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Vet 413 - Infectious Diseases > Exam 5 > Flashcards

Exam 5 Flashcards

1
Q

4 CNS Immune Rules

A
  1. immune access is restricted but not insurmountable
  2. lower [antigen presenting cells]
  3. low levels of MHC
  4. meningeal lymphatic system plays important role
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2
Q

Why is immune response in CNS undesirable?

A
  1. Rigid bone casing (skull)

2. Impact on neurons (inflammation can damage these non-renewing cells)

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3
Q

3 sites of entry for immune cells into the CNS

A
  1. Blood-Brain Barrier
  2. Blood-CSF Barrier
  3. Meningeal Barrier
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4
Q

Access to Brain Parenchyma via BBB (general info)

A
  • governed by complex tight junctions that are extremely difficult for cells to pass
  • made worse by presence of glia limitans and astrocyte foot processes
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5
Q

Access to CSF (general info)

A
  • lack of tight junctions allows for specialized function of allowing lymphocytes more ready access to CSF (CD4+ T cells)
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6
Q

Access to Meninges (general info)

A
  • 3 layers (dura, arachnoid, pia)

- simple one layer vascular structure unlike that of the BBB

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7
Q

T/F: Immune responses in the CNS are typically initiated in the CNS

A

F

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8
Q

What is the main route of entry of immune cells into the CNS?

A
  • Blood-CSF Barrier
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9
Q

Microglia (general info)

A
  • brain resident immune cells
  • primary phagocytes and clean up debris
  • express low levels of MHC-2 + TLRs (ability to activate macrophages); can release cytokines and chemokines
  • primarily held in check by endogenous factors
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10
Q

Astrocytes (general info)

A
  • pH balance, osmoregulatory, cytokine and chemokine (to help recruit activated T cells)
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11
Q

CSF Evaluation (cause of increased protein)

A
  • inflammation leading to elevated globulins
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12
Q

CSF Evaluation (n cell counts)

A
  • very low (<2 in dogs)
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13
Q

CSF Evaluation (bacterial disease)

A
  • neutrophil predominance)
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14
Q

CSF Evaluation (fungal, protozoal disease)

A
  • mixed phagocyte response
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15
Q

CSF Evaluation (viral disease)

A
  • mononuclear cell increase)
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16
Q

West Nile Virus (4 routes of CNS entry)

A
  1. impaired BBB
  2. endothelial infection
  3. virus is transported in wbcs
  4. retrograde axonal transport
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17
Q

West Nile Virus (immune response and consequence)

A
  • infected cells in brain produce T cell chemoattractant (CXCL10) that recruit CXCR3+ T cells (WNV specific)
  • delayed response = high viremia + inflammation = encephalitis
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18
Q

Anthrax (Bacillus antracis) (General facts)

A
  • spore forming - lasts forever in env.; exposure to air triggers spore formation
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19
Q

Anthrax (Bacillus antracis) (2 pathogenic factors)

A
  1. capsule – resistant to host immunity

2. three-component toxin (binding antigen, edema factor, lethal factor)

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20
Q

Anthrax (Bacillus antracis) (Clinical Signs)

A
  • cutaneous: necrotic lesions
  • inhaled: ‘wool sorters dz’
  • ingestion: spores from cont. food
  • rapid progression to death
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21
Q

Anthrax (Bacillus antracis) (diagnostic)

A
  • Tissue exam, culture, PCR (CDC controlled)
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22
Q

Rabies (rhabdovirus) (general info)

A
  • wildlife is natural reservoir
  • transmitted via saliva
  • not env. resistant
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23
Q

Rabies (rhabdovirus) (clinical signs)

A
  • Early: behaviour change, anorexia, depression

- Late: pruritis, hyperesthesia, hydrophobia, paresis, seizures, death (universally fatal)

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24
Q

Rabies (rhabdovirus) (diagnostics)

A
  • post-mortem CNS exam
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25
Q

Q-fever (Coxiella burnetii) (general info)

A
  • intracellular bacterium w/ env. protective phase
  • extremely low infectious dose (1-10 org)
  • like to live in macrophages
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26
Q

Q-fever (Coxiella burnetii) (Clinical signs)

A
  • ADR
  • Acute: fever, chills, headache, flu
  • Chronic: endocarditis, pneumonitis, joint dz
    Small Ruminants = abortion
    most people/ animals recover
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27
Q

Q-fever (Coxiella burnetii) (diagnostics)

A
  • IHC, PCR
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28
Q

Brucellosis (general facts)

A
  • gram neg facultative intracellular

- most species get it, but effectively eliminated from US aside from bison in Yellowstone

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29
Q

Brucellosis (Clinical dz)

A
  • repro dz in animals

- humans: undulent fever, chronic infection

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30
Q

Brucellosis (Diagnostics)

