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Vet 413 - Infectious Diseases > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Toxoplasma gondii (hosts)

A

definitive: felids only
intermediate: warm-blood animals (includ. birds)

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2
Q

Toxoplasma gondii and Neospora spp. (Life-cycle stages w/in intermediate host)

A

Tachyzoites: pathogenic stage; invasive; rapid asexual reproduction; highly inflammatory
Bradyzoites: latent stages with low immunogenicity

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3
Q

Neospora caninum (hosts)

A

intermediate: warm blood mammals
definitive: canines

hughesi def. host is unknown

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4
Q

Sarcocystis spp. (hosts)

A

dif. hosts for dif. species

- host sheds sporulated oocyst that contains 2 sporocysts

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5
Q

Neospora caninum (pathology)

A

congenital transmission:

  • neuromuscular dz
  • myositis
  • polyradiculoneuritis
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6
Q

Neospora caninum (transmission mech)

A
  • transplacental transmission; bradyzoite cysts come out of latency during pregnancy and migrate into the fetus inducing their pathology
  • shed oocytes rare in dog feces
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7
Q

Neospora caninum (diagnosis)

A
  • serum for antibodies
  • CSF for antibodies
  • PCR of CSF (v. sensitive, low specific)
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8
Q

Neospora in cattle (clinical signs, pathogenesis, diagnosis)

A

Clinical signs: elevated abortion rates, autolysed fetuses, non-sup. cellular infiltrates w/ focal necrosis in brain
Pathogenesis: both vertical (congenital inf. and calves will have super high pre-colostral Ab) and horizontal (abortion storms) trans.
Diagnosis: look at aborted fetus’ brain and heart for leasions

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9
Q

Factors determining susceptibility to viral dz

A

Viral side: genome and epigenetic

Host side: genome, epigenetic, immune response, and receptor expression

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10
Q

Steps in viral infection and dissemination

A
  1. Entry and 1* replication at point of entry
  2. 2* viral replication (either local or systemic)
  3. Shedding from host
  4. Clearance from host
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11
Q

T/F: Distance that virus travels is inverse to the size of the host

A

True

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12
Q

5 routes of viral entry into CNS

A
  1. via sensory neurons
  2. via motor neurons
  3. neurons in the nasal planum (olfactory)
  4. infect WBCs that traverse the blood brain barrier
  5. infect endothelial cells directly
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13
Q

Rabies (route of infection)

A

afferent up the motor neurons closest to infected wound up into the CNS (non-systemic entry); splits into two routes near the brain and enters into the salivary glands to promote spread of itself

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14
Q

4 mech of virus-cell interactions

A
  1. Cytocidal: inhibition of protein, DNA and RNA synthesis
  2. Persistent, productive: little metabolic disturbance, some loss of cell fx
  3. Persistent, non-productive: no effects, virus is ‘dormant’ but can be reactivated via trauma
  4. Transformation: alteration in cell morphology, immortalization, produce tumors that can continue into neoplasia
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15
Q

Viral Shedding

A

You don’t need to be presenting with symptoms in otder to be shedding the virus
depends on the virus, but can be before symptoms, after them, or with no relevant symptoms

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16
Q

Define:
Microbiota
Microbiome
Metagenome

A

Microbiota: the community of microbes
Microbiome: the genome of said community
Metagenome: genome of the community and host

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17
Q

Tolerance vs Immunity

A

Tolerance: formed against self and food antigens. consists of a stage 1 with no stage 2 (associated inflammatory response with antigen)

Immunity: involves Ab production, Th1, Th2, Th17, CD8; forms against commensal bacteria, fungi, viruses, and true pathogens; involves both steps of T and B cell activation

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18
Q

2 ways to analyze the microbiome and immunity

A
  1. 16s rDNA – v highly conserved; for bacteria

2. Germ free animals allow comparison of animals w/ the specific flora vs one with no flora at all.

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19
Q

Inside-out Immune Detection (skin vs gi)

