Term
| What is the organism responsible for distemper? What species are susceptible to infection? |
|
Definition
morbilivirus (related to measles) Dogs and ferrets are the domestic species that are susceptible
**** large wild cats, seals, and wild canids/mustelids (weasels) are also suceptible |
|
|
Term
| How is distemper virus transmitted? |
|
Definition
primarily shed via respiratory and occular secretions (also in urine)
primarily transmitted via aerosolization but ingestion is also possible |
|
|
Term
| What type of antibody response to distemper virus is associated with development of CNS signs? |
|
Definition
low antibody response
*** these patients have mild or subclinical respiratory disease associated initial viral infection, the virus then persists in the lungs for up to 60 days before the development of CNS signs |
|
|
Term
| What antibody response to distemper virus is associated with a low prevelence of CNS signs? |
|
Definition
good antibody response (adequate host immunity- ex. well vaccinated dam and puppies)
*** although the virus may enter the CNS the immune system is effected at clearing the infection before significant damage is done |
|
|
Term
| T/F the majority of respiratory disease associated with distemper occurs secondary to primary viral replication within respiratory tissues |
|
Definition
FALSE
most respiratory signs associated with distemper are the result of secondary bacterial infections |
|
|
Term
| What CNS sign is pretty specific to viral infections (Ex. distemper)? |
|
Definition
|
|
Term
| What clinical signs occur less commonly than respiratory and CNS signs with distemper infection? |
|
Definition
hyperkeratosis of foot pads and nasal planum
enamel hypoplasia
optic neuritis, retinal atrophy with "gold medallion lesions"
hypertrophic osteodystrophy
pustular dermatitis |
|
|
Term
| What is a rare sequelae of distemper infection that occurs in old dogs? |
|
Definition
old dog encephalitis
**** occurs in immunocompetent animals that clear initial systemic infection but virus persists within CNS tissue resulting in chronic encephalomyelitis |
|
|
Term
| What is the best way to diagnose distemper virus infection? |
|
Definition
submit nasal and conjunctival swabs for real time PCR
*** PCR is highly sensitive and specific, can differentiate between vaccine and natural infection |
|
|
Term
| What is the treatment for distemper virus? How can you prevent infection? |
|
Definition
supportive care +/- antibiotic therapy (if secondary bacterial infections)
prevent infection with vaccination, modified live for puppies at 6-8 wks of age, then again 2-4 wks later (to ensusure good immunity if maternal interference) and CLEAN the environment (enveloped virus -> easily killed with most cleaners) |
|
|
Term
| What is the prognosis for dogs diagnosed with distemper infection? |
|
Definition
guarded if CNS sings
variable for non-neuro, many do live with appropriate therapy (supportive +/- antibiotics) |
|
|
Term
| What three systems can be affected by distemper infection? |
|
Definition
|
|
Term
| When is it safe for animals that have been successfuly treated for distemper infection to interact with other dogs without risk of transmission? |
|
Definition
| 2 weeks beyond resolution of clinical signs |
|
|
Term
| What is the etiology of infectious canine hepatitis? |
|
Definition
canine adenovirus type 1
non-enveloped virus --> hard to kill, need to use quaternary ammonia (vs. distemper is enveloped and easy to kill with household cleaners) |
|
|
Term
| What is the pathogenesis of infectious canine hepatitis? |
|
Definition
| virus is shed in all body secretions (esp. oronasal) --> direct cytopathic effect on target organs --> anterior uveitis, hepatic/renal necrosis (ie. predilection for highly vascular organs) |
|
|
Term
| What is the prognosis for patients with infectious canine hepatitis? |
|
Definition
grave (most infected animals die)
**** so VACCINATE (CAV-2 MLV, because CAV-1 vaccine causes corneal edema (blue eye)) |
|
|
Term
| T/F positive coronavirus serology is diagnostic for feline infectious peritonitis |
|
Definition
FALSE
**** most animals exposed to feline corona virus will NOT develop FIP, additionally vaccinated cats may be positive on serology (vaccination is not typically recommended) |
|
|
Term
| What is the common signalment and clinical signs associated with FIP? |
|
Definition
| young animal with a waxing/waning fever, weight loss, and anorexia |
|
|
Term
| What is the most clinically important protein in the corona virus envelope? |
|
Definition
