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VET433A > Week 9 - Infectious > Flashcards

Week 9 - Infectious Flashcards

1
Q

What is Toxoplasma gondii?

A
  • Obligate intracellular coccidian parasite
  • Definitive host Felidae
  • Intermediate hosts cats and other animals - any warm blooded
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2
Q

Bradyzoites exist as cysts in the ____

A

TISSUE

Bradyzoites are a bunch of tachyzoites together, essentially - latent infection

slow dividing

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3
Q

Toxoplasma oocysts are shed in the feces and transform into _______

A

tachyzoites, the actively forming dz that spread infection. they turn into bradyzoites

fast dividing

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4
Q

Sexual cycle (enteroepithelial life cycle) of Toxoplasma occurs in ___

A

ONLY CATS

There are 2 life cycles for Toxo - asexual can happen in any species warm blooded.

Sexual cycle does NOT cause clinical dz

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5
Q

What are the routes of infection for Toxoplasma?

A
  • Transplacental/congenital - most severe in nature
  • Bradyzoite cyst ingestion - hunting prey animals that are infected
  • Oocyst-contaminated FOOD, water or soil ingestion (from feces)
  • Blood product transfusion
  • Organ transplantation
  • Ingestion of infected goat milk
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6
Q

What is sporulation of the toxoplasma oocyst?

A

after defecating millions of eggs – the oocysts can sporulate, thus increase in resistance

takes 1-21 days

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7
Q

Cats do/don’t reshed infection after first exposure.

A

DON’T

  • In immune/already exposed cats, the sexual cycle is ARRESTED and oocysts are not shed
  • Immunity may last for several years to lifelong
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8
Q

What’s the difference between brady and tachy cyst/oocyst ingestion?

A

Bradyzoite cyst ingestion
* Oocysts produced by 97% of naïve cats
* Prepatent period (time between infection and shedding of dz) 3 to 10 days
* 100 million oocysts/day for 7-10 days

Tachyzoite/oocyst ingestion
* Oocysts produced by 20% of naïve cats
* Prepatent period is > 18 days
* Fewer oocysts shed for several weeks

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9
Q

How can reactivation of Toxo happen in cats/intermediate hosts?

A
  • High doses steroids can cause animals to reshed oocysts
  • Severe immune suppression that causes brady to become tachy
    – High doses steroids
    – HIV infection
    – Chemotherapy
    – Anti-rejection
  • PREGNANCY NOT associated with bradyzoite cyst reactivation!!
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10
Q

What are the general CS for Toxo?

A
  • Most infections subclinical
  • Young animals often most
    susceptible
  • Age, sex, host

susceptibility/species, parasite
strain and number of organisms
may also be important

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11
Q

What are the CS for Toxo in cats?

A
  • Enteroepithelial cycle usually subclinical
  • Extraintestinal cycle
    –Stillbirth, neonatal death
    –Anorexia, lymphadenopathy, fever, dyspnea, coughing, CNS signs, vomiting, diarrhea, icterus, abdominal effusion, pancreatitis, splenomegaly, myositis
    –Uveitis, chorioretinitis

Dogs
* Similar to cats
* Ocular disease less common
* Chronic neuromuscular disease

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12
Q

What are the CS for Toxo in humans?

A
  • Immunocompetent
    -Mild, flu-like illness
  • AIDS and transplant patients
    -> 95% of cases due to bradyzoite cyst reactivation
    -Encephalitis, chorioretinitis, occasional pneumonia
  • Transplacental infections
    -Often asymptomatic at birth: later show chorioretinitis and mental
    retardation
    -Spread to fetus less common in early pregnancy but disease more
    severe
  • < 20% of women show signs
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13
Q

How do you DIAGNOSE Toxo?

