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Vet 413 - Infectious Diseases > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Type 1 Interferons

A

IFN alpha, beta

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2
Q

Describe the fx of IFN a/b in response to viral infection

A
  1. Internal cytoplasmic sensors of viral RNA (TLR 3, 7/8, 9) stimulate release of IFN a/b
  2. Block the spread of virus to uninfected cells via the destruction of mRNA and protein synthesis
  3. IFN’s stimulate chemokine production CXCL 9, 10, 11 that recruit lymphocytes and stim. MHC-1 expression
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3
Q

What stimulates NK (Natural Killer) cells?

A

IFN a, b, and IFN-y (via ILC-1)

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4
Q

What is unique about the function of NK cells?

A

The ability to kill virus-infected cells without any prior exposure (no need for TCR or BCR).

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5
Q

How do NK cells recognize the cells it must kill?

A

Viruses often down-regulate MHC-1 on the surface of the cell to inhibit CD8 response. MHC-1 inhibits activation/ degranulation of NK cells.

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6
Q

Two ways to activate CD8 T cells

A
  1. Intracellular/ endogenous pathogen processing and presentation on MHC-1 – TCR
  2. Cross-Presentation: extracellular pathogen presented via activated DC
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7
Q

T/F: CD8 primarily defend against extracellular pathogens

A

F: they are primarily intracellular

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8
Q

Mechanisms of attack for CD8 T Cells

A
  1. Cytokine secretion: IFN-y, TNF-a, Lymphotoxin-a

2. Trigger apoptosis: 2 mech. (LFA-1/ICAM-1)(Death Receptor)

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9
Q

Describe LFA-1 and ICAM-1 mech. of apoptosis (CD8 T cells)

A

LFA-1 and ICAM-1 are non-specific adhesion molecules that form an immunological synapse between the CD8 and target cell. This allows perforins, granzymes, and granulolysin to be directed specifically towards the target cell.

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10
Q

Function of Perforins (CD8TC)

A

Perforins are glycoproteins that are used to penetrate the cell wall and form complement-like structures that allow injection of granzymes to trigger the apoptosis pathway

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11
Q

Fas-Fas Ligand pathway

A

Secondary way to kill virus infected cells; the main way is the LFA1 ICAM1 pathway thought; mainly used during negative selection in the thymus

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12
Q

B Cell activation

A
  1. BCR recognizes whole antigen

2. B Cell processes antigen and presents it to T Helper 2 Cell w/ CD40/40L

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13
Q

Antibodies (and fx)

A
  • IgA: barrier fx, neutralizes and prevents infections
  • IgG: neutralizes, opsonizes, ADCC w/ NK cells
  • Compliment activation w/ IgM and IgG
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14
Q

T/F: any level of virus load will trigger the adaptive immune response. it will just take longer to respond if there is less load

A

F: there is a specific cut-off level that the adaptive immune system won’t respond to if load is below that level

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15
Q

2 possible end results of B cell activation

A
  1. antibody secreting plasma cells

2. non-secretory memory B cells

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16
Q

Advantage of Activated Memory B cells

A
  • have more CD80 and MHC2 than naive
  • higher affinity of surface Ig and increased levels of co-stimulatory molecules allow them to initiate rxns w/ Tfh cells at lower antigen levels = faster response
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17
Q

Understand the idea of Affinity Maturation

A

yeah

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18
Q

How to use Ab to determine chronicity of dz

A
  • IgM (acute) vs IgG (chronic) levels
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19
Q

Do memory T cells undergo somatic hypermutation?

A

No, only B cells do that

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20
Q

How long do the core vaccines confer immunity for?

A

roughly 7 years

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21
Q

What is the rationale for increased interval between vax?

A

potential for adverse effects since we are activating the immune system every time. risk of overstimulation

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22
Q

Methods to determine Ab titer (Distemper, Adenovirus-1, Parvovirus, Leptospira)?

