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Nutrition > Recap 4 > Flashcards

Recap 4 Flashcards

1
Q

How does Mannheimia haemolytica affect mucus?

A

Produces neuraminidase (glycoside hydroxylase) which reduces viscosity of mucus

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2
Q

Bacterial exotoxins :
Produced by
Action via
Gram+

A

Secreted by living G+
Some act via A-B toxin system = bind to cell membrane with R (B-subunit) and deliver toxin via A-subunit (botulism, tetanus, Corynebacterium, anthrax)
E.coli hemolysin
S.aureus also has a-toxin = pore forming cytotoxin
G+ = thick meshlike outer layer of peptidoglycan (murein)

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3
Q

Lipoteichoic acid (origin)

A

Release from dead G+ (located in cell wall)

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4
Q

Endotoxin :
Release
Toxicity

A

Released from dead G-
Toxicity of LPS due to lipid A immunogenicity due to polysaccharide = activation of proinflamm cytokines and NO -> active complement and coag cascade = endotoxic shock

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5
Q

Virulence factor of siderophore

A

Mediate release of iron from IC iron stores
- enterobactin = E.coli, salmonella
- Bacillibactin, petrobactin (B.anthracis)

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6
Q

Key mechanisms of ATBresistance

A
  • Enzymatic deactivation (B-lactamase)
  • Alteration of atb binding sites (penicillin-binding protein)
  • Alteration of a metabolic pathway (sulfonamide-resistant bacteria that use preformed folic acid in place of PABA)
  • Reduced atb accumulation in bacteria through decreased membrane permeability to the atb and/or enhanced efflux via membrane pumps
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7
Q

Bacterial horizontal gene transfer

A
  • Conjugation : direct bacteria-bacteria contact via plasmid
  • Transformation : chromosomal DNA in which free in EC fluid as a result of lysis of its host bacterium are taken up via bacteria
  • Transduction : bacteria-Sp virus (bacteriophage) transfer DNA between 2 closely related bacteria
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8
Q

Types of enteric colibacillosis

A
  1. ETEC : don’t invade enterocytes, secrete toxins that affect enterocytes fct not structure, secretory diarrhea
  2. EPEC : don’t invade enterocytes, affect microvillus border (structure) = osmotic D+ (malabsorption)
  3. EHEC : invade mucosal enterocytes, structural damage/necrosis to colon enterocytes (cell lysis) = malabsorption
  4. Enterotoxemic and septicemic collibacillosis : from enteropathogenic strains = enterotoxins invade/absorb by capillaries in lamina propria
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9
Q

Pathogenesis of ETEC

A
  • Express K99 (F5) or F41 (fimbria adhesin) = allow to bind to receptors in mucus layer and to ganglioside and glycoprotein-R on cell membranes
  • Heat labile (LT) and heat stable (ST) enterotoxins -> binds to R interact with 2nd messenger -> increase IC cAMP (LT) and cGMP (ST) = open chloride channels irreversibly = IC Cl ions move to EC in lumen
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10
Q

Pathogenesis of EPEC

A
  • Express adhesins P and S fimbriae, EPEC adherence factor, intimin
  • Injury to brush border disrupt cytoskeleton by injecting EspA, EspB, EspD in cytoplasm of enterocytes = active transduction pathway + acute inflammation = loss of microvilli (attaching/effacing injury) = decrease digestive enzyme activity -> osmotic D+
  • Some strain produce verotoxin = kills enterocytes and cells in lamina propria = erosions, ulcers
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11
Q

Pathogenesis of EHEC

A
  • ++++ colon specific
  • Verotoxin = acute inflamm, invade enterocytes and toxin kills
  • Some strains produce Shiga toxin
  • H+ colitis with erosion/ulcers = expose lamina propria to LPS
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12
Q

In Salmonella what is the mechanism of injury in by what are the lesions caused by? colonize? Survival?