A
  • culture, PCR, serology
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31
Q

Coccidiodes (Valley Fever) (everything)

A
  • C. immitus and posadasii
  • Clinical Dz: fungal pneumonia, disseminated granulomas
  • Diagnostics: histopath, serology, fungal culture (v dangerous)
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32
Q

Leptospira (general facts)

A
  • most common zoonotic agent worldwide

- pnetrates mucous membranes

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33
Q

Leptospira (Clinical dz)

A
  • Acute: liver, lung, kindey damage
  • Fetal loss
  • transmission through urine
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34
Q

Leptospira (diagnostics)

A
  • PCR (kidney or urine)
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35
Q

Yersinia pestis (clinical dz)

A
  • bubonic, septic, pneumonic

- swollen LN, death

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36
Q

Yersinia pestis (diagnostics)

A
  • culture, PCR, IHC on tissues
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37
Q

Francisella Tularensis (Clinical dz)

A
  • high fever, lethargy, lymphadenopathy, hepatitis, septicemia and death
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38
Q

Francisella Tularensis (diagnostics)

A
  • Culture, PCR, IHC on tissues
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39
Q

Contagious ecthyma (everything)

A
  • very contagious

- lesions on face, muzzle, lips, teats

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40
Q

Mucosal Immune System (MALT)

A
  • comprised of lymphoid organs and follicles in the upper respiratory tract epithelium
  • rich in DCs, T and B cells and is overlaid w/ M cells (lack microvilli and mucus layer) (site of entry for many pathogens) ( specialized cells for antigen uptake)
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41
Q

Mucosal Immune System (IgA)

A
  • as you move down into the reps tract, [IgA] relative to [IgG] decreases
  • long lived IgA producing plasma cells localized for resp. tract
  • IgA can bind and neutralize pathogens or toxins on the resp. epithelium
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42
Q

Mucosal Immune System (Mucocilliary Escalator)

A
  • paralized by brodetella bronchiseptica

- heavily reliant on an in tract mucus layer

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43
Q

Mucosal Immune System (Resp. epithelium)

A
  1. TLRs and NODs drive pro-inflammatory pathway
  2. Production of chemokines which attract neutrophils and macs – and immature DCs
  3. production of IL-1, -6 for mac activation
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44
Q

Mucosal Immune System (Consequences of Inflammation)

A
  • over-productive responses of cytokine/ chemokines (cytokine storm) can leads to ARDS (Acute Respiratory Distress Syndrome) causing serious damage
  • chronic inflammation w/ persistent antigen presentation => granuloma formation, fibrosis, remodeling
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45
Q

Lower airway lavage (normal contents)

A
  • only really pulmonary alveolar macrophages and lymphocytes
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46
Q

Obligate vs Facultative Intracellular Bacteria

A

Obligate - must be grown intracellularly; cannot be grown in culture
Facultative - can be grown on artificial media

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47
Q

Listeria (species, strains, clinical dz)

A
  • gram + intracellular bacteria
  • ruminants (humans, animals, birds)
  • L. monocytogenes, L. invanovii
  • septicemia, encephalitis, abortions
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48
Q

Yersinia

A
  • rodent based zoonotic disease
  • humans and domestic animals (cats)
  • Cat Facts (regional lymphadenitis (mandibular) w/ ADR progressing into systemic dz)
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49
Q

T/F: dog and cat fleas transmit Yersinia (along with the rodent flea)

A

False: only the rodent flea transmits Yersinia pestis

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50
Q

Francisella tularensis (mortality?, reservoir, trans, species)

A
  • highly infectious, zoonotic reportable disease
  • 30-60% of untreated cases are fatal
  • reservoir (lagomorphs, rodents)
  • transmission (ticks, water, infected prey)
  • cats most commonly infected
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51
Q

Brucella

A
  • non-motile, gram neg, coccobacilli
  • v environmentally resistant
  • several animals and zoonotic
  • B. melitensis, B. abortus, B. suis
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52
Q

Brucella ( pathogenesis and clinical dz)

A
  • penetrates through in tact mucosal surfaces
  • intracellular survival
  • Dz: Humans (undulant fever, reticulo-endothelial system, mild lymphadenopathy, splenomegally, hepatomegaly, abortions have been reported)
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53
Q

Central Tolerance (T and B Cells)

A

T Cells: tissues express tissue-specific antigens that are selected against w/in the thymus (via the AIRE gene)
B Cells: BCR recognizing self-antigen will induce apoptosis

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54
Q

Peripheral Tolerance

A
  • T and B cells that escape central tolerance can still be filtered in the periphery
  • important in generation of Treg (CD25+, CD4+, FoxP3+) – iTreg for tolerance of food antigens via expression of TFG-B and IL-10
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55
Q

