapsing-remitting course. This subtype is charcterized by progressive worsening of neurologic function. Primary progressive MS Characterized by worsening neurologic function (accumulation of disability) from the onset of symptoms, without early relapses or remissions and prognosis is worse for this group of patients
44
What are infections linked to Guillain-Barre syndrome?
Camplyobacter jejuni Cytomegalovirus Epstein Barr virus Varcilla-zoster virus Mycoplasma pneumoniae
45
What events can trigger Guillain-Barre syndrome?
Upper respiratory tract infection or diarrhoea precedes onset in two thirds of cases Immunisation Pregnancy Surgical procedure Lymphoma
46
What are the first symptoms of guillai Barre syndrome?
Numbness, Parasthesia, weakness, pain in the limbs Progressive bilateral and relatively symmetrical weakness of the limbs Most patients have initially weakness, numbness and tingling in the distal parts of the lowerlimbs that ascends to the proximal legs
47
What cells in MS produce IL-10 and TGF-B?
FoxP3+ Tregs and type 1 tregs
48
How does IL-10 suppress the immune system?
Supress T-Cell response by inhibiting the production IL-2, IL-5 and TNFB and also through inhibitng the upregulation of MHC Class II as well as B7 co-stimulatory ligand on DCs and macrophages anatgonizing effective antige presentation and T cell co-stimulation
49
How does TGF-B suppress the immune system?
TGF-B blocks cytokine production by T cells, as well as cytoxicity and proliferation
50
What is meningitis?
Infection & inflammation od meninges
51
What is encephalitis?
Inflammation and infection of the brain
52
What is meningoecephalitus?
Encephalitis with meninges
53
What is encephalomyelitis?
Encephalitis with involvements of the spinal cord
54
What are the 4 princinple routes by which infectious agents enter the CNS?
1.Hematogenous from blood 2.Direct inoculation by trauma or surgery 3.Spread from nearby infection 4.Retrograde through pripheral nerves
55
What part of the spinal cord does poliovirus infect?
The grey matter, anterior horn cell of the spinal cord causes lower motor neuron lesion
56
What are the genotypes of poliovirus?
PV 1, 2, 3
57
What is the genus of poliovirus?
enterovirus
58
What type of virus is poliovirus?
family: Picornavirus with a very small RNA +SS RNA non-enveloped
59
What is the most common form of poliovirus?
PV1
60
What can inactivate poliovirus?
Chlorination of water
61
What is the mode of infection of poliomyelitis?
Ingestion of contaminated foof and drinks by stool from infected human (feco0oral transmission)
62
What is the incubation period of poliomyelitis?
7 to 14 days
63
How can you diagnose poliomeylitis?
Through a nasopharyngeal swab and in the stool
64
What are the stages of polio infectiion?
1.Inapparant (asymptomatic) The virus multiplies in the intestinal lymphoid tissues without invading the blood or CNS, excreted in faeces 2.Abortive infection (most common) The virus invades the blooc (viraemia) but not CNS. Mild symptoms: fever, malaise, headache, nausea and vomiting 3.Aseptic meningitis (non-paralytic poliomyelitis) The virus reaches reaches the CNS 4.Paralytic poliomyelitis Destroys lmns of the spinal cord causing flaccid paralysis
65
In what stage does protective immunity develop?
Innaparant stage
66
What is the clinical picture of aseptic meningitis?
headache, neck stiffness ad back pain ussually resolves spontaneously but may progress to paralysis
67
What are the polio endemic areas?
Nigeria, Afghanistan, Pakistan
68
Which areas are certified free of poliovirus?
Americas, western pacific, europe ans south east asia
69
What is the first inactivated polio vaccine ?
Salk vaccine
70
What is the live attenuated oral polio vaccine?
Sabin vaccine
71
What are the advantages of using oPV?
Inexpensive Easy to administer (orally) Produces excellent local immunity in the intestine (IgA) Provides herd immunity (passes in stool)
72
Why have most developed countries switched to IPV?
It cannot revert
73
What is the immune basis of gullain Barre syndrome?
1.Through molecular similarity between myelin epitopes and glycolipids expressed on Caamplyobacter, Mycoplasma and other infectious agents (molecular mimicry) which precede attacks of gUllain-Barre syndrome 2.Antibodies directed against these infectious agents cross-react with specific antigens of myelin components 3.Binding of these antibodies to target antigens on the peripheral nerves may lead to conduction block before there is strucural nerve damage
74
What is the pathogenesis in Guillain-Barre syndrome?
1.Lipo-oligosaccharides on the c.jejuni outer membrane may elicit the production of antibodies that cross-react with gangliosides, such as GM1 on peripheral nerves 2.Antibodies binding leads to complement activation followed by membrane attack complex (MAC) formation 3.Macrophages then invade from the nodes into the periaxonal space, scavenging the injured axons
75
What are the antibodies of gangliosides?
GM1, GD1a, GT1a, and GQ1b
76
What are the immunological features of Guillain-Barre syndrome?
Mononuclear cell infiltration of affected peripheral nerves Antibodies to meylin components Peripheral T cell activaton
77
What is Guillan barre CSF diagnostic testing?
Elevated CSF protein levels in over 80% of ptients after 2 weeks No or few mononuclear cells ANti ganglioside antibodies, particularly anti-GM1 antibodies Electrodiagnostic studies: demonstrate evidence of demyelination
78
What are the treatment opotions of Guillan barre?
Large doses of intravenous immunoglobulin (IVIG) (In severly affected patients as soon as a diagnosis is made) Plasma exchange
79
What is CTLA-4?
The alternative receptor of b7 co-stimulatory ligands, is important for treg function. TRegs bearing surface CTLA-4 exert inhibitory effect on T-cells by a number of mechanisms
80
How do we rener naive T cells inactive?
Delivering negative signals to dendritic cells via CTLA-4 which down reglate B7 ligands on the latter renderig them incapable of activating naive t cells
81
How is the barrier of activation of autoreactive t cells is lowered for mS patients?
An increased frequency of IFN-Y secreting Tregs relative t healthy controls

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