A

Acute coagulative necrosis by toxins and by acute inflammation
= enterotoxins (exotoxin), endotoxin and LPS (membrane injury, cell lysis), acute inflammation
Colonize M cells and apical cell membrane of enterocytes (salmonella is motile = flagella)
In the cell (macro), survive within a Salmonella containing vacuole (SCV ; phagosome or phagolysosome can block fusion)
Can kill macrophages via type 1 secretory system (apoptosis, active caspase 1)

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13
Q

Pathogenesis of enterotoxemia by C.perfringens

A
  1. Ingestion of spores or can be found in normal flora
  2. Attachement and retraction on microvilli with type 4 pili
  3. Phase 1 = injury to enterocytes
  4. Phase 2 = mucosa is colonized, bacteria proliferate and produce +++++ cytotoxins spread by diffusion to mucosa/LP/SM/muscle
    - Alpha, beta = enterocyte membrane toxin
    - Epsilon = increase enterocyte and endothelial cell permeability by acting on their cytoskeleton and altering junction complex = affect absorption of toxin by vascular system
    - Iota = disrupts cytoskeleton = cell lysis
  5. Toxins goes systemic (+++ epsilon bc increase permeability) -> brain (focal, symmetric encephalomalacie), kidney (pulpy kidney dz)
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14
Q

Pathogenesis of B.anthracis

A

3 exotoxins cause cell lysis
1. Protective antigen (PA, B part) = Facilitate entry of itself into cells by endocytosis and form a pore through which the remaining 2 toxins can enter the cells -> binds to TEM8 and CMG2
2. Edema factor (EF, A part) = Disrupt cell membrane, water and electrolyte transport -> cell lysis
EF binds to Ca, calmodulin to form adenyl cyclase that convert ATP to AMPc
3. Lethal factor (LF, A part) = Destroys MAPKK which regulates MAPK = leads to cell death

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15
Q

Virulence factor in R.equi enteritis

A

Vaps = virulence associated proteins

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16
Q

Pathogenesis of Johne’s disease (Mycobacterium avium spp paratuberculosis)

A
  • Requires iron for growth inside phagosome (iron stored as ferritin)
  • Mycobacteria secrete iron-chelating proteins (exochelin, iron-reductase, siderophore)
  • R on macrophages in phagocytosis of bacteria = mannose-binding-R, CD14-R
  • Mycobacteria suppress ability of macrophages to be activated by cytokines such as IFNy
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17
Q

Pathogenesis of Lawsonia

A
  • Lawsonia surface AG (LsaA) = adhesion or invasion
  • endocytosis in crypts in proliferative zone
  • rapidly escape phagosome before fusion with lysosome and reside free in cytoplasm
  • prolif IC with prolif of crypt enterocytes (hypertrophy/hyperplasia)
    = inhibits normal maturation of crypt cells and increase rate of cell division = ++ mitosis
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18
Q

Pathogenesis of Brachyspira hyodysenteriae

A

Anaerobic motile spirochete
- lysis of epithelial cells of colon and cecum by hemolysin and protease
- goblet cells mucus = mucin = strong chemoattractant for spirochetes (replicate in mucigen droplets and increase production of mucus)
- majority in mucus layer
- anerobe = prod of NADH to protect against oxidative stress

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19
Q

Pathogenesis of Clostridium haemolyticum

A

Tropism for Kupffer cells
- Produce phospholipase C and hemolysin = destroy membranes
- follows injury caused by liver flukes (promotes anaerobic state)

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20
Q

Virulence factors of Strep equi subs zooepidemicus

A
  • SzP : Surface M-like protein = determine which organ is colonized through ligand-R interactions (antiphagocytic properties)
  • C5a peptidase (certain strain), invasin, fibronectin-binding protein = biofilm formation
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21
Q

Virulence factors of bovine pneumonic pasteurellosis/mannheimiosis (M.haemolytica)

A

Leukotoxin, LPS (binds CD14, B2 integrin, TLR on alveolar macro), adhesin, capsular polysaccharide (inhibe phagocytosis, disrupt complement-lysis), outer membrane protein (chemotactic for neutro, disrupt phagocytosis), protease (reduce viscosity of mucus), fimbriae and pili adhesin
**Leukotoxin = causes lysis and apoptosis of alveolar macrophages and neutrophils, attach through cells by passive absorption and cell surface B2-integrin-R (CD18)
High concentration = necrosis by creating pores in cell membrane
Low concentration = apoptosis, active neutro induce proinflamm cytokines