A

Distemper - Virus Neutralization
Adenovirus-1 - Virus Neutralization
Parvovirus - HAI
Leptospira - MAT

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23
Q

What are the 4 key components of every major immune response/ module?

A
  1. T helper subset (Th1, Th2, Th17)
  2. Innate Lymphoid Cells (assist the T cells)
  3. Phagocytes (do the dirty work)
  4. Antibody Isotypes (connect phag-pathogen)
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24
Q

Components of Type 1 Immune Response/ Modules

A

Th1, ILC-1, macrophages, IgG

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25
Q

Components of Type 2 Immune Response/ Modules

A

Th2, ILC-2, mast cells/ basophils/ eosinophils, IgM

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26
Q

Components of Type 3 Immune Response/ Modules

A

Th17, ILC-3, neutrophils, IgG

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27
Q

How do T cells determine their differentiation pathway?

A

Signal 3 –> activation of T cell in presentation of specific cytokines. Cytokines can come from APC (in the case of Th1) or from the ILCs

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28
Q

Describe counter regulation of opposing Th subsets

A
  • Th1 and Th2 subsets will antagonize each other
  • IFN-y produced by Th1 will completely inhibit the Th2 pathway
  • IL-4, -13 from Th2 will counter Th1
  • Treg produce TGF-b that counters Th1 and Th2
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29
Q

T cells make a fate decision. What does this mean?

A

Fate Decision refers to the concept that once a T cell differentiates into Th1 or Th2, they will stay that way

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30
Q

Describe the process involved in the T cell fate decision.

A

expression of master transcription factors that direct expression of certain cytokines that positive feedback upon themselves and prevent transition into a different subset

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31
Q

Which T cell subsets are considered ‘plastic’

A

Th17 and Treg

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32
Q

T/F: Autoimmune T cells can sometimes arise from exTh17 cells that turn into Th1.

A

True

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33
Q

How do we mount a variable T cell response in different locations in the body?

A

T cell differentiation is determined by the sentinel lymph node. Can mount a Th2 response to helminths in the GI tract while the rest of the body dose Th17 for extracellular bacteria from the invasion

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34
Q

Active vs Passive Immunity

A

Passive – immunity not generated in the patient, giving the patient preformed Ab, protection is immediate but not long lasting
Active – induces an immune response that will not be immediate, but will be long-lasting

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35
Q

Characteristics of Ideal Vaccine

A
  • confers long-lasting immunity
  • free of side effects
  • stable, long shelf life
  • adaptable to mass vaccination
  • able to stim. immune response distinguishable from that induced via active infection (DIVA vax)
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36
Q

3 Types of Adjuvents

A
  1. Depot
  2. Particulate
  3. Immunostimulatory
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37
Q

Depot Adjuvents

A
  • slows removal of antigen providing longer exposure to the host
  • triggers granuloma formation that can last for extended periods of time
  • mineral oil, aluminum salts/ alum
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38
Q

Particulate Adjuvents

A
  • mimic microorganisms to enhance delivery to antigne presenting cells
  • emulsions, microparticles, immunostimulating complexes, and liposomes
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39
Q

Immunostimulatory Adjuvents

A
  • Promote cytokine production by host

- can be selective for Th1 (saponins) or Th2 (Bordatella pertussis)

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40
Q

Recombinant Vax USDA categories

A
  1. vax that contains inactivated recombinant organisms or purified antigens derived from recombinant organisms
  2. vax containing live organisms that contain gene deletions or heterologous marker genes
  3. vax that contain live expression vectors expressing heterologous genes for immunizing antigens or other stimulants
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41
Q

DNA Vaccines

A

plasmid is used as vector; it contains genes for immunization; taken into cell where antigenic protein is made and produces good cell mediated immunity

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42
Q

DIVA vaccines

A
  • removal of genes that code for unnecessary antigens

- immune response to those removed regions = true infection and not vaccination

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43
Q

Advantages of Live Vaccines

A

Fewer doses, no adjuvents needed
decreased chance of hypersensitivity
relatively cheap