4 Mechanisms of Autoimmunity

A
  1. Exposure of previously hidden antigens
  2. Exposure to cross-reacting antigens
  3. Alterations of self-antigen
  4. Dysregulation of the immune response
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56
Q

Autoimmunity (Exposure of previously hidden antigens)

A
  • sequestered antigens not able to interact w/ immune system

- lens of eye, sperm, CNS tissue

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57
Q

Autoimmunity (Exposure to cross-reacting antigens)

A
  • attack self tissues that bear similar antigenic determinants
  • Strep B. M protein and cardiac myosin
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58
Q

Autoimmunity (Alterations of self-antigen)

A
  • chemical groups may bind to self cells or tissue to form a new antigen
  • TMS, penicilin, etc. bind to rbcs drive IMHA
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59
Q

Autoimmunity (Dysregulation of the immune response)

A
  • loss of suppression
  • viral infection may interfere w/ n reg. mech
  • lymphoid tumors associated w/ this due to loss of n control mech.
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60
Q

Systemic Lupus Erythematosus (Mech, Clinical signs, diagnostics)

A
  • multiple body systems are affected
    Mech: immune complex deposition
    Clinical signs: associated w/ IMHA, IMTP, glomerulonephritis, polyarthritis, skin lesions (typical butterfly rash)
    Diagnostics: ANA (anti-nuclear antibody) Test, LE cell test (pathopneumonic)
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61
Q

Diabetes mellitus (immune mediated)

A
  • Coomb’s Type 4-ish

- T cell destruction of B cells within the pancreatic Islets of Langerhans

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62
Q

Thyroiditis (immune mediated)

A
  • Ab production against thyroglobulin (find via IFA or ELISA)
  • presenting complaints mimic hypothyroidism
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63
Q

Pemphigus (immune mediated)

A
  • 3 locations (P. vulgaris, P. folliaceous, Bullous P.)

- P. vulgaris is most sever and an attack on desmoglian 3

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64
Q

IMHA

A

2 types: extravascular vs intravascular hemolysis

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65
Q

Coonhound Paralysis/ Guillan-Barre Syndrome

A
  • ascending flacid paralysis

- peripheral nerve demyelination

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66
Q

Myasthenia Gravis

A
  • Ab production against ACh receptors at the neuromuscular junction
  • treatment: ACh-esterase inhibitors
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67
Q

VKH Disease

A
  • uveodermatological syndrome (present with sudden blindness or chronic uveitis
  • depigmentation of hair and skin follows
  • humans: autoimmune attack on melanin containing cells (not well documented in dogs)
  • overall reduction in melanin content in cells
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68
Q

Canine Diabetes mellitus (autoimmune breed disposition)

A
  • Cavalier King Charles Spaniel has multiple SNP w/ IL-10 gene
  • Samoyed has the highest relative risk
  • Genes associated w/ Th1/Th2 response appear to modulate risk
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69
Q

Thyroiditis (autoimmune breed disposition)

A
  • Borzoi breed - autosomal recessive inheritance
  • Beagle colony documented
  • Dobermans - genetic ass. first found here
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70
Q

Viruses in BRDC

A
  1. Bovine Respiratory Syncytial Virus
  2. Infectious Bovine Rhinotraceitis (Bovine Herpes Virus-1)
  3. Parinfluenza-3
  4. Bovine Coronavirus
  5. Bovine Viral Diarrhea Virus
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71
Q

Bovine Respiratory Syncytial Virus

A
  • enveloped, neg. sense, single stranded RNA
  • only partial protection by maternal antibodies
  • stays in respiratory tract
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72
Q

Bovine Respiratory Syncytial Virus (Clinical signs)

A
  • LRT infection w/ bronchiolitis
  • Dyspnea, increased resp rate, wheezing
  • coughing, open-mouth breathing
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73
Q

Bovine Respiratory Syncytial Virus (Immune Response)

A
  • in absence of normal Th1 response, body will develop strong Th2 (+Th17)
  • Ab to F and G protein - neutralizing
  • CTLs against nucleoprotein
  • vaccine enhanced disease may appear
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74
Q

Bovine Herpes Virus-1, Infectious Bovine Rhinotraceitis

A
  • enveloped, ds DNA

- likes to hang out in trigeminal ganglion

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75
Q

Bovine Herpes Virus-1, Infectious Bovine Rhinotraceitis (Clinical Signs)

A
  • rhinotracheitis

- conjunctivitis

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76
Q

Bovine Herpes Virus-1, Infectious Bovine Rhinotraceitis (Immune Response)

A

Innate: infects mucosal epithelial cells and triggers TLRs; complement can neutralize virus; Type 1 IFN present at 5 hours post infection; BHV-1 reduces MHC1 expression

Adaptive: virus interferes w/ antigen loading into MHC1 by binding TAP protein and peptide transport