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22
Q

Pathogenesis of M.bovis (bovine tuberculosis)

A

Use multiple membrane pathogen PRR to enter macrophages = complement receptor (CR1, 3, 4), mannose, surfactant protein, CD14
Can activate alternative pathway of complement and use C3b and C3bi fragments to opsonize its surface and bind complement-R
Waxy cell wall hard to digest = granuloma, giant cells

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23
Q

Virulence factors of porcine pleuropneumoniae (Actinobacillus pleuropneumoniae)

A

Use porcine transferrin as source of iron
Apx toxin = pore forming exotoxins that lyses cells (ApxI-III)

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24
Q

Pathogenesis of atrophic rhinitis

A
  1. B. Bronchiseptica = Dermonecrotic toxin (DNT) and adenylate cyclase-hemolysin toxin -> squamous metaplasia = disrupts mucus layer promote multocida infection
  2. P. Multocida = P.multocida toxin (PMT) = blocks fct of osteoblasts = bone remodelling
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25
Q

Virulence factor of Mycoplasma hyopneumoniae

A

Cilium adhesin expressed on bacterium = binding process -> interact with glycosaminoglycan and heparin on cell membranes

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26
Q

Pathogenesis of B.bronchiseptica in dogs (tracheobronchitis)

A

Colonize ciliated epithelium via nonfimbrial adhesins = filamentous hemagglutinin and perfactin
Release exotoxins (adenylate cyclase-hemolysin and DNT) and endotoxin = impair fct

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27
Q

Virulence factor of leptospirosis

A

Surface-associated protein (outer membrane of leptospiral protein)
Pore-forming hemolysin
Protease
Sphingomyelinase
Collagenase

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28
Q

Pathogenesis of edema disease

A

Hemolytic strain of E.coli -> absorb (shiga or verotoxin) = fibrinoid arteriopathy ++ brain = ischemia, malacia
Lysis of endothelial cell and smooth muscle cells of arteriols (express R for toxins = globotetraosylceramide, galactosylgloboside, globotriaosylceramide) = disrupt protein synthesis = permability = edema

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29
Q

Virulence factor of UPEC (E.coli)

A

Adhesin type 1 fimbria, P fimbria, S fimbria = bind to receptors called uroplakins expressed on apical surface of umbrella cells
Tips of type 1 fimbria express ligand called FimH adhesin = bind to uroplakin receptors (UPIa)

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30
Q

Target cells of leptospira

A

Primary target in kidney = proximal convoluted tubules (cortex)
Later = loops of henle (medulla)

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31
Q

Virulence factors of Brucella

A

Class A scavenger receptors on target cells
Blocks phagosolysosome fusion by LPS, cyclic B-1,2-glucan and HSP

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32
Q

Pathogenesis of Strep equi equi

A
  1. Target = epithelial cells -> M-like proteins (SeM, SzPSe) = adhesins
  2. Bact multiplied EC in NL
  3. SeeH (cell wall protein) interacts with macro = increase proinflamm cytokines = increase permeability and edema
  4. Peptidoglycan bact wall interacts with C3 complement in edema via alternative complement pathway -> produce chemotactic factors
  5. Streptokinase interacts with plasminogen in edema fluid to form active plasmin which hydrolyzes fibrin = increase spread of bacteria
  6. Secrete leukocidal toxin and streptolysin S (pore-forming toxin)
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33
Q

Virulence factors of Corynebacterium pseudotuberculosis

A
  • Phospholipase D (exotoxin) = increase permeability (helps macro spread), injures cell membrane
  • Waxy mycolic acid coat on cell surface = acute inflamm, formation of granuloma
34
Q