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44
Q

Advantages of Dead Vaccines

A

Stable on storage
Unlikely to cause disease
Unlikely to be contaminated

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45
Q

Vaccination of the young animal

A
  • almost guaranteed lack of maternal Ab by 16 weeks of age so vaccination should work well then
  • can lose maternal protection prior to 16 weeks so vaccination protocols begin long before then
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46
Q

Reasons for Vaccine Failure

A
  1. Correct Administration, animal responds
  2. Correct Administration, animal does not respond
    3 Incorrect Administration
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47
Q

Role of genetics in vaccine variability

A

inbreeding can reduce the variability of MHC alleles and cause reduced ability to respond to some antigenic peptides

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48
Q

3 Types of Adverse Vaccine Responses

A

Errors, “Normal” Toxicity, and Inappropriate Response

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49
Q

Adverse Vaccine Response Error (end-results)

A

immunosuppression, clinical disease, fetal death

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50
Q

Adverse Vaccine Response N Toxicity (end-results)

A

fever, malaise, inflammation, pain

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51
Q

Adverse Vaccine Response not-N Response (end-results)

A

Type 1 - against adjuvant
Type 3 -
Type 4 - granuloma or sterile abscess
Fibrosarcoma in Cats

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52
Q

Antimicrobial Resistance Mechanisms

A
  • reduced permeability to antimicrobial agents
  • antimicrobial agent modification
  • active efflux
  • target modification
  • alternate metabolic pathways
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53
Q

Disk Diffusion (pros and cons)

A

pros: easy, inexpensive, no special equipment
cons: no MIC, no slow-growing or fastidious microbes

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54
Q

Broth Dilution (What is it and pros and cons)

A
  • serial dilution of drug that help determine MIC for a pathogen
    pros: gives MIC, trends in resistance, good for fastidious or slow growing organisms
    cons: specialized equipment needed, expensive
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55
Q

MIC vs Breakpoint

A

MIC - minimum inhibitory concentration

Breakpoint - the [drug] at which the pathogen is considered susceptible to an antimicrobial

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56
Q

T/F: MIC is specific for each species and isolate

A

T

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57
Q

T/F: MIC helps determine dosing [ ] while breakpoint determines frequency

A

F; MIC is for both dosing and frequency

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58
Q

Methicillin resistant Staph (general facts)

A
  • Altered penicillin-binding protein so no B-lactams or carbapenems will work at all
  • check for resistance w/ oxacillin
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59
Q

Subcutaneous Mycoses

A
  • typically associated with injuries
  • infections are chronic and insidious; establish in skin and produce a localized infection of surrounding tissue and lymph nodes
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60
Q

T/F: Subcutaneous Mycoses consist of all fungi and yeast

A

False: SM consist of dematiaceous or hyaline molds and dimorphic fungi

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61
Q

Oomycosis

A
  • not from the fungal family, but clinically and morphologically look the same
  • Pythium and Lagendium –> pyogranulomatous dz in animals
62
Q

Phaeohyphomycosis

A
  • caused by dematiaceous fungi
  • hyphae are present
  • CNS involvement is common (often goes systemic)
63
Q

Cryptococcus neoformans

A

Pathology: ulcerative lesions involving the URT, CNS (meningitis), Eye
Species: mainly cats
Pathogenesis: stim. Treg to suppress inflammatory response in order to gain time to reproduce
Reservoir: dust, dirt, pigeon poop, amoeba

64
Q

Systemic Mycoses (general characteristics)

A
  • most agents are saprophytic fungi
  • dimorphic (mostly)
  • infection via inhalation
  • pyogranulomatous lesions
  • generally, non-contagious
65
Q

Coccidiosis (systemic mycoses) (general facts)

A
  • dimorphic fungi
  • mainly dogs (some horses) gets pulmonary dz and osteomyelitis
  • C. immitis, and C. posadasii
66
Q

Coccidiosis (reservoir and transmission)

A

Reservoir: arthroconidias (very environmentally resistant form of spore, part. to dry, heat, acid)
Transmission: inhalation of arthroconidia