| spike protein (coronaviruses that have a spike protein are more invasive (better able to bind to macrophages) than those without a spike protein) *** most coronaviruses do not have this protein |
|
|
Term
| What type of cornoavirus is more likely to cause FIP? What type is more commonly used in a research setting? |
|
Definition
type 1 --> FIP
type 2 --> research (very amenable to tissue culture) |
|
|
Term
| What is the most common clinical presentation of coronavirus infection in a cat? |
|
Definition
| subclinical infection is most common, symptomatic cats are typically young and present with mild diarrhea |
|
|
Term
| What is the etiology of FIP? |
|
Definition
feline corona virus that undergoes internal genetic mutation to a more virulent form --> clinical FIP
*** all feline coronaviruses have the potential to cause FIP |
|
|
Term
| What is the best way to prevent feline corona virus infection and FIP? |
|
Definition
| good environmental management (virus is shed in feces and persists in the environment and fomites for long periods of time) |
|
|
Term
| T/F horizontal transmission of FIP is uncommon |
|
Definition
TRUE
**** horizontal transmission of feline corona virus is common through contact with feces or fomites, however, FIP arises secondary to internal genetic mutation which cannot be transmitted to naive animals |
|
|
Term
| What cells are affected by FECoV? Which cells are affected by FIPV mutation? |
|
Definition
FECoV --> intestinal epithelial cells (subclinical or mild diarrhea)
FIPV --> infection and replication within macrophages --> increased vascular permiability/exudation + pyogranulometous lesions |
|
|
Term
| What type of immunity may be protective against the development of FIPV from FECoV? |
|
Definition
cell mediated
early T cell response signals macrophages to destroy the virus and will prevent the development of clinical signs
***late or weak cell mediated immunity allows macrophages to get infected and disseminate the virus |
|
|
Term
| What strength of cell mediated response to FIPV infection is associated with development of wet (effusive) form? development of dry (pyogranulometous) form? |
|
Definition
antibodies + inadequate CMI -> wet
antibodies + partially protective CMI --> dry
*** if CMI is strong the cat will not develop overt disease but may become persistently infected and immunosuppression may instigate recrudescence |
|
|
Term
| What breeds are more susceptible to developing FIP? |
|
Definition
|
|
Term
| What is antibody dependent enhancement (ADE) and how does this relate to the pathogenesis of FIP? |
|
Definition
Antibodies bind to the virus tagging it for macrophages which engulf the virus-antibody complexes --> in the absence of adequate T-cell signalling the macrophage doesn't destroy the virus which exploites the macrophage for reproduction and dissemination
ie. antibodies accelerate the disease process by attracting more cells for the virus to exploit |
|
|
Term
| What population of cats has the highest incidence of FCoV infection (and FIP)? |
|
Definition
| cattery kittens 6-12 months of age |
|
|
Term
| abdominocentesis of a kitten affected with wet FIP (inadequate CMI) would result in fluid with what characteristics? |
|
Definition
| modified transudate (high protein, low cells) secondary to immune complex vasculitis -> increased vascular permiability |
|
|
Term
| What are the most common sites for pyogranulomeous lesions associated with dry FIP (partially protective CMI)? |
|
Definition
eyes and CNS
(also liver, spleen, kidneys, and LN) |
|
|
Term
| What occular pathology is associated with FIP? |
|
Definition
anterior uveitis, keratic precipitates (cellular deposits on the posterior surface of the cornea), hyphema/hypopyon, chorioretinitis and retinal detachement
*** remember, occular lesions associated with k9 distemper include optic neuritis and retinal atrophy with "gold medallion lesions" |
|
|
Term
| What is the only way to definitively diagnose FIP antemortem? |
|
Definition
organ biopsy (perivascular pyogranulometous inflammation and IHC for viral antigen)
** IHC is gold standard for diagnosis of FIP |
|
|
Term
| T/F electronmicroscopy of feline feces will not identify subclnical FCoV shedding, or FIPV |
|
Definition
|
|
Term
| Although most cats are exposed to FECoV in the enviornment and will therefore be positive of serology what are three indications for testing cats? |
|
Definition
introducing a new cat the the environment (ideally FECoV negative, otherwise can contaminate the environment)
breeding animals (breed negative animals to negative animals and positive animals to positive animals)