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77
Q

Parainfluenza-3

A
  • causes epithelial necrosis and reduced ciliary clearing resulting in 2* infection
  • usually seen in cows w/ poor colostral AB
  • causes mild resp. dz
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78
Q

Bovine Coronavirus

A
  1. Calf Diarrhea
  2. Sporadic Hemorrhagic Diarrhea; Winter Dysentery
    • high morb, low mort.
  3. Shipping Fever

Isolate from manure or resp samples
Ab titers to check

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79
Q

Bovine Viral Diarrhea Virus

A
  • immunosuppressive effects
  • infection of pregnant dam during early gestation can cause persistently infected fetus
    Clinical Dz
    1. Targets lymphoid tissue (eg. Peyer’s Patches)
    2. abortion early in gestation
    3. Diarrhea
    4. Mucosal Disease –> mutation of non-cytopathic into cytopathic under persistent infection causing fatal mucosal sloughing
80
Q

Main difference between Staph and Strep? (Catalase)

A
  • Staph is Catalase Positive

- Strep is Catalase Negative

81
Q

Streptococcus (general facts and sorting techniques)

A
  • chains or strips of cocci together
  • hemolytic (alpha, beta, gamma); B is more pathogenic
  • Lancefield grouping: sorting based off of surface carbs
82
Q

Streptococcus ( 4 Disease types)

A
  1. Upper resp infection w/ lymphadenopathy (strep equi)
  2. Neonatal septicemia (horses, dogs, cats)
  3. Secondary pneumonia - opportunistic path (strep. zoo, strep. canis)
  4. Miscellaneous - UTI, mastitis, abscesses, necrotizing fasciitis
83
Q

Streptococcus (4 strains)

A
  1. Strep equi
  2. Strep zoo
  3. Strep suis (zoonotic)
  4. Strep canis (pneumonia, UTI, skin lesions)
84
Q

Streptococcus (pathogenesis)

A
  • Antiphagocytic capsule
  • M protein (important in horses)(inhibit complement deposition)
  • extracellular enzymes
  • pyrogenic exotoxins (superantigen stimulation, non-sepcific T cell activation)
85
Q

Staphylococcus (4 strains)

A
  1. Staph. aureus (all but dogs really)
  2. Staph pseudintermedius (dogs and cats)
  3. Staph hyicus
  4. Coagulase neg staphs (low path)
86
Q

Staphylococcus (Disease Types)

A
  • skin infection
  • wound infection
  • contagious mastitis (staph. aureus)
  • Bumble Foot (staph. aureus)
  • Greasy Pig Dz (Staph. hyicus)
87
Q

Staphylococcus (Virulence Factors)

A
  • Protein A (binds IgG Fc region)
  • Capsule (antiphagocytic, stop Ab binding)
  • hemolysins
  • epidermolytic/ exfoliative toxins
  • superantigens
88
Q

Biofilms

A
  • convert from planktonic to communal growth w/in a polysaccharide matrix to evade host immune system and antibiotics
89
Q

Classical Swine Fever Virus (Hog Cholera) (general facts)

A
  • enveloped positive sense ssRNA

- endemic to most of world (not in US)

90
Q

Classical Swine Fever Virus (Hog Cholera) (pathogenesis)

A
  • oronasal infection, gains access to tonsilar crypts as 1* site of replication
  • targets include macrophages, DCs, endothelial cells
  • spreads to lymphoid organs, spleen, LN, bone marrow, thymus
91
Q

Classical Swine Fever Virus (Hog Cholera) (Effects on Immune System)

A
  • central and peripheral lymphoid depletion
  • increases [IFN-a] released from DCs that are then inhibited by virus
  • macs are infected and activated –> vasoactive mediators such as IL-1
92
Q

Classical Swine Fever Virus (Hog Cholera) (Clinical Signs)

A
  • Fever, skin lesions
  • neuro effects
  • death w/in 15 days
  • v similar to African Swine Fever
93
Q

Classical Swine Fever Virus (Hog Cholera) (Diagnostics)

A
  • Direct immunofluorescence on histo

- Indirect Immunofluorescence on Elisa for AB

94
Q

Foot and Mouth Disease (general facts)

A
  • disease of cloven hooved animals (not horses)
  • high contagious (food, water, direct, aerosol)
  • vaccination along borders keeps it at bay
95
Q

Foot and Mouth Disease (Clinical Signs)

A
  • drooling, shivering, anorexia
  • pyrexia
  • decreased production
  • blisters and sores on feet and mucosal surfaces
  • myocarditis in the young (fatal)
96
Q

Vesicular Stomatitis Virus

A
  • cattle, horses, pigs, insects
  • DDx: important for cattle as clinical signs are similar to hoof and mouth dz
  • zoonotic
97
Q