67
Q

Histoplasma capsulatum var. capsulatum (reservoir and affected species)

A

Reservoir: birds as passive carriers, bats have intestinal infection
Affected species: all species, mainly dogs tho

68
Q

Histoplasma capsulatum var. capsulatum (transmission and pathogenesis)

A

Transmission: inhalation
Pathogenesis: intracellular yeast; LN, lungs, and parenchymateous organs contain white, nodular lesions; macs filled with yeast

69
Q

Blastomyces dermatitidis (general facts)

A
  • dimorphic fungi
  • humans, dogs (cats and horses rare)
  • can survive w/in phagocytes
70
Q

Aspergillus spp. (general facts)

A

Asp. fumigatas is the most frequent in animals and humans
Path:
- Avian: respiratory dz => elevated death rates
- Ruminants: abortions and mastitis

71
Q

Defenses of respiratory tract

A
  • Physical barriers (nasal passages, epiglottis and larynx, resp. mucocilliary apparatus)
  • Immune Defense
72
Q

Bovine Respiratory Disease Complex (define)

A
  • a complex of pathogens, host factors, and environmental conditions that leads to resp. dz
  • “shipping fever”
73
Q

BRDC (4 causative viruses)

A
  1. Bovine resp. syncytial virus
  2. Infectious Bovine Rhinotraceitis
  3. Parainfluenza
  4. Bovine Viral Diarrhea
74
Q

BRDC (pathology and prevention)

A
  • death of epithelial cells, disruption of mucocilliary apparatus, and immunosuppression
  • Vaccination, anhelmenthic, slow feed changes
75
Q

BRDC (4 causative bacteria)

A
  1. Mannhemia hemolytica
  2. Pasteurella multocida
  3. Histophilus somni
  4. Mycoplasma
76
Q

BRDC (Mannhemia hemolytica)

A
  • secretes RTX toxin known as leukotoxin (pore forming toxin that affects PMNs and platelets)
  • fibrinonecrotic pneumonia
77
Q

BRDC (Pasteurella multocida)

A
  • causes bronchopneumonia

- can also causes hemorrhagic septicemia

78
Q

BRDC (Histophilus somni)

A
  • vascular damage -> fibrinonecrotic pneumonia

- other dz: septicemia w/ thromboembolic vasculitis; abortion

79
Q

BRDC (Mycoplasma)

A
  • v host specific, lack cell wall
  • Look like friend egg on culture growth
  • variety of dz: pneumonia, septicemia, and contagious mastitis in cattle
    (conjunctivitis in sheep and goats)
80
Q

Enzootic Pneumonia of Sheep

A

effectively the same dz process and pathogenesis of BRDC

81
Q

Porcine Atrophic Rhinitis (2 bacteria)

A
  1. Pasteurella multocida (PMT toxin – osteolysis and stimulates fibroplasia)
  2. Bordetella bronchiseptica (paralysis of respiratory cilia)
82
Q

Porcine Pneumonia (3 bacteria)

A
  1. Pasteurella multocida
  2. Actinobacillus pleuropneumoniae
    - porcine necrotizing pleuropneumonia caused by RTX toxin called Apx – [low] = resp. burst leading to tissue damage; [high] = destruction of phagocytes
  3. Haemophilus parasuis (bronchopneumonia in pigs – Glasser’s Disease)
83
Q

Frank vs Opportunistic pathogens

A

Frank - not normal flora

Opportunistic - part of the normal flora that invades as a secondary infection normally

84
Q

Strep equi equi (pathology, pathogenesis)

A
  • Strangles
  • Frank pathogen
  • Pathology: URT infection w/ lymphadenopathy, but can disseminate systemically to lung, spleen, brain, mesenteric LN
  • Pathogenesis: extracellular infection transmitted via aerosol or direct contact; capsule and M-proteins are antiphagocytic and prevent compliment deposition
85
Q