high titers in a sick patient that has suspect clinical signs (chronic fever and weight loss) and comes from a single cat home (and probably wasn't exposed as a kitten ie. NOT from a cattery)) |
|
|
Term
| T/F a negative FECoV titer rules out FIP |
|
Definition
FALSE
(peracute infections prior to antibody production, antigen-antibody complex formation leaves non free in the serum, antibody production is exhausted late in disease) |
|
|
Term
| What FIP serum tests are available but are of limited diagnostic value? |
|
Definition
7B protein test (some non-FIP FECoV have this protein, and some FIPV do not have this protein)
mRNA PCR (false positives)
Real time PCR (only works for viremic patients, cats with dry form of FIP are often not viremic) |
|
|
Term
| What is the treatment and prognosis for FIP infection in cats? |
|
Definition
immunosuppressive doses of prednisone (try to supress antibody dependent enhancement and immune complex deposition)
prognosis is poor |
|
|
Term
| What are some breeding precautions that should be adopted to limit FECoV transmission to kittens? |
|
Definition
| test queen prior to partuition --> if queen is positive remove the kittens from mom at 4-6 weeks (prior to this point kittens will be protected from contracting FCoV by maternal antibodies) and test kittens after 10 weeks for seroconversion |
|
|
Term
| Why is FIP vaccine rarely reccomended? |
|
Definition
sensitizes humoral immunity but has no effect on CMI ---> increased antibody production in response to antigen challenge --> ADE and vasculitis
*** remember, antibody-virus complexes are phagocytized by macrophages which subsequently are infected by the virus and dissemintated <-- animals do NOT die of FIP if they do not make antibodies |
|
|
Term
| What is the most most common form of fungus that poses a threat of infection to dogs? |
|
Definition
infective spores (blasto, histo, coccidio and crypto)
*** only exception is aspergillosis in which fungal hyphae are infective form |
|
|
Term
| What triggers the transformation of most fungal infections from spores to yeast forms? |
|
Definition
body temp following inhalation or ingestion (histo) --> systemic infection
*** exception is aspergillosis which exists in its mycelious fungal hyphae form both inside the body and in the environment |
|
|
Term
| What is the cytologic appearance of a blastomycosis yeast? |
|
Definition
big blue broad-based budding yeast
*** often associated with pyogranulometous inflammation |
|
|
Term
| Why are fungal mycoses not infective from animal to animal? |
|
Definition
spores are infective forms, fungi exists as yeast inside the body
*** the presence of an infected animal indicates environmental contamination which CAN pose a threat of new infection in animals and people |
|
|
Term
| What radiographic findings are most commonly appreciated in cases of fungal pneumonia? |
|
Definition
diffuse interstitial nodular infiltrate
*** can also present with alveolar or mass pattern or combo of all three |
|
|
Term
| describe the skin lesions often associated with systemic blasto infection? |
|
Definition
| multifocal, can occur anywhere on the body, ulcerative with serosanguinous to purulent drainage |
|
|
Term
| What anatomic site is associated with persistent infection and relapse of systemic blasto infection? |
|
Definition
the eyes
*** assess patients for uveitis, retinal granulomas, optic neuritis, glaucoma and lens rupture |
|
|
Term
| What is the best way to diagnose blasto? |
|
Definition
cytology (big blue broad-based budding yeast)
*** collect samples from LN (organism disseminates through lymphatics), skin lesions, tracheal wash or vitreous. Can also dx via histopathology |
|
|
Term
| What fungal organisms shoud NEVER be cultured in the hospital and why? |
|
Definition
NEVER culture blasto or histo as these cultures will produce infective spores that pose a public health risk
*** culture for ALL fungal pathogens is generally an INEFFECTIVE means of diagnosis |
|
|
Term
| What is the drug of choice for treatment of blastomycosis? |
|
Definition
microencapsulated intraconazole (spranox) --> microencapsulation increases bioavalability, do not use compounded itraconazole
**** also consider using anti-inflammatories (NSAIDS if well hydrated or low anti-inflammatory doses of glucocorticoids) during first few days of tx to reduce risk of the patient developing systemic inflammatory response syndrome (SIRS) as the blasto organisms start to die |
|
|
Term
| How long should blasto and histo be treated for? |
|
Definition
1 month past resolution of detectable disease (ex. clear thoracic rads, normal fundic exam, resolved skin lesions etc.)