Porcine Resp and Repro Syndrome (PRRS) Virus

A
  • replicates in swine macrophages
  • late term abortion or stillbirths and neonatal pneumonia
  • Severe necrotizing interstitial pneumonia
  • transmission: direct contact, fomites, semen of infected boars
98
Q

Equine Infectious Anemia (general facts)

A
  • noncontagious dz affecting horses

- transmission is bloodborne (mech. by biting insects or iatrogenic)

99
Q

Equine Infectious Anemia (pathogenesis and clinical signs)

A
  • incubates in body for 15-45 days
  • macrophages are infected and release pro-infl cytokines
  • Acute phase (1-3 days): fever, depression, and IMTP
  • Chronic phase (fever, IMTP, anemia, petechia on mm, muscle weakness, meningitis and encephalitis)
100
Q

Equine Infectious Anemia (Diagnosis and Treatment)

A
  • Diagnosis: look for EIA specific IgG (Coggins, ELISA)

- Treatment: quarantine or euthanasia (no cure)

101
Q

Cowpox (general info)

A
  • Cats: ulcerated cutaneous lesions post-contact w/ rodents

- people get cowpox from cats and it’s usually self-limiting

102
Q

Hantavirus (transmission, 2 syndromes)

A
  • rodents are sub-clinically infected (aerosol) and they transmit to humans (dead end host) and our companion species
  • 2 distinct syndromes: Hemorrhage syndrome w/ renal dz (rest of the world) and Pulmonary syndrome (US)
  • dogs and cats can be subclinical
103
Q

Staph. pseudintermedius/ aureus (general info)

A
  • skin commensals of dogs and cats
  • may becomes severely drug resistant (mecA gene encodes faulty PBP2a for meth resist staph)
  • dz in humans only when break in n host defenses
104
Q

Plague and Tularemia

A
  • rare but highly infectious to humans
  • both cause fever, lymphadenopathy, abscesses, pneumonia
  • Plague: trans. via rodent fleas
  • Tularemia: trans. via biting fleas, ticks
105
Q

Bite Wounds (2 pathogens)

A
  1. Pasteurella multocida and canis
    - most prevalent infection for dog and cats bite
  2. Capnocytophagia
    - rarely causes dz in dogs and cats
    - C. canimorsus: cellulitis, gangrene, bacteremia, meningitis, endocarditis (humans)
106
Q

Bartonella (general info)

A
  • chronic, largely subclinical infections in cats
  • lives within erythrocytes and endothelial cells (also macs)
  • trans: fleas are intermediate host
107
Q

Bartonella (Dz in humans)

A
  • cat scratch dz
  • papules that transition into local lymphadenopathy
  • vasculoproliferative dz, ocular dz, granulomatous dz, relapsing fever
108
Q

Bartonella (Dz in cats)

A
  • chronic and widespread dz
  • fleas essential for transmission and can survive for days in env
  • not all cat strain pathogenic in people
  • pyogranulomatous cardiovascular dz
109
Q

Bartonella (Dz in dogs)

A
  • B. vinsonii and henselae
  • bacteremia is much lower than cats (often incidental hosts)
  • endocarditis in aortic valve, protein losing nephropathy, granulomatous dz, vasc. proliferation
110
Q

Bartonella (Diagnostics)

A
  • not seen on blood smears
  • Serology (not useful in cats)
  • Culture and PCR (good for cats)
111
Q

Leptospira (transmission)

A
  • direct via urine
112
Q

Leptospira (pathogenesis)

A
  • penetrates mucous membranes for lung, liver, kidney damage
113
Q

Leptospira (Clinical dz)

A
  • anorexia, pyrexia, vomiting, dehydration
  • anuria or oligurea (renal)
  • icterus (liver)
  • Dyspnea (lung)
114
Q

Leptospira (Diagnostics)

A
  • Microscopic Agglutination Test (MAT)
115
Q

Psittacosis (dz in birds)

A
  • pneumonia, air sacculitis, pericarditis, hepatitis, etc.

- particularly in stressed birds

116
Q

Psittacosis (dz in humans)

A
  • similar to Q fever and brucellosis
  • flu-like symptoms, cough, fever
  • [erocardotos. endocarditis, myocarditis, hepatomegaly, splenomegaly
117
Q

Psittacosis (diagnosis)

A
  • birds: antigen, PCR, serology

- humans: PCR, serology

118
Q

Mycobacterial Infections in Dogs/ Cats (3 types)

A
  1. Tuberculous mycobacteria (disseminated disease)
  2. Non-tuberculous mycobacteria (disseminated or focal cutaneous)
  3. Lepromatous mycobacteria (cutaneous)
119
Q

Retroviruses (general info)

A
  • envelope makes them v env. susceptible

- transitions from RNA to DNA within the animal host (forming a pro-retrovirus)

120
Q

Retroviruses (Genome organization)

A
  • Simple: FeLV

- Complex: FIV

121
Q

Retroviruses (Life Cycle)

A
  • generate DNA from RNA (forming a pro-virus)
  • they are generally life-long (maybe latent)
  • endogenous retroviruses –> most animals have tons of innate retroviral dna that does not work due to many reasons
122
Q

Retrovirus induced oncogenesis (3 ways)

A
  1. Insertional mutagenesis (upregulate host oncogene via insertion of LTR sequence from the retrovirus next to said oncogene)
  2. Oncogene capture (virus steals a host’s oncogene, making the virus oncogenic. inactivates the virus’s ability to replicate w/out assistance)
  3. Oncogenic Viral proteins
123
Q

T/F: All retroviruses eventually cause tumors.