Rhodococcus equi

A
  • almost exclusively foals
  • facultative intracellular pathogen so requires Th1 response of resolution
  • pyogranulomatous inflammation
86
Q

Coreynebacterium pseudotuberculosis

A
  • transmitted by biting fleas
  • facultative intracellular pathogen
  • ventral abscesses and occasionally disseminates to abd. or thoracic cavity
  • (sheep get caseous lymphadenitis)
87
Q

List the 3 Frank pathogens ass. w/ resp. tract dz in horses

A
  1. Strep equi equi (Strangles)
  2. Rhodococcus equi
  3. Corenybacterium pseudotuberculosis
88
Q

List the 4 Opportunistic pathogens ass. w/ resp. tract dz in horses

A
  1. Strep equi zooepidemicus
  2. Actinobacillus equuli hemolyticus
  3. Actinobacillus equuli equuli
  4. Bardetella bronchiseptica
89
Q

Strep equi zooepidemicus

A
  • part of n flora

- pneumonia, abscesses, neonatal infection/ septicemia

90
Q

Actinobacillus equuli hemolyticus

A
  • much more pathogenic than …equuli

- RTX toxin Aqx ( [low] = resp. boost; [high] = membrane damage to phagocytes) leads to necrotizing pneumonia

91
Q

Actinobacillus equuli equuli

A
  • septicemia in foals and can disseminate to cause microabscesses in kidneys
92
Q

Bordetella bronchiseptica (equine)

A
  • generally younger horses

- path: binds to the cilia and secrete toxins that paralyze them –> pneumonia

93
Q

Bordetella bronchiseptica - SA

A
  • aerobic gram neg. cocci
  • shared among dogs and cats, poss. zoonotic
  • growing number of MDR strains
  • path: binds to the resp. cilia and secrete toxins that paralyze them
94
Q

Mycoplasma spp (particularly M. cynos) - SA

A
  • can causes URT and LRT dz

- commensal dz

95
Q

Canine Parainfluenza Virus

A
  • paramyxovirus

- enveloped, single-stranded RNA virus

96
Q

Canine Influenza Virus (general facts, 2 strains, pathology, trans, dx)

A
  • orthomyxovirus
  • enveloped RNA virus w/ high mutation rate
  • low prevalence, primarily shelter outbreaks
  • H3N8 (horses) and H3N2 (more important)
  • path: no symptoms (20%); mild to sever URT dz w/ H3N2 being more pathogenic
  • trans: not well understood
  • Diagnosis: PCR gold, Ab detection bronze d/t vax
97
Q

Canine Herpesvirus

A
  • enveloped DNA virus

- latency in trigeminal ganglia

98
Q

Canine Coronavirus (resp.)

A
  • lawnmower pathogen because it destroys all cilia
99
Q

Canine Adneovirus-2

A
  • (adenovirus-1 causes hepatitis)

- encapsidated virus = v resistant

100
Q

Canine Distemper Virus

A
  • immunosuppression from the SLAM protein predisposes to secondary infection
  • also respiratory, GI, and neuro signs
101
Q

Canine Pneumovirus

A
  • mild resp. dz
102
Q

Canine Inf. Resp. Dz Complex (Epidemiology and Diagnosis)

A

Epid: aerosol transmission, variable shedding
Diagnosis: Airway lavage w/ PCR

103
Q

Canine Resp. Vax

A
  • Intranasal or oral (preferred for shelters)

- Recommendations: two doses of parenteral 3-4 wks apart or 1 dose intranasal/oral

104
Q

Feline calicivirus (FCV) (path, carrier status)

A
  • encapsidated RNA virus
  • Pathology: Lingual ulcerations, lethargy, fever, pneumonia, conjunctavitis, sneezing, nasal discharge, hepatic splenic pancreatic necrosis
  • Carrier status: can shed constantly w/out symptoms
105
Q

Feline Herpesvirus (FHV) (path, carrier status)