*** usually require at least 6 months of tx |
|
|
Term
| Although blasto has a fair to good prognosis if treated appropriately what are three negative prognostic indicators? |
|
Definition
severe pulmonary involvement, CNS involvement, more than 3 body systems affected
*** relapse is common, may be recrudesence of persistent infection (ie. occular) or reinfection |
|
|
Term
| What is unique about histoplasmosis transmission? |
|
Definition
| infective spores may be ingested --> primary GI infection (in addition to inhalation --> pulmonary involvement) |
|
|
Term
| What is the cytologic appearance of histoplasma yeast? |
|
Definition
| many intracellular small round yeast with a thin clear halo, packed within macrophages |
|
|
Term
| Histoplasma yeast has a predilection for which host cell type? |
|
Definition
|
|
Term
| What environmental factors are associated with the presence of histoplasma? |
|
Definition
histoplasma is associated with bird and bat feces, found in temperate to tropical climates associated with ohio, mississippi and missouri rivers in the USA
**remember crypto is also associated with bird (pigeon) feces and is ubiquitous throughout the entire world |
|
|
Term
| Which systemic fungal disease has a shorter incubation period blasto or histo? |
|
Definition
histo (2 wks)
vs. blasto (1-3 months) |
|
|
Term
| What intestinal lesions are associated with ingestion and primary GI infection with histoplasmosis? |
|
Definition
| thickened, friable, hemorrhagic/ulcerated --> large and/or small bowel diarrhea, hematochezia, melena, PLE |
|
|
Term
| What is the best way to diagnose histoplasmosis? |
|
Definition
CYTOLOGY (many small round yeasts with a thin halo within macrophages)
*** collect cytology samples from LN, liver/spleen/lung aspirates, rectal scraping, or bone marrow (only if abnormal CBC, bone lesions are less common with histo than with blasto) |
|
|
Term
| What is the treatment for histoplasmosis? |
|
Definition
itraconazole (microencapsulated isn't necessary) +/- amphotericin B for severe disseminated disease
*** if lesions are restricted to the lungs the infection can be self limiting but treatment is always recommended to reduce the risk of further dissemination |
|
|
Term
| although prognosis for histoplasmosis is fair to good with treatment what are three negative prognostic indicators? |
|
Definition
| CNS, ocular, and bone lesions |
|
|
Term
| What is the cytologic appearance of coccidiodes? |
|
Definition
| large endospore-filled spherules --> induce intense inflammatory reaction and are often obscured by swarms of neutrophils |
|
|
Term
| What triggers coccidiodes spores to transform into spherules? |
|
Definition
| inhalation and CO2 exposure |
|
|
Term
| What region of the US is assocaited with coccidiodes? |
|
Definition
south western US
*** hot, sandy, alkaline soil |
|
|
Term
| Although most coccidiomycoides infections are subclinical what three factors can lead to dissemination and clinical disease? |
|
Definition
immunosupression, pregnancy, massive exposure
**** recommend screening with thoracic rads prior to breeding in endemic areas (SW USA) |
|
|
Term
| Of all the systemic mycosis which organism is associated with myocardial and pericardial lesions? |
|
Definition
|
|
Term
| What is the most common site of coccidiomycosis dissemintation in dogs? |
|
Definition
|
|
Term
| Which species is more likely to develop clinical signs related to direct innoculation of coccidiodes spores rather than inhalation? |
|
Definition
| cats -> skin lesions are the most common manifestatino of coccidiomycosis -> abcesses, masses with drainage, and local lyphadenopathy |
|
|
Term
| Because coccidiodes spherules incite such an intense inflammatory response they are difficult to find on cytology (hidden in swarms of neutrophils), what other diagnostic tests are available for diagnosis of cocidiomycosis? |
|
Definition
tube precipitation test (IgM) --> IgM is the first antibody produced in response to infection, positive tube precipitation test indicates active infection (**** remember, incubation period for coccidio is 2 wks)
complement fixation antibodies (IgG) -> IgG will predominate 4-6 wks post initial exposure. Low titers suggest acute disease or previous subclinical infection, high titers (>1:32) suggest severe disseminated disease
**** false negatives are possible for both serologic tests (esp. if immunocompromised), interpret in light of clinical signs |
|
|
Term
| What species is more likely to have a positive complement fixation antibody titer for coccidiomycosis? |
|
Definition
cats have a longer period of positive titers than dogs
*** remember, compliment fixation tests IgG (present 4-6 wks post initial exposure) |
|
|
Term
| What fungal disease responds well to the older (cheaper) azole drugs? |
|
Definition
coccidiomycosis
*** may require lifelong therapy as frequent relapses are common if treatment is discontinued |
|
|
Term
| Although the prognosis for localized respiratory infections of coccidiomycosis is good, what are some negative prognostic indicators? |
|
Definition
CNS or multiple bone involvement
**** although patients with disseminated coccidiomycosis often respond to treatment the disease is difficult to cure and life long therapy is often required |
|