Pathogenesis of botulism and tetanus

A
  1. Toxins produced in anaerobic microenvironment
  2. Access to myoneural/neural-neural jct from a wound
    HEMATOGENE - botulism toxin
    RETROGRADE AXONAL TRANSPORT - tetanus
    BOTULINUM :
    - neurotoxins in capillaries -> reaches cell membrane of peripheral nerves (lower motor neuron) -> enters neuron by endocytosis
    - toxin type A to G cleaves some SNARE protein (don’t cross BBB)
    - toxin binds ganglioside on motor neurons -> goes in cytoplasm where toxin A cleaves synaptobrevin (mediates fusion of NT) = prevents release of acetylcholine
    TETANUS
    - gain access by entering cytoplasm of distal process of neurons by endocytotic vesicles in viable nerve in periphery of wound -> retrograde axonal transport -> release in interstitial fluid of neural-neural jct by exocytosis -> free toxin binds to cell membrane of inhibitory interneurons of spinal cord -> internalized via endocytosis = disrupt release of inhibitory NT (disrupt synaptic fusion complex) = BLOCKS RELEASE OF GABA-aminobutyric acid (inhibitor NT)
35
Q

What are the proteins forming the synaptic fusion complex?**

A

SNARE : neurotransmitter vesicle protein (VAMPs/synaptobrevin) and presynaptic plasma membrane proteins (syntaxin, synaptosomal-associated protein, SNAP-25)

36
Q

Pathogenesis of Listeria monocytogenes

A

Penetrating injury oral mucosa -> cranial nerve -> CNS via retrograde axonal transport -> brainstem -> entry cells by internalins type A et B that use target cell-R (E-cadherins)
Reside in endosome IC in cell bodies of neurons = début pas d’inflammation
Cytoplasm of neurons = free proliferation promoted by listeriolysin O (inhibe immune response = hide from defense mechanism)
Surface A protein ActA = propel themselves via actin polymerization and pseudopod = invagination (double-membrane endocytosis -> lysis by listeriolysin O, phospholipase C, lecithinase) = bacteria released in cytoplasm of new cell

37
Q

Viral replication cycle

A
  1. Attachment (attachment proteins = virulence factors on capside or envelops)
  2. Entry (by endocytosis, phagocytosis, fusion)
  3. Spread (by uncoating)
  4. Replication
    DNA virus = DNA genome tranfer to nucleus = uses cell nuclear organelle to transcribe mRNA and replicate new DNA. Viral RNA leave nucleus translated in cytoplasm and assemble in new virus
    RNA = genome can replicate new viral RNA from cytoplasmic viral mRNA via own viral RNA-dependent RNA polymerase or make viral DNA from RNA via RNA-dependent DNA polymerase -> use target cell nuclear and cytoplasmic organelles to transcribe/translate new proteins and viral RNA
  5. Shedding (release or egress) = exit cell via budding or cell lysis
    Non envelopped = via cell lysis only
    Envelopped = by budding from cell membrane usually no lysis (except herpèsvirus)
38
Q

What are mechanisms of genomic change?***

A
  1. AG drift/genetic drift = natural mutation in viral genome over time
  2. Antigenic shift = when 2 or more different strains of the same virus or strains of 2 or more different virus combine (reassortment) to form new virus (when infect the same cell)
    Also occurs from recombination = IN DNA VIRUS rearrangement within viral genome and deletion or duplication of viral genes and acquisition of unrelated genetic material = occurs when strand of DNA is broken
  3. Reassortment = ONLY IN RNA VIRUS because they have discrete genomic segments (like chromosome) that behave independently of one another = during viral replication
  4. Defective interfering viruses = DNA, RNA = virus that can’t replicate by themselves = compete with nondefective viral genomes for limited supply of replication enzymes
39
Q

Caracteristics of Rotavirus

A

Non enveloppé
RNA
VP4, VP7 = attachment protein
NSP4 = enterotoxin

40
Q

Arbovirus (vesicular stomatitis)

A

Envelopped, RNA
Attachment protein glycoprotein G binds to LDL-R
Targets squamous epithelial cells

41
Q

BVD (pestivirus)

A

Envelopped, RNA
Glycoprotein E1, E2 = attachment crypt enterocytes
Vasculopathy in submucosal Peyer patch = necrosis of vascular wall
Lympho of Peyer initially prolif -> massive lysis (virus induced apoptosis)

