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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
What is the signalment of Nocardiosis?
-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
26
What is the pathogenesis for Norcardia?
-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)
27
What are skin CS for Actinomyces/Nocardia?
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
What are other CS for Actinomyces/Nocardia?
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
How do you DIAGNOSE Actinomyces/Nocardia?
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 3. Histopathology
30
How do you TREAT Actinomyces/Nocardia?
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
Mycoplasmas are not mycobacteriums. What's the major difference?
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
What are etiologic agents of mycobacterium?
M. tuberculosis (humans) and M. bovis (cattle) > (MTBC - tuberculosis) M. avium complex M. lepraemurium
33
What are MTBC Mycobacteria?
-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
Who is most susceptible to M.t uberculosis?
DOGS -Pulmonary predilection -Most dogs subclinically infected -Potentially zoonotic, this is the bad guy
35
How is M. Bovis transmitted?
-Ingestion of unpasteurized milk or uncooked meat or offal -target in cats: GI -traget in dogs: respiratory
36
Non-tuberculosis mycobacterium
-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
What is the pathogenesis of M. avium?
-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
Which are the rapidly growing mycobacterium?
-M. smegmatis and M. fortuitum most common -Inoculated into skin via trauma -Enhanced pathogenicity in adipose -Cats most susceptible
39
What are CS for rapidly growing mycobacterium? (M. smegatis and M fortuitum)
Cutaneous and subcutaneous granulomas (mycobacterial panniculitis) -Especially inguinal area -Resemble cat fight abscesses, later ulcerate, drain -No systemic signs
40
What is Lepromatous mycobacteria?
-M. leprae, M. lepraemurium -Localized cutaneous nodules which may ulcerate -difficult/impossible to culture
41
What dz can Lepromatous mycobacteria cause?
Canine leproid granuloma syndrome -CA, Australia -short-coated breeds -Usually head, pinnae -Never cultured
42
How do you DIAGNOSE mycobacteria?
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 4. 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) 5. PCR
43
How do you TREAT M. tuberculosis?
-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
How do you TREAT M. Avium complex?
-Treatment difficult -Fluoroquinolones, doxycycline and/or clarithromycin/azithromycin
45
How do you TREAT Rapidly growing mycobacterium?
Skin lesions -High doses fluoroquinolone or doxycycline, then surgical excision -3-6 months of doxycycline or a FQ -Rarely, lifelong treatment
46
What are the ground rules when choosing to use IMMUNOSUPPRESSIVE DRUGS
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
Examples of glucocorticoids
Prednisone, prednisolone, dexamethasone dex more potent than pred
48
MOAs of glucocorticoids
* 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
Glucocorticoids stop which pathway?
the Arachidonic Acid Pathway no production of Prostaglandins, Thromboxanes, or Leukotrienes
50
What is the starting dose for Glucocorticoids?
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
What are side effects of glucocorticoids? (Pred)
-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
What is Cyclosporine 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
What's the dose of Cyclosporine A for immune suppression?
* 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
What are adverse effects of cyclosporine 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
what type of metabolism is cyclosporine A?
* p450 enzyme metabolism
56
What kind of immunosuppressive drug is Azothioprine?
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
Azathioprine (Imuran): Adverse Effects - Dogs
* 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
Can Azothioprine be used in cats?
NO NO NO Severe adverse effects in cats, especially marrow suppression
59
How does Azathioprine affect the enzyme Thiopurine S-methyltransferase (TPMT)?
* 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
What is Chlorambucil?
-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
What 4 things should we keep in mind when tapering meds?
-Use objective measure to assess remission -Aim for <6 months of therapy -Taper by ~25% at each check-in -Balance adverse effects
62
IMHA is a Type 2 hypersensitivity. What are some prognostic factors for IMHA?
* Intravascular hemolysis * Absence of regeneration * Auto-agglutination * Thrombocytopenia * Hyperbilirubinemia
63
IMPA is a type 3 hypersensitivity. What does IMPA stand for?
immune mediated poly arthritis COMMON in dogs, UNCOMMON in cats Usually NONEROSIVE polyarthritis Genetic predisposition may exist -DLA-DRB1 alleles
64
How do you TREAT IMPA?
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
Which drugs trigger IMPA?
* Chloramphenicol * Itraconazole * Propofol * Trimethoprim-sulfamethoxazole * Metronidazole

VET433A (8 decks)

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