A

CLIN PATH
* +/- nonregenerative anemia, leukocytosis
* +/- hypoalbuminemia, hypoproteinemia
* Chronic infections may show hyperglobulinemia
* +/- increased CK, Tbili, ALP, ALT, lipase

CYTOLOGY
* CSF tap normal or increased protein and WCC
* Tachyzoites rarely seen in body fluids

RADIOLOGY
Thoracic
* Diffuse interstitial to alveolar pattern
* Pleural effusion
Abdominal
* Interstitial masses/mesenteric lymphadenopathy
* Hepatomegaly
* Peritoneal effusion

FECAL EXAMINATION
* Diseased cats RARELY shed oocysts and shedding period is short
* Examine FRESH feces to determine human health risk
* Sheather’s centrifugal sugar flotation
* Cannot differentiate from H. hammondii and B. darlingi

SEROLOGY
-high IgM within 2 weeks - consistent with dz
-IgM titers > 64
-or fourfold or greater, increasing or decreasing, IgG or other antibody titers

ORGANISM DETECTION
* Histopathologic detection of tachyzoites (NOT bradyzoite cysts), aided by immunohistochemistry
* PCR

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14
Q

What is the risk of owning a cat in terms of Toxo?

A

pets of low risk of infection

-30% of dogs and cats seropositive in the US

Pet cats of little risk
* Short shedding period
* Immunity to reshedding
* Uncommon reactivation
* Meticulous groomers

Seronegative cats greatest risk to seronegative women

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15
Q

What is Neospora?

A

PROTOZOA - Neospora caninum

  • Transplacental transmission following ingestion of tissue cysts by carnivores or oocysts by herbivores
  • Dogs (especially farm dogs), cattle, sheep, horses, goats, deer
  • Not cats or humans
    *dogs definitive host
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16
Q

What are the CS of Neospora?

A

Herbivores
* Abortion

Dogs
* Neuromuscular abnormalities and sometimes dermatologic, pulmonary, hepatic, and myocardial disease
* Ascending paralysis and muscle atrophy
and stiffness in dogs < 6 months of age

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17
Q

What is the pathogenesis in dogs?

A
  • Purebred dogs
  • Chronically infected bitches REACTIVATE during gestation with transplacental infection
    -Successive litters affected
    -Most pups in the litter
  • Congenital subclinical infection may be followed by reactivation late in life following immunosuppression
  • Postnatal infection probably uncommon
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18
Q

How do you DIAGNOSE Neospora?

A
  • Serology (IFA)
    -Serum and/or CSF
    -Cross-reactions with T. gondii insignificant
  • PCR
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19
Q

How do you prevent Neospora?

A
  • Limit access of dogs to raw meat and placental materials on farms
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20
Q

Which atypical bacteria are there?

A

Actinomyces, Nocardia, Mycobacteriosis

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21
Q

Actinomyces and Nocardia are similar. How?

A

-Filamentous, branching, Gram- positive bacteria
indistinguishable by Gram staining

-Opportunists
-Chronic pyogranulomatous inflammatory lesions
-Sulfur granules
-Sporadic disease
-Not transmitted between animals

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22
Q

What is the pathogenesis of Actinomyces?

A

-Actinomyces is commensal bacteria in oropharyngeal and GI inhabitant. ANAEROBE

-Not in the environment

-when mucous membranes break (foxtail, dog fight), actinomyces is then introduced

-Grass awns contaminated in the oropharynx, migrate from respiratory or GI tract ® thoracic and abdominal cavities
–Diagnosis may be delayed months to years

-Bite wound inoculation
–Cervicofacial actinomycosis
–Limb or subcutaneous tissue infections

-CNS actinomycosis: hematogenous spread, or extension from from head/neck (basilar meningitis)

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23
Q

Is nocardia anaerobe or an aerobe? Where is it found?

A

-aerobe

-found in soil - ubiquitous soil saprophyte
–House dust, beach sand, garden soil, swimming
pools

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24
Q

What is the signalment of Actinomycosis?

A

-Common - since found in mouth
-Young adult to middle-aged large breed dogs
-Usually immune competent

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25
Q

What is the signalment of Nocardiosis?

A

-Uncommon to rare
-Usually cats or young adult dogs
-1/4 to 1/3 of dogs (and humans) are immunosuppressed
–opportunistic infection when animals don’t have a good immune system

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26
Q

What is the pathogenesis for Norcardia?

A

-Inhalation ® pleural and/or systemic spread
-Bite, scratch, or foreign body wounds > subcutaneous nocardiosis
-Hematogenous dissemination to other organs
(CNS, eyes, joints, bones, kidney and heart)

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27
Q

What are skin CS for Actinomyces/Nocardia?