A

Skin: epithelial cells’ TLRs constantly sample the environment to stimulate mucus and AMP production and IgA secretion (from plasma cells in lamina propria)

GI: TLRs do the same here; also, dendritic cells sitting underneath M cells will constantly sample antigen, migrate to mesenteric lymph nodes, and drive IgA secretion into the lumen

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20
Q

Outside-in microbial control

A

all i got is that certain microbiota allow for an increased response to other pathogens, so a loss of those specific ones will predispose you to illness

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21
Q

Some causes of dysbiosis in gi

A
  1. Antibiotics

2. Prior Th1 response

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22
Q

Antibiotics vs Antimicrobial

A

Antibiotic: substance produced by microorganisms that act against another microorganism
Antimicrobial: all agents that kill or inhibit the growth of all types of microorganisms

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23
Q

Broad vs. Narrow spectrum

A

hi

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24
Q

Why might you give IV vs oral vs topical administration

A

IV: ciritical condition, compromised gi

oral: easier for owners, long-term use, gi tract specific
topical: too toxic for iv, oral

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25
Q

Time dependency vs Concentration dependency

A

Time: efficacy best determined by time spent above MIC; ideal Cmax>2-4MIC

Concentration: efficacy best determined by Cmax:MIC

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26
Q

Post-antibiotic effect

A

the ability to produce a beneficial effect even below MIC

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27
Q

Drug synergism vs antagonism

A

Synergism: two drugs put together provide more benefit than each one individually
Antagonism: drugs that inhibit each other.

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28
Q

Drugs that inhibit cell wall synthesis

A

B-lactams, Carbepenems, Glycopeptide Abx (Vancomycin), Bacitracin, Polymyxin

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29
Q

B-lactam (general facts + mech of action)

A

penecillins and cephalosporins
broad spectrum, bacteriocidial
time dependent
Mech: B-lactam ring binds to Penecillin Binding Protein and inhibits cell wall synthesis

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30
Q

B-lactam (adverse effects)

A
  • disruption of intestinal microflora
  • vomiting and diarrhea
  • CNS excitation at higher doses
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31
Q

B-lactamase

A

breaks the B-lactam ring to inhibit the metabolic activity of the antibiotic

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32
Q

B-lactamase inhibitor

A

no antibacterial activity on their own

ex. clavulinic acid w/ amoxicillin

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33
Q

Carbapenems

A

broadest antibacterial action of the B-lactam group (not a B-lactam tho)

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34
Q

Acute viral infection (clinical signs)

A

general: fever, malaise (super broad)

specific to site of infection: ulceration, rash, loss of gi mucosa, edema

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35
Q

Acute, Latent, Persistent, Chronic

A

Acute – get the virus, mount immune response, and resolve
Latent – phase in a virus cycle in which proliferation of virus ceases
Persistent – long standing, infections that may involve productive infection w/out rapidly injuring the host (papillomavirus)
Chronic – virus can be easily found in body at all times (FIV)

36
Q

Are all persistent viruses bad?

A

no…

37
Q

Parvovirus virulence mech

A

VP2: on virus binds to n transferrin receptor on cells for internalization
VP1: lipolytic enzyme to allow escape from endosome

38
Q

Parvovirus (general facts)

A

sing-stranded DNA
replication only occurs in the nucleus of dividing cells (cannot induce replication so must find quickly replicating cells)
non-enveloped – extremely durable in environment

39
Q

Parvovirus (host specificity)

A

very host specific but seems to have made many jumps from species to species in the past

40
Q

Parvovirus (canine lesions) (feline lesions)

A

Hemorrhagic enteritis/ enterocyte necrosis
Neonates: CNS and cardiac lesions

Feline:
panleukopenia w/ mild enteritis
Neonates: cerebellar hypoplasia

41
Q

Parvovirus (pathogenesis)

A

oronasal exposure –> lymphatics –> going systemic hematogenously but only affects the rapidly dividing cells

42
Q

Parvovirus (Diagnostics (canine and feline))