A
  • large, enveloped DNA Virus
  • infects epithelial cells and sensory neurons w/ latency in the trigeminal ganglia
  • Path: repro dz (abortions, resorption, or birth defects); often severe dz w/ oculonasal discharge (oral ulcers can occur but smaller than FCV)
  • Carrier Status: stress induced shedding (intermittent)
106
Q

Chlamydia felis

A
  • important ocular pathogen

- does not cause resp. signs in the absence of conjunctivitis

107
Q

Mycoplasma and Bordetella bronchiseptica

A
  • uncommon in cats so look for other causes first
  • myco -> URT w/ conjunctivitis
  • bord -> URT, LRT
  • PCR both; culter for bord
108
Q

T/F: the order of environmental susceptibility for feline resp. pathogens is FHV > FCV > Chlamydia

A

F: FCV > FHV > Chlamydia

FCV is encapsidated while FHV is enveloped making FCV much more resistant

109
Q

Diagnosis of FCV, FHV, C. felis

A

PCR

110
Q

Vaccination of cats regarding resp dz

A

does not ‘cure’ or prevent, but reduces the shedding rate of those infected

111
Q

Principles of antifungal therapy

A
  • most antifungals are fungistatic, fungi grow slowly, and so treatment must be of sufficient duration to allow n processs to take place
112
Q

Amphotericin B (moa, toxicity, gen facts)

A
  • severe systemic fungal infections, broad spectrum
    MOA: fungistatic, -cidal at [high]; binds ergosterol to increase permeability of cell membrane (selectively toxic)
    Toxicity: Nephrotoxicity, Phlebitis, fever and vomiting (can reduce nephrotoxicity by using lipid-complex formulation)
113
Q

Azoles (two types)

A
  1. Imidazole

2. Triazole

114
Q

Triazoles (moa and toxicity)

A

MOA: inhibition of CYP450 to decrease ergosterol synthesis causing a change in fungal membrane fluidity
toxicity: hepatotoxicity concerns an drug-drug interaction problems

115
Q

Ketoconazole (imidazole)

A
  • extensive hepatic metabolism
  • Toxicity common: nauseau, anorexia, vomiting, hepatic dz and failure (cats), inhibition of mammalian P450s, cortisol, and testosterone synth
116
Q

Itraconazole (trazole)

A
  • all fungi

- well tolerated w/ minor concern for hepatotoxicity and cutaneous vasculitis

117
Q

Flucytosine (synthetic)

A
  • give w/ Amphotericin B to treat condida and cryptococcus
  • Tox: bone marrow suppression
  • Resist: permease/ deaminase enzyme changes
  • MOA: entry into cell w/ permease and deaminase and causes inh. of protein and DNA synth
118
Q

MOA of Amphotericin B and Azoles

A

Amphotericin B - binds directly to ergosterol

Azoles - CYP450 inh. to decrease ergosterol synth

119
Q

Acyclovir/ Valacyclovir (Use, MOA, tox.)

A
  • Herpesvirus
  • MOA: inhibitor of DNA polymerase
  • tox: val is toxic in cats
120
Q

Famciclovir/ penciclovir (MOA)

A

MOA: inhibitor of DNA ploymerase; subs. for guanosine

non-linear PK in cats

121
Q

Idoxuridine (IDU)/ Trifluiridine (TFT)

A

FHV-1

MOA: subs. thymidine -> interupts transcription

122
Q

Zidovudine (Target, MOA)

A

Retroviruses

MOA: thymidine analog, inhib of reverse transcriptase (higher affinity for viral RT than mammalian DNA polymerase)

123
Q

West Nile Virus (general facts)

A

enveloped single-stranded positive-sense RNA virus

124
Q

West Nile Virus (Transmission/ Host cycle)

A
  • primary host is birds (part. crows) that can generate high enough viremia to allow mosquitoes to finish the cycle
  • mosquitoes can transmit virus to humans or horses
125
Q

West Nile Virus (Equine Pathology)

A
  • 80% asymptomatic
  • 20% WN viremia (febrile, depression)
  • <1% CNA disease (40-60% of those who become recumbant will die)
126
Q