42
Q

Morbillivirus (rinderpest)

A

Envelopped, RNA
Target CD150 (signaling lympho activation molecule), SLAM (lympho, mono, macro, epithelial cells, alimentary, integumentary)

43
Q

Parapoxvirus (ecthyma contagious)

A

DNA, envelopped
F1L attachment protein vind to glycosaminoglycan heparin sulfate receptors
Synthesis of vascular endothelial growth factor by infected endothelium = angiogenesis

44
Q

Aphtovirus (foot-and-mouth disease)

A

RNA, non envelopped
VP1-4 = attachment
R-integrin VB1, VB3 and VB6

45
Q

GIT (Coronavirus)

A

RNA, envelopped
S protein on envelop bind sialic acid in mucus layer to amino-peptidase N on apical surfaces
E2 = entry

46
Q

Enterovirus (swine vesicular disease)

A

RNA, non envelopped
VP1-4 = attachment
R = ICAM

47
Q

Calicivirus (vesicular exanthema of pigs)

A

RNA, non envelopped

48
Q

Parvovirus

A

DNA, non envelopped
Requires a target cell-derived duplex transcription template = only available when cells are in the S phase
Bind to canine transferrin-R, feline neuraminic acid and transferrin-R

49
Q

Arbovirus (Wesselbron’s disease, flavivirus)

A

RNA , envelopped
Cible hepatocytes, Kupffer

50
Q

Phlebovirus (Rift Valley Fever)

A

DNA, non enveloped
Lysis of epithelial cells (liver, kidney) and endothelial cells everywhere
Fiber protein = attachment
R = Coxsackievirus-adenovirus integrin

51
Q

Equine influenza = orthomyxovirus

A

RNA, enveloped
Hemagglutinin (HA) = entry
Neuraminidase (NA) = shedding
HA, NA = bind to target cell (R composed of sialyloligosaccharide)

52
Q

Herpesvirus (IBR) = alpha-herpesvirus

A

DNA, enveloped
Attachment = glycoprotein B, C, D
Herpesvirtus entry mediator A, nectin 1, nectin 2 (herpes entry proteins C, and B), 3-O-sulfated heparin sulfate
Enter nerve ending of trigeminal and olfactory nerves -> go to other nerves via retrograde axonal transport -> neurons = latent infection ; no CMH II, low CMH I = less recongition of CTL, macro, microglial
Latency = virus in nucleus but no viral protein synthesized
ACTIVATION = reestablish replication by axonal transport to mucosa, infect adjacent epithelila cells

53
Q

Pneumovirus (virus syncitial bovin)

A

RNA, enveloped
Syncitial cell with intracytoplasmic inclusion body
Attachment = glycoprotein G
Fusion = glycoprotein F
TLR3-4 = inflammation

54
Q

Lentivirus (maedi-visna)

A

RNA, enveloped
Persistently infect monocytes precursor cells
Virus infect immature monocyte precursors in bone marrow -> reservoir + dissemine -> all cell permanently infected because genome inserted into chromosomal DNA of target cells
Chronic inflamm in lung, brain, mammary, synovia (where macrophages are permissive to genome integration)
Demyelinating encephalitis

55
Q

Arterivirus (SRRP)

A

RNA, envelopped
R = sialoadhesin, scavenger receptor-CD163, heparan sulfate
Acute inflammation can injure mucociliary apparatus = bacterial infections

56
Q

Herpesvirus-cytomegalovirus (inclusion body rhinitis)

A

DNA, enveloped
Infect/injure erythroid precursors cells in bone marrow = neonatal anemia

57
Q

Feline calicivirus

A

RNA, non enveloped
Virulent systemic felin calicivirus infection, acquired tropism for endothelial cell -> lysis, vascular injury, CIVD

58
Q

Orbivirus (african horse sickness)

A

RNA, non enveloped
Similar to bluetongue
Non contagious
Bite from midges
Capsid structural protein VP2, VP5
NS3 = inserted in target cell membranes, cytotoxic (viroporin)
Source = semen (accessory sex glands)