A
  1. Firm to fluctuant swellings, +/- draining tracts
    -Contain serosanguinous to purulent fluid, sometimes
    with ‘sulfur granules’
    -Sulfur granules most common in actinomycosis
    -Tomato soup-like exudate
28
Q

What are other CS for Actinomyces/Nocardia?

A
  1. Fever, anorexia, weight loss
  2. Pleural effusion and pyogranulomatous pneumonia
  3. Bronchointerstitial patterns, hilar lymphadenopathy,
    lobar consolidation, extrapulmonary masses, pleural
    effusion
    -Pericardial involvement
  4. Abdominal involvement
    -Abdominal distention, mass lesions, organomegaly
  5. Retroperitoneal space involvement
    -Spinal pain, sometimes pelvic limb paralysis/paresis
  6. CNS involvement
    -Neurologic signs such as hyperesthesia and tetraparesis

hilar lymphadenopathy can also be fungal too

29
Q

How do you DIAGNOSE Actinomyces/Nocardia?

A
  1. Gram stain
    -Thin, Gram positive, beaded branching filaments
  2. Culture
    -Alert laboratory
    -Slow growing, susceptible to overgrowth
    -Incubate 2-4 weeks
    -Smooth and moist or wrinkly, velvety colonies (molar tooth)
    -Multiple specimens, biopsy specimens if possible

Nocardia grows on simple media. May be acid fast – might retain stain.

Actinomyces is NOT ACID fast - does not retain stain

  1. Histopathology
30
Q

How do you TREAT Actinomyces/Nocardia?

A
  1. Prolonged treatment with high doses of antimicrobials to prevent relapse
    -Cutaneous infections 1-3 months
    -Pulmonary infections 6 months
    -Systemic infections 12 months
  2. Drain abscesses or pyothorax first

Actinomycosis - PENICILLIN, good prognosis
Nocardia - TMS, guarded prognosis

31
Q

Mycoplasmas are not mycobacteriums. What’s the major difference?

A

Mycobacteriums have THICK CELL WALLS.

-Gram positive, aerobic, nonmotile bacteria
-Cell wall rich in mycolic acid (lipid):
–Acid-fast: retains carbol fuschin after heating and acid exposure

-Resistant to phagocytosis
-Resistant in the environment
-Resist many disinfectants
-inactivated by direct sunlight and dilute household bleach

32
Q

What are etiologic agents of mycobacterium?

A

M. tuberculosis (humans) and M. bovis (cattle) > (MTBC - tuberculosis)

M. avium complex

M. lepraemurium

33
Q

What are MTBC Mycobacteria?

A

-Highly pathogenic

-Facultatively or obligately intracellular

-Differentiation difficult

-Maintained by infection of reservoir mammalian hosts
-Survives only 1-2 weeks in the environment
-Reverse zoonosis

34
Q

Who is most susceptible to M.t uberculosis?

A

DOGS

-Pulmonary predilection

-Most dogs subclinically infected
-Potentially zoonotic, this is the bad guy

35
Q

How is M. Bovis transmitted?

A

-Ingestion of unpasteurized milk or uncooked meat or offal

-target in cats: GI
-traget in dogs: respiratory

36
Q

Non-tuberculosis mycobacterium

A

-saprophytic, survive > 2 years in the environment

-Slow-growing (M. avium complex)
–Produce tuberculous lesions, disseminate

-Rapidly-growing (RGM)
–M. thermoresistible, M. fortuitum, M. smegmatis

37
Q

What is the pathogenesis of M. avium?

A

-Acid soils high in organic matter
-Avian carcasses or feces
-No spread from animals to people
-Lesions resemble TB lesions
-Cats and dogs are quite resistant to infection
–Miniature schnauzers, Bassett hounds

38
Q

Which are the rapidly growing mycobacterium?

A

-M. smegmatis and M. fortuitum most common

-Inoculated into skin via trauma
-Enhanced pathogenicity in adipose

-Cats most susceptible

39
Q

What are CS for rapidly growing mycobacterium? (M. smegatis and M fortuitum)

A

Cutaneous and subcutaneous granulomas (mycobacterial
panniculitis)
-Especially inguinal area
-Resemble cat fight abscesses, later ulcerate, drain
-No systemic signs

40
Q

What is Lepromatous mycobacteria?