A

Canine: Fecal ELISA, viral shedding may be intermittent, Serology (HAI, ELISA)

Feline: Clinical signs w/ panleuk

43
Q

Biological vs Mechanical vectors

A

Mechanical: simple mechanical transmission of the pathogen
Biological: pathogen development must occur within the intermediate host (heartworm)

44
Q

R0 value and idications

A

R0:
>1 – epidemic since the pathogen will infect more people than required to simply maintain population
<1 – has negative growth and will die out
=1 – will persist endemically

45
Q

Population turnover

A

the rate of gross loss (movement or death) relative to the total population
ie: our vet school has a turnover of 25%

46
Q

Morbillivirus characteristics (canine distemper virus)

A
  • enveloped virions w/ glycoprotein spikes
  • neg-sense single stranded RNA
  • not host specific
47
Q

Surface proteins of morbillivirus (Distemper)

A 
- H (hemagglutinin) antigen:
SLAM (leukocyte binding causing immunosuppression)
Nectin 4 (epithelial tissues)
- F (fusion) protein:
Cell fusion and virus penetration
48
Q

Distemper virus (pathogenesis/ ology)

A
  • jumps into macrophages that bring it to lymph nodes; reproduce in lymph node and spread throughout the body
  • disease varies considerably: ocular discharge and upper resp. tract dz (brochointerstitial pneumonia), GI dz, enamel hypoplasia, severe encephalitis, chronic CNS lesions (old dog distemper)
49
Q

Peste des Petits Ruminants

A
  • Sheep and goats
  • looks like distemper
  • Clinical signs (Depression, Diarrhea, Dehydration, Death, Pneumonia)(severe acute enteritis)(bronchointerstitial pneumonia)
50
Q

Distemper Vaccines

A
  • attenuated live give the best results but are fully virulent for many non-domestic species
51
Q

Potentiated-Sulfonamides (spectrum, MOA, Selectivity)

A
  • broad spectrum (Gram + and -)
  • bactericidal at folic acid synthesis
  • highly pathogen specific
52
Q

Potentiated-Sulfonamides (adverse effects)

A
  • Crystalluria
  • Hypersensitivity rx
  • Hepatic necrosis
  • Keratoconjunctivitis Sicca
  • Thyroid met. disorders
53
Q

Potentiated-Sulfonamides (resistance mech)

A
  • impaired uptake

- decreased sensitivity

54
Q

5 Drugs that target Ribosomes

A
  1. Aminoglycosides
  2. Tetracyclines
  3. Chloramphenicol
  4. Lincosamides
  5. Macrolides
55
Q

Aminoglycosides (drugs)

A
  • Gentamicin, amikacin, neomycin, kanamycin
56
Q

Aminoglycosides (general facts)

A
  • MOA: 30s ribosomal subunit
  • bactericidal
  • transport into cell requires O2 pump (no effect in anaerobes)
  • aerobic Gram (-)
57
Q

Aminoglycosides (adverse effects)

A
  • Ototoxicity (lots of phospholipids)
  • Nephrotoxicity
  • —- ensure adequate hydration, use once daily, monitor renal values, combination therapy
58
Q

Aminoglycosides (resistance)

A
  • inactivating enzymes
  • decreased uptake
  • modification of ribosome
59
Q

Tetracyclines (drugs)

A
  • chlortetracycline, oxytetracycline, doxycycline, minocycline
60
Q

Tetracyclines (general facts)

A
  • broad spectrum (gram + and -)
  • MOA: 30s ribosomal subunit
  • bacteriostatic
  • high intracellular accumulation
61
Q

Tetracyclines (adverse effects)

A
  • GI
  • Esophageal lesions
  • tooth discoloration/ inhibition of growth of long bones
  • renal tubular necrosis (chronic)
  • death in horses (IV doxcycline)
62
Q

Tetracyclines (resistance)

A
  • effflux of drug
  • altered binding site
  • inactivation via bacterial enzymes
  • cross-resistance is common
63
Q