59
Q

Gamma herpesvirus (catarrhal maligne)

A

DNA, enveloped
Lysis of vascular endothelial cells and hyperplasia and lysis of lymphocytes in lymphoid tissues
Lymphoproliferative vasculitis
Dead-end host because virus spread requires cell free virus in body fluid which doesn’t happen

60
Q

Pestivirus (classical swine fever)

A

RNA, enveloped
Erns and E2 envelope glycoprotein

61
Q

Asfivirus (african swine fever)

A

DNA, enveloped
Envelop glycoprotein p12, p54, p30

62
Q

Canine herpesvirus type 1*

A

DNA, enveloped
Glycoprotein B, C, D
Low body temperature helps

63
Q

PIF (enteric coronavirus mutated)

A

RNA, enveloped
Mutation = antigenic shift/drift of 3c gene occurs within mucosal macrophages
S1, S2, M, E = attachment
R = feline aminopeptidase-N
Response:
- Strong cell mediated = no PIF
- Weak cell mediated = dry/non effusive
- No cell mediated = wet/effusive
- Effective humoral = increase severity
If adequate AC -> form AC-AG complex on basement membrane of endo cells = type 3 hyperS = active complement -> neutro
Type 4 hyperS involved in some pyogranulomas

64
Q

Equine infectious anemia (lentivirus)

A

RNA, enveloped
Bloodborne
Surface envelope protein = gp120, gp90
R = equine lentivirus receptor 1
Cell-free virus absorb on surface of GR act as hapten -> phagocytosis + hapten presented to lympho -> humoral response -> hyperS 2
If hapten active complement -> GR lysis, if not GR phagocytosed by macro
Control of disease linked to effective AC-response against virus = 6-8 mois

65
Q

Deltavirus (bovine leukemia virus)

A

RNA, enveloped
Transformation of LB+++ (gene transactivation)
Provirus infected LT
Gp51, gp30 enter naive LB that express bovine leukemia virus-binding-R
LB expressing IgM and cell surface CD5 and CD11b more susceptible to infection
Bovine leukemia virus Tax protein (p34tax) stimule prolif of LB, increase virus replication, interact target cell genes and transactivated genes that modulate cell growth and differenciation

66
Q

Circovirus type 2

A

DNA, non enveloped
Virus requires dividing cells in the S phase
Macrophages = non permissive (only infected for leuco traffick)
Lymphocytes = permissive

67
Q

Retrovirus (feline leukemia virus)

A

RNA, enveloped
LB = spread virus by leucocytes trafficking
LT = primary target for cell infections
Requires rapidly dividing cells
Persistent LT infection = SC
Surface glycoprotein (SU) and transmembrane protein TM

68
Q

Lentivirus (feline immunodeficiency virus)

A

RNA, enveloped
infect CD4+ LT
Surface glycoprotein SU, transmembrane protein TM
Target cells express feline CD134 and CXCR4 cofactor

69
Q

Rabies lyssavirus ***

A

RNA, enveloped
- Viral takeover of RNA transcription\translation in neurons disrupts NT fcts, dysfunction ions channels, synthesis of NO
- infects neurons, glial cells, epithelial cells (salivary)
Attach viral G protein binding to NT-R (acetylcholine) = enter striated muscle -> replicate -> enter interstitial fluids of myoneural jcts binds acetylcholine-R and other gangliosides in cell membrane of unmyelinated axon terminals of lower motor neurons of peripheral nerves
- Spread via retrograde axonal transport (using dynein light chain microtubule-based transport) -> replicate -> travel to dendrite via axonal where buds in dendritic process into synaptic cleft of neural-neural jct (gray matter, ventral gray horn, spinal cord)
- Spread via afferent and efferent neural pathway to infect epithelial cells of salivary glands = facial 7 et glossopharyngien 9

70
Q

Alphaherpesvirus (equine encephalomalacie)

A

DNA, enveloped
Dysfct of endothelial cells in small arterioles of brain and spinal cord
Immune complex hyperS