A

F: Lintivirus (FIV, HIV, etc) and Spumavirus do not cause tumors

124
Q

Alpharetrovirus

A

Avian Leukosis Virus

  • lymphoma, sarcoma
  • can be slowly (insertional) or acutely (capture) transforming
  • only retro w/ ability to oncogene capture while maintaining ability to self-replicate
125
Q

Betaretrovirus

A

ENTV

  • sheep/goats –> nasal adenocarcinoma
  • envelope protein itself is oncogenic
  • LTR is specific for nasal turbinates

JSRV

  • sheep –> pulmonary adenocarcinoma
  • LTR specific for lungs
126
Q

Deltaretrovirus

A

Bovine Leukemia Virus

  • B cells and macrophages
  • has its own oncogenic viral protein (tax)
  • persistant lymphocytosis (can cause lymphoma in 1%)
127
Q

Gammaretrovirus (everything)

A

FeLV

  • macs/ t cells/ hematopoietic progenitor cells
  • neoplasia, pancytopenia (anemia), immunodeficiency
  • trans: milk, saliva
  • diagnosis: antigen test (highly viremic)
  • types: progressive, regressive, abortive, focal
128
Q

Lentivirus

A

Small Ruminant Lentivirus

  • inflammatory problems, not immunodeficiency
  • see arthritis across the body

Feline Immunodeficiency Virus

  • macs, CD4 T, CD8 T, B Cells
  • CD4 makes it immunodeficiency
  • Dx: serology
  • transmits via bites –> persistent infection requires direct transfer of living infected cells
129
Q

What are vector-borne diseases?

A
  • transmitted by another organism and pathogen cannot exist for long outside of vector or host
  • animals and humans can be intermediate or definitive hosts
130
Q

What are the most important types of vector for disease in the US?

A
  • hard ticks (part. ixodes)
131
Q

Classic symptoms for tick-borne diseases?

A
  • thrombocytopenia
  • anemia
  • icterus (large animals)
  • fever
132
Q

Rickettsiales (general info)

A
  • not easily culturable
  • gram neg, aerobic, obligate intracellular bacteria
  • replicate via binary fission w/in phagosome
133
Q

Spotted Fever (R. rickettsi)

A
  • Rocky Mountain Spotted Fever
  • major pathogen of dogs and people
  • dogs may be sentinel species
  • vector: ticks… new tick just found across entire US
134
Q

R. rickettsi (pathogenesis)

A
  • infects endothelial cells to cause vasculitis (edema, necrosis, coagulopathy)
  • consumption of platelets d/t adhesion to endothelium
  • spreads directly from cell-cell to avoid immune detection
135
Q

Ehrlichiosis (vector, replication)

A
  • vector: Lone Star Tick

- replication: intracellular binary fission w/ cell rupture to spread

136
Q

Ehrlichiosis (pathogenesis)

A

Canine and Human Ehrlichiosis

  • monocytes and granulocytes
  • form morulae

Heartwater

  • lymphatic replication leads to bacteremia and subsequent invasion of endothelial cells (CNS)
  • identified as intracellular colonies
137
Q

FIV (Types of Disease)

A
  • CD4, CD8, B cells, macrophages
    1. Acute (wks - months)
    2. Asymptomatic (v chronic stage)
    3. Terminal (related to AIDS in humans) (here we see the markedly decreased CD4 lineage induce an immunodeficiency –> coinfections, stomatitis, neoplasia)
138
Q

FIV (Immunodeficiency pathogenesis)

A
  • CD4 T cells drops over time
  • initially CD4:CD8 < 1 ; over time CD8 will begin to drop
  • dec CD4 = dec Th1 (dec CD8) and Th2 (dec B cells)
139
Q

FIV (mech of oncogenesis)

A
  • decreased immune surveillance
140
Q

FeLV (Types of Disease)

A
  • CD4, CD8 T cells, macrophages, hematopoietic stem cells, =/- epithelial cells
    1. Abortive
    2. Focal
    3. Regressive
    4. Progressive (immunodeficiency, neoplasia, anemia)
141
Q

FeLV (Immunodeficiency pathogenesis)