A

-M. leprae, M. lepraemurium

-Localized cutaneous nodules which may ulcerate

-difficult/impossible to culture

41
Q

What dz can Lepromatous mycobacteria cause?

A

Canine leproid granuloma syndrome

-CA, Australia
-short-coated breeds
-Usually head, pinnae
-Never cultured

42
Q

How do you DIAGNOSE mycobacteria?

A

1.Presentation + acid fast stained cytology

2.Tuberculous granulomas
–Focal necrosis surrounded by plasma cells, macrophages and a fibrous tissue capsule
–Giant cells uncommon in dogs and cats
–Calcification may be present

3.RGM and lepromatous mycobacteria
–Pyogranulomatous inflammation

  1. Isolation
    -Multiple deep tissue biopsies
    - Tuberculous mycobacteria may take 4-6 weeks to grow on solid media, faster in liquid media
    - RGM: 3-5 days
    - Requires egg-enriched media (eg. L-J media)
  2. PCR
43
Q

How do you TREAT M. tuberculosis?

A

-Combinations of drugs for > 6 months

-Isoniazid-ethambutol/pyrazinamide- rifampin/streptomycin in humans

-Treatment of affected dogs and cats not recommended, but has been successful

-Streptomycin, isoniazid, rifampin

44
Q

How do you TREAT M. Avium complex?

A

-Treatment difficult
-Fluoroquinolones, doxycycline and/or
clarithromycin/azithromycin

45
Q

How do you TREAT Rapidly growing mycobacterium?

A

Skin lesions
-High doses fluoroquinolone or doxycycline, then surgical excision
-3-6 months of doxycycline or a FQ
-Rarely, lifelong treatment

46
Q

What are the ground rules when choosing to use IMMUNOSUPPRESSIVE DRUGS

A
  1. Do everything possible to ensure immune-
    mediated disease is really immune-mediated disease
    -may need a lot of testing
  2. Warn the owner that infection or neoplasia may go undetected despite your best efforts to uncover it
  3. Think before you clip - bc glucocorticoids slow hair growth
  4. Minimize excessive immunosuppression
    * Degree of immunosuppression relates to
    * drug and number of drugs used,
    frequency, dose, chronicity
    * Pre-existing immune defects/concurrent
    disease
    * Including age and breed
    * Never use more than 2 drugs at a time
    * Target is “pulse” immunosuppression
  5. Maintain contact with your patient
47
Q

Examples of glucocorticoids

A

Prednisone, prednisolone, dexamethasone

dex more potent than pred

48
Q

MOAs of glucocorticoids

A
  • Suppression of cytokine production
  • Decreased antibody response
  • Reduced T cell activation
  • Decreased phagocytosis
  • Decreased inflammatory cell influx
  • Decreased Fc receptor expression by macrophages
  • Lymphopenia, eosinopenia - stress leukogram
49
Q

Glucocorticoids stop which pathway?

A

the Arachidonic Acid Pathway

no production of Prostaglandins, Thromboxanes, or Leukotrienes

50
Q

What is the starting dose for Glucocorticoids?

A

Starting dose 1 mg/kg PO q12h

No higher than 30 mg to 40 mg total q12h

NEVER WITH NSAIDs - leads to GI perforation

51
Q

What are side effects of glucocorticoids? (Pred)

A

-hair loss
-muscle atrophy - temporal muscle
-calcionosis cutis
-fat redistribution to belly

  • PUPD, polyphagia (D)
  • Panting (D)
  • Muscle wasting, weakness (D)
  • Hepatomegaly (D)
  • Calcinosis cutis (D)
  • Hypercoagulability (D)
  • GI ulceration with anemia (D)
  • Alopecia, thin skin, impaired hair regrowth (D, C)
  • Lethargy, behavioral changes (D, C)
  • Opportunistic infections (especially bacterial) (D, C)
  • Sodium retention (D, C) (C>D)
  • Early growth plate closure (D, C)
  • Diabetes mellitus (C)
52
Q

What is Cyclosporine A?