71
Q

Alphaherpesvirus (pseudorabies)

A

DNA, enveloped
Target neuron cell bodies
Dysruption of neurons ++++CTL
Use retrograde axonal transport to enter brain

72
Q

Morbilivirus (distemper)

A

RNA, enveloped
Dysfct of neuronal, epithelial, mesenchymal, neuroendocrine, hematopoietic cells
Demyelination leucoencephalomalacie
Viral H protein and fusion protein called viral F protein
R = CD150 (SLAM)

73
Q

Feline parvovirus induced cerebral hypoplasia

A

NS1 produced by virus = highly toxic

74
Q

Viral papilloma, warts, sarcoids **

A

DNA, non envelopped
Dysfct of genes that regulate cell prolif/differenciation/adhesion
E5 = active R PDGF, EGF, inhibe CMH I
E6 = inhibe p53, BAK, active telomerase, BCL2, mTOR, MYC
E7 = active HIFa, inhibe Rb, p21, favoris bris DNA
Integrins (a6B4) and potentially heparin sulfate mediate attachment
Bovine L1 major capside protein and L2 minor capside protein
Target cells= basal cells (non permissive), reservoir for persistent infection = replicate genome but can’t produce infected virions
Maturation of virus occurs as cells differenciate to upper layers= virus complete cycle
Viral protein prevent cells from stopping cell cycle = now capable of division
Some strains are unable to integrate into target cells gene = benign (non permissive cells of stratum basale) if integrate = malign (permissive cells of suprabasal layer)

75
Q

FeLV subtypes

A
  1. FeLV A = only subgroups transmitted between cats, persistent infection of bone marrow (LT = precursor), immunosuppressive (+ cell-mediated immunity)
    Less lympho (CTL) virus induced lysis + suppress IFN, IL secreted by LT + dysfct of activation of macro and neutro phagocytosis
    R = feline thiamine transport protein (FeTHTR1)
  2. FeLV B = antigenic shift (recombination) of FeLV A, neoplastic transformation
    R = feline phosphate transporter protein 1 or 2 (FePit1 or 2)
  3. FeLV C = point mutation (antigenic drift), anemia, R = FeLVCR
  4. FeLV T = infects LT, immunodeficiency syndrome, R = FePit1
    FeLIX = secreted by LT = restrict tropism to LT
    VIRUS PRODUCE REVERSE TRANSCRIPTASE (REOVIRUS) TO TRANSCRIBE VIRAL RNA INTO PROVIRAL DNA = INSERTION INTO CHROMOSOMAL LT
    FOCMA expressed on cell membranes of transformed cells (not found on infected, non transformed cell)
76
Q

Blastomycosis adhesion

A

BAD1 : blastomyces adhesion factor 1 = adhesion to CR3, CD14 on alveolar macrophage cell membrane

77
Q

Pathogenesis of tuberculosis

A

Enters macrophages by phagocytosis mediated by receptors MBL and CR3 -> blocks phagolysosome formation -> replicate in vesible
PAMP recognized by innate immune receptors :
- lipoarabinomannan binds TLR2
- unmethylated CpG nucleotides bind TLR9
IFNy stimulates defensins, autophagy, prod of NO
Macro activated by IFNy differenciate into epithelioids = form granuloma

78
Q

What are lepra cells?

A

In leprosis, they are lipid laden macrophages filled with mass globi acid-fast bacilli
Multibacillary because abundant bacilli

79
Q

How is aspergillus recognized by alveolar macrophages?

A

Via TLR2 and lectin-dectin-1 = reconnait beta-1,3-glucan in cell wall -> activate phagocytes

80
Q

Leishmaniasis virulence factors

A
  • Lipophosphoglycan = glycocalyx that activates complement but prevent MAC insertion -> opsonize with C3b binds MAC-1 and CR1 = phagocytosis
  • Gp63 = proteinase that cleave complement and some lysosomal enzymes
81
Q

Dx methods for cells in mitosis, apoptosis

A

Mitosis : Ki67, PCNA, AgNOR
Apoptosis : caspase, annexin, TUNEL

Nutrition (13 decks)

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