A
  • decreased leukocytes (PMNs) and function of leukocytes
142
Q

FeLV (mech of oncogenesis)

A
  1. Insertional oncogenesis
  2. Oncogene capture
  3. Decreased immune surveillance
143
Q

Rabies (transmission mech)

A
  • biting via saliva
144
Q

Rabies (pathogenesis)

A
  • bite wound + infection
  • virus multiplies in myocytes
  • travels p peripheral nerves into CNS
  • multiplies in CNS + encephalitis
  • virus moves out through peripheral/ cranial nerves (salivary glands, mucosal surfaces, most organs)
145
Q

Rabies (Clinical Stages)

A
  1. Prodromal: behavioural changes
  2. Excitive/ furious: air biting, pica, muscle spasms, tremors and seizures
  3. Paralytic/ dumb: LMN diseas
146
Q

Rabies (Diagnosis)

A

Antemortem: sudden behavioral change w/ flaccid paralysis, Direct FA

Postmortem: submit whole head refrigerated (looking for Negri bodies in the hippocampus for carnivores and Purkinje fibers in herbivores)

147
Q

Rabies (Post-exposure Measures for Unvax Pets)

A
  • euthanize

- quarantine for 4 months w/out contact to humans or animals

148
Q

Rabies (Post-exposure Measures for late vax pets)

A
  • quarantine w/ o for 45 days + vaccinate
149
Q

Rabies (Post-exposure Measures for vax pets)

A
  • quarantine w/ o for 45 days + vaccinate
150
Q

Rabies (Post-exposure Measures for Humans)

A
  • confine for 10 days and observe
  • do not vaccinate, but administer prophylaxis
  • wash wounds under pressure for 15 minutes
  • irrigate w/ copious amounts of warm, soapy water or QUAT
151
Q

Rabies (Post-exposure Prophylaxis)

A
  • being immediately and don’t wait for test results
152
Q

Anaplasmosis (vector and pathogenesis)

A

Vector: Ixodes
Pathogenesis: Bovine (RBC destruction d/t lysis or immune mediated) Canine (thrombocytopenia, fever, lameness)

153
Q

Borreliosis (vector and replication)

A

Vector: Ixodes (same as Anaplasma)
Replication: not intracellularly like the rickettsia

154
Q

Borreliosis (Lesion and path)

A
  • classical ‘target lesion’ for Lyme Disease

- most dogs are subclinical (IMpolyarthritis for those who are not or lyme-nephritis)

155
Q

Babesiosis (transmission, pathogenesis, clinical signs)

A

Trans: sporozoites develop in tick salivary gland
Pathogenesis: parasite antigens incorporated onto RBC membrane; free antigen may bind RBC and platelets resulting in hemolysis (complement driven); direct damage via parasitism and damage
Clinical Signs: Fever, anemia, thrombocytopenia, icterus

156
Q

Cytauxzoonosis (species, pathogenesis)

A
  • strictly felids

- infects mononuclear cells, replicates, bursts out and lysis everything resulting in a pancytopenia

157
Q

Hepatazoonosis (transmission, pathogenesis)

A

Trans: ingestion of infected tick
Pathogenesis: penetrates gi tract, infects WBCs, travels to muscle; muscle cysts present as pyogranulomas, myositis, pain, weakness

158
Q

List one cause of infectious Secondary Immunodeficiency

A

Distemper Virus (dogs)
Infectious Bursal Disease (Birds)
FIV, FeLV (Cats

159
Q

List on cause of non-infectious Secondary Immunodeficiency

A 
Hyperadrenocorticism (Cushing's)
Stress
Malnutrition
Immunosenescence
Medical Immunosuppression
160
Q

Tetanus and Botulism (types of paralysis)

A
  • Tetanus: spastic paralysis

- Botulism: flaccid paralysis

161
Q

T/F: Tetanus and Botulism toxins bind reversibly to the pre-synaptic membrane receptor for ACh release.

A

F: they bind irreversibly

162
Q

C. Botulinum (Etiology)

A
  • seven toxins (A-G)
  • most potent toxin known
  • cats relatively resistant
163
Q

C. Botulinum (Pathogenesis)

A
  • most cases from ingestion of pre-formed toxin
  • inhibits ACh release from cholinergic neurons at neuromuscular jxn and autonomic synapses
  • recovery requires formation of new terminal axons
164
Q

C. Botulinum (Clinical Signs)

A
  • LMN (weakness, etc) and Autonomic (tachycardia, etc) problems
165
Q

C. Botulinum (Diagnosis)

A
  • history and clinical signs

- botulinum toxin analysis

166
Q

C. Botulinum (Treatment)

A
  • only supportive care available

- antitoxin is controversial and not readily available

167
Q

C. Tetani (Etiology)

A
  • single neurotoxin, tetanospasmin
168
Q

C. Tetani (Epidemiology)

A
  • wound contaminated via env. spores
  • germination under anaerobic conditions
  • contaminated surgeries, pregancy, or parturition associated w/ fetal death
    dogs and cats are resistant; horses prone
169
Q