A
  • Cyclic peptide
  • Interacts with cyclophilins in lymphocytes, blocking formation of transcription factors needed for T cell
    activation and cytokine synthesis (mainly Il-2)

-inflammation-mediator

-leads to DECREASED IL-2

  • Sandimmune®
  • Neoral®
  • Atopica®
  • Gengraf®
  • Topical formulations for KCS
    (Optimmune)
53
Q

What’s the dose of Cyclosporine A for immune suppression?

A
  • 3-5 mg/kg q12h initial

For atopic dermatitis
* 5 mg/kg q24h until clinical improvement (1-2 months)
* Taper to q48h then q72h

54
Q

What are adverse effects of cyclosporine A?

A
  • GASTROINTESTINAL SIGNS – MOST COMMON
    -give with food
  • Gingival hyperplasia
  • Verrucous dermatopathy
  • Hirsuitism
  • Hepatotoxicity
  • Nephrotoxicity
  • Lameness
  • Neoplasia (lymphoma, up to 10% chance)
  • gammaherpesvirus?
  • Opportunistic infections
55
Q

what type of metabolism is cyclosporine A?

A
  • p450 enzyme metabolism
56
Q

What kind of immunosuppressive drug is Azothioprine?

A

Nucleocide Analog - stops cellular replication

chemo drug – targets rapidly dividing cells

  • Almost always used in combination with glucocorticoids
  • Delayed onset of action
  • 1-2 mg/kg q24h PO until remission (10-14 days), then q48h
  • Glucocorticoid-sparing

-hepatotoxic!

57
Q

Azathioprine (Imuran): Adverse Effects - Dogs

A
  • Gastrointestinal upset - Most common
  • Impaired hair growth
  • Bone marrow suppression
    -Monitor CBC q2 weeks for first 3 months then
    every 2-3 months
    -Uncommon
  • Hepatotoxicity
    -Monitor liver enzymes q2-4 weeks
  • Pancreatitis
  • Profound muscle weakness and tetraparesis
58
Q

Can Azothioprine be used in cats?

A

NO NO NO

Severe adverse effects in
cats, especially marrow
suppression

59
Q

How does Azathioprine affect the enzyme Thiopurine S-methyltransferase (TPMT)?

A
  • Converts active metabolites of azathioprine to inactive metabolites
  • Human patients with GENETICALLY LOW TPMT ACTIVITY ARE AT RISK FOR MYELOTOXICITY
  • Dogs TPMT activity > cats (another reason not to give to cats)
  • Dog levels vary but poorly correlated with myelotoxicity
60
Q

What is Chlorambucil?

A

-chemo drug

-Used most often in cats
–2 mg every other to every 3rd day

  • IBD, lymphoma, immune disease
  • Low potency
  • Adverse effects uncommon
    –GI adverse effects
    –Bone marrow suppression

-not rapidly acting, nor super potent

61
Q

What 4 things should we keep in mind when tapering meds?

A

-Use objective measure to assess remission
-Aim for <6 months of therapy
-Taper by ~25% at each check-in
-Balance adverse effects

62
Q

IMHA is a Type 2 hypersensitivity. What are some prognostic factors for IMHA?

A
  • Intravascular hemolysis
  • Absence of regeneration
  • Auto-agglutination
  • Thrombocytopenia
  • Hyperbilirubinemia
63
Q

IMPA is a type 3 hypersensitivity. What does IMPA stand for?

A

immune mediated poly arthritis

COMMON in dogs, UNCOMMON in cats

Usually NONEROSIVE polyarthritis

Genetic predisposition may exist
-DLA-DRB1 alleles

64
Q

How do you TREAT IMPA?

A

Consider adding azathioprine, cyclosporine
* Most commonly azathioprine
* Cyclosporine alone an option (ie. no
prednisone)
* No concurrent NSAIDs with prednisone!!

  • Monitor joint fluid cytology?
  • May relapse
  • Avoid vaccinations?
  • Erosive polyarthritis may be refractory
65
Q

Which drugs trigger IMPA?

A
  • Chloramphenicol
  • Itraconazole
  • Propofol
  • Trimethoprim-sulfamethoxazole
  • Metronidazole

VET433A (8 decks)

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