West Nile Virus (diagnosis)

A
  • IgM capture ELISA

- also PCR from blood

127
Q

West Nile Virus (Treatment)

A
  • supportive therapy, antiinflammatories, heavy bedding, sling, hyperimmune plasma
128
Q

West Nile Virus (Prevention)

A
  • Vaccination w/ annual booster in spring
129
Q

Influenza A Virus (General facts)

A
  • enveloped RNa virus w/ HA and NA surface proteins

- segmented genome (8 segments)

130
Q

Influenza (infection, replication)

A
  • HA binds to sialic acid receptors upon the epithelial cells
  • NA allows for release of the influenza virus post-replication
131
Q

Influenza (Antigenic shift vs drift)

A

Drift - normal mutations causing change in genome but not a change in subtypes
Shift - multiple influenza viruses infecting the same cell allowing for recombination of subtypes

132
Q

Influenza (Transmission and Pathogenesis)

A

Avian - alpha2,3 in gut
Mammals - alpha2,6 receptor in lung
Pigs - alpha2,3 and 2,6 allows for infection via both

133
Q

Zoonotic influenza, pandemic influenza, vs seasonal flu

A

Zoonotic Influenza - viruses transmitted from animals to humans w/ limited human–human
Pandemic Influenza - new virus infects humans, causes dz, and spreads from humans–humans
Seasonal Flu - recurrent influenza viruses; variants of previous pandemic viruses

134
Q

Influenza (OG source)

A
  • wild aquatic birds
135
Q

Influenza (Avian Influenza, Equine Influenza, Canine)

A

Avian – extremely important w/ high and low path variants; H5N1
Equine – H3N8; high morbidity, low mortality; jumped form horses to greyhounds
Canine – H3N2

136
Q

Influenza (Prevention and Treatment)

A

Prevention – non-core vaccine

Treatment – antivirals (Tamiflu) blocks NA

137
Q

Coronavirus (general facts, surface proteins)

A
  • enveloped single-stranded RNA virus w/ club-shaped spikes

- S (determines tropism) and N surface proteins

138
Q

Coronavirus (replication)

A
  • normal replication w/ nested set protein production
139
Q

Coronavirus (Transmission)

A
  • aerosol (resp symptoms)

- fecal-oral (GI symtoms – blunting, malabsorption, maldigestion)

140
Q

Coronavirus (Diagnosis)

A

PCR (gold) and Immunostaining

141
Q

Transmissible Gastroenteritis (TGEV) of Swine

A
  • severe gi signs, dehydration, death in neonates

- precursor to Porcine resp. coronavirus (mild resp. dz in piglets)

142
Q

Porcine Hemagglutinating Encephalomyelitis Virus

A
  • neural dz leading vomiting and wasting
143
Q

Canine Enteric Coronavirus

A
  • mild gi upset
144
Q

Canine Respiratory Coronavirus

A
  • lawnmower

- shelter and boarding facilities

145
Q

Bovine Coronavirus

A
  • diarrhea in calves < 3mnths of age
  • sporadic hemorrhagic diarrhea in older
  • resp. signs in all ages
146
Q

Equine Coronavirus

A
  • Enteric, febrile, neuro (d/t hyperammonemia)
147
Q

FIP (Feline Infectious Peritonitis) (2 viruses)

A
  1. Feline Enteric Coronavirus - not bad at all and basically they all got it; infectious
  2. FIP Virus - mutation in FECV causing severe clinical signs to manifest; non-infectious
148
Q

FIP (Feline Infectious Peritonitis) (facts)

A

clinical signs = death

149
Q

FIP (Feline Infectious Peritonitis) (pathogenesis)

A
  • pyogranulomatous vasculitis
  • immunosuppressed
  • antibody dependent disease enhancement
150
Q

FIP (Feline Infectious Peritonitis) (clinical signs)

A

Wet FIP - effusive

Dry FIP - pyogranulomatous lesions

Vet 413 - Infectious Diseases (4 decks)

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