C. Tetani (Pathogenesis)

A
  • site of toxin entry influences clinical presentation
  • toxin travels along axons & migrate into an inhibitory interneuron vesicle
  • inhibits GABA and glycine release (inhib. neurotransmitters)
  • recovery depends on regeneration of new axon terminals
170
Q

C. Tetani (Localized Clinical Signs)

A
  • 5-10 days post-trauma
  • most common in dog/ cats
  • stiffness in muscle/ limb near wound
  • prox. to head affects rate of CNS sign onset
171
Q

C. Tetani (Generalized Clinical Signs)

A
  • usual form in horses and humans
  • hyperthermia
  • generalized increase in muscle tone, stiff gait
  • tetany
172
Q

C. Tetani (most common cause of death)

A
  • respiratory paralysis
173
Q

C. Tetani (Diagnosis)

A
  • History and clinical signs
  • elevated CK
  • Serum AB to tetanus toxins
174
Q

C. Tetani (5 Treatment options)

A
  • Antitoxin: clears unbound toxin
  • Antibiotics: kill the bacteria
  • Sedatives: prevent CNS excitability (that would otherwise cause seizures)
  • wound debridement and cleaning with H2O2 (increase local [O2]
  • Supportive Care
175
Q

Best stain to identify mycobacterium on a slide?

A

Acid-fast stain

gram stain not always good, but they should all be gram positive

176
Q

T/F: Mycobacterium have a cell wall that makes them environmentally vulnerable.

A

F: The cell walls makes them very resistant to everything and also contains Mycolic Acid which is a main virulence mechanism they have.

177
Q

What strains cause Tuberculosis?

A

Mycobacterium Tuberculosis Complex

M. tuberculosis, M. bovis

178
Q

Is Tuberculosis a reportable disease?

A

Fosho

179
Q

Tuberculosis (pathogenesis)

A
  • organisms replicate locally/ taken up by macrophages
  • cell mediated immunity influences course of disease (ie granuloma formation)
  • Primary complex –> lesion at local lymph node
180
Q

Tuberculosis (Disease patterns)

A
  • erratic appetite leading to emaciation
  • large LN
  • cough, diarrhea
181
Q

Tuberculosis (rum. lesions)

A
  • caseous necrotic nodules in lung
182
Q

Tuberculosis (dogs and cats - strain)

A
  • M. bovis
183
Q

Tuberculosis (primates)

A
  • M tuberculosis, and M. bovis
  • airborne route in densely packed areas
  • can get M. bovis via ingestion
184
Q

Tuberculosis (Avian)

A
  • M. avium complex

- lives at higher temperatures than other M.

185
Q

Tuberculosis (Diagnosis)

A

Tuberculin Tests (type 4 hypersensitivity test so have to wait ~72 hours for results)

186
Q

Johne’s Disease (strain and path)

A

M. avium paratuberculosis

- causes chronic, irreversible wasting

187
Q

Johne’s Disease (reservoir)

A
  • ruminants
188
Q

Nosocomial Infection vs Health-care associated infection

A

Nosocomial: acquired in the hospital environment

Health-care ass.: acquired as a result of healthcare interventions (ie placing a catheter)

189
Q

Risk factors for Health-care associated infections (4)

A
  1. immunosuppression
  2. invasive devices
  3. anesthesia
  4. surgery
190
Q

Pathogens that causes Health-care associated inf. (viral and bacterial)

A

Viral: FCV
Bacterial: Bordetella, Staph, C. diff
Fungi: microsporum

191
Q

Prevention of health-care associated infections

A
  • monitor site/ system q8 hours
  • fever watch
  • fasting, et tube management, avoid excessive sedation
  • Standard practice infection control
192
Q

Disinfection, Sterilization, Antiseptics

A

Disinfection: elimination of many or all microbes from inanimate objects
Sterilization: complete elimination of all microbes
Antiseptics: reduction in number of microbes on living tissue and skin

193
Q

Gold Standard vs Index Tests

A

Gold Standard: the best test at determining disease/non-disease (can have downsides)
Index Test: the practical alternative to the gold standard that is often cheaper, less invasive, etc

194
Q

Sensitivity vs Specificity

A

Sensitivity: if you have the disease, you will always come back positive (might get a few false +)

Specificity: if you don’t have the disease, you will not come back positive (ideally to not mis-identify a disease - if the + would mean euthanasia)

195
Q

Analytical vs. Clinical Se/Sp

A

Analytical: how does test perform in lab
Clinical: how does test perform in real life (with variability of populations and such)

Vet 413 - Infectious Diseases (4 decks)

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