Chloramphenicol (general facts)

A
  • broad spectrum
  • Bacteriostatic
  • do not use in food animals
  • widely distributed throughout the body
  • glucoronidation
64
Q

Chloramphenicol (adverse effects)

A
  • peripheral neuropathy
  • bone marrow depression
  • CYP450 inhibitor
  • antagonism if given with macrolides
65
Q

Toxoplasma gondii (specificity, life cycle)

A
  • obligate intracellular protozoan parasite
  • def. host - cat
  • int. host - everything gets tissue cysts (muscle and brain)
66
Q

Toxoplasma gondii (transmission)

A

Endogenous trans-placental trans. (common in Neospora, but rare in Toxo)
Exogenous trans-placental trans. (naive ingestion during preg.; common in both Neospora and Toxo

67
Q

What animals does Toxoplasma gondii cause dz?

A

Cats - often asymptomatic or present w/ immunosuppression

Sheep and Goats - Abortion

68
Q

Immune response to Toxoplasma gondii

A

Innate response – antigen drives NK cell secretion of IFN-gamma leading to intracellular macrophage destruction of pathogens
Adaptive – Ab have no effect; CD4 and 8 produce IFN-gamma

69
Q

T/F: Toxoplasma gondii oocysts are extremely resistant to inactivation

A

T

70
Q

Abx treatment of Toxoplasma gondii and how it works

A

many of the drugs target the apicoplast (responsible for synthesis of Fatty acids)

71
Q

Diagnosis of Toxoplasma gondii

A

IgG vs IgM titers (high sensitivity)

72
Q

Salmonella (general info)

A
  • gram - bacteria
  • fecal-oral route of infection
  • local gi to systemic dz
  • Large # of animal reservoirs
73
Q

Salmonella (virulence factors)

A

SPI1 – promotes uptake of salmonella pathogens

SPI2 – modify cell to suit salmonella’s needs

74
Q

Salmonella (immune response)

A

Th1 and Th17 response (mostly Th17 since salmonella is not considered intracellular)

75
Q

Lincosamides - Clindamycin (MOA)

A

MOA: protein synth. inhibitor

76
Q

Lincosamides (Adverse Effects)

A
  • contraindicated in horses and ruminants and pocket pets
  • vomiting (cats)
  • loose stool (dogs)
77
Q

Macrolides - erethryomycin, tylosin (MOA)

A

inhibit protein synthesis

78
Q

Macrolides (Adverse Effects)

A
  • GI
  • hyperthermia in foals
  • antagonism w/ chloramphenicol
  • CYP450 inhibition
79
Q

Fluoroquinolones - enrofloxacin (MOA)

A
  • inhibition of DNA replication and transcription via inh. of DNA gyrase and topoisomerase IV
80
Q

Fluoroquinolones (adverse effects)

A
  • gi upset
  • articular cartilage damage in puppies and foals
  • neural effects (seizures)
  • bone marrow suppression (dogs)
  • retinal degeneration (cats)
    CYP450 inhibition
81
Q

Fluoroquinolones (resistance mech)

A
  • alteration of target enzymes

- decreased drug permeability into bact. cell

82
Q

Rifampin (MOA)

A
  • inactivation of DNA dependent RNA polymerase
83
Q

Rifampin (adverse effects)

A
  • orange-red urine, tears, saliva
  • hepatitis
  • thrombocytopenia, anemia, anorexia
84
Q

Metronidazole

A
  • MOA: breaks DNA strands/ inhibits repair
  • Resistance is rare
  • Adverse Effects:
    inappetance (horse)
    Nausea and vomiting (dog)
    neurotoxicity
    urine discoloration
    -NOT permitted in food animals
85
Q

Sarcocystis neurona

A 
Equine Protozoal Myeloenchephalitis (EPM)
- asymmetric nerve damage
- muscle atrophy
- C.N. dysfunction
- limb ataxia
(can also be caused by N. hughesi)

Vet 413 - Infectious Diseases (4 decks)

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