|
Term
| What is the cytologic appearance of cryptococcus? |
|
Definition
| round to oval yeast, narrow based budding with thick clear capsules |
|
|
Term
| What is the most common systemic mycosis of cats? |
|
Definition
|
|
Term
| What is the most common clinical presentation of cryptococcosis? |
|
Definition
young cat with nasal or facial deformity
*** cryptococcosis primarily affects the upper respiratory tract |
|
|
Term
| What is the most common presentation of cryptococcosis in dogs? |
|
Definition
CNS > eyes > nasal cavity
** likely enters through nasal passages and invades CNS through cribiform plate. Remember, cats are much more commonly infected with crypto than dogs |
|
|
Term
| What are two ways to diagnose cryptococcosis? |
|
Definition
| cytology or serology --> latex cryptococcal antigen agglutination (LCAT): titers correlate with severity of disease |
|
|
Term
| What is the value of checking cryptococcosis titers after making the initial diagnosis? |
|
Definition
because titers correlate with severity of disease they can be used to assess response to treatment
*** treat patients until titer is negative (clinical signs resolve sooner than titer values) |
|
|
Term
| How does FeLV infection impact treatment of cryptococcosis in cats? |
|
Definition
| FeLV + cats must be treated for life |
|
|
Term
| What is a favorable prognostic indicator associated with cryptococcosis? |
|
Definition
decrease in titer (LCAT) of 10 fold over the first 2 months of treatment
**** prognosis is good to excellent except for CNS disease (guarded) |
|
|
Term
| What is the only systemic mycosis NOT caused by a yeast? |
|
Definition
aspergillosis
*** exists as dichotomously branching hyphae in the environment and in the body |
|
|
Term
| What populations are at risk for developing aspergillosis? |
|
Definition
| immunosuppressed individuals and german shepherds |
|
|
Term
| What is the best way to diagnose aspergillosis? What is the prognosis? |
|
Definition
dx --> cytology
prognosis --> grave |
|
|
Term
| What class of drugs used to treat systemic mycosis are fungistatic at pharmacologic doses? |
|
Definition
azoles
*** these are the current drugs of choice, best absorbed in acidic environments (give with a meal --> stimulates gastric acid secretion) |
|
|
Term
| Which of the azoles can penetrate into the brain, eyes, and prostate? |
|
Definition
fluconazole
*** still choose itraconazole for blasto because blood brain barrier is compromised by significant inflammation and organism is more sensitive to itraconazole (microencapsulated!) |
|
|
Term
| If you have been treating a patient with itraconazole for blastomycosis and he develops cutaneous lesions what should be your next course of action? |
|
Definition
cytology of the lesions! Blasto can cause cutaneous lesions and organisms will be easily recovered from them; however, itraconazole can cause vasculitis and ulcerative skin lesions which will not contain any blasto yeasts
*** if cytology is positive --> increase dose of itraconazole, if negative --> switch to a different antifungal |
|
|
Term
| What three adverse effects are associated with itraconazole? |
|
Definition
| GI (anorexia and vomiting), hepatic necrosis (elevated ALT), cutaneous (vasculitis and ulcerative skin lesions) |
|
|
Term
| Which azole drug is associated with the most severe side effects? |
|
Definition
ketoconazole
**** super cheap but less effective than the others and associated with more severe GI and hepatic toxicities |
|
|
Term
| Which azole should NEVER be used in cats? |
|
Definition
voriconazole --> neurotoxicity
**** monitor dogs for neurotoxicity as well |
|
|
Term
| What class of drugs used to treat systemic mycosis are fungicidal at pharmacologic doses? What is the most significant side effect associated with this drug? |
|
Definition
amphotericin B
**** reliably associated with nephrotoxicity, SQ protocol and liposomal formulations ($$$$$) are safer than straight up IV administration |
|
|
Term
| You work at a practice in minnesota. A 4 year old MN Labrador present to you for anorexia, a fever, and skin lesions. You find Blastomyces organisms on skin cytology. What two diagnostic tests are most valuable to "stage" this disease? |
|
Definition
| thoracic rads and fundic exam |
|
|
Term
| You move to philadelphia to avoid dealing with fungal disease. A 10 year old FS Mini Schnauzer presents to you for geriatric screening and you find a diffuse interstitial lung pattern on radiographs. Her owner is shocked. The dog just won championship titles in shows in AZ and MN last week and seems to be the picture of health. What is the likely diagnosis and prognosis? |
|
Definition
| coccidiomycosis, carries a good prognosis |
|
|
Term
| Which systemic fungal diseases commonly cause subclinical infections? |
|
Definition
|
|
Term
| What is the only systemic mycosis not generally diagnosed on cytology? |
|
Definition
| Coccidiosis (spherules are difficult to identify) <-- tx based on serology |
|
|
Term
| Which systemic mycoses require life long treatment? |
|
Definition
| aspergilosis +/- cryptococcosis (definitely if concurrently FeLV +) |
|
|
Term
| How is rabies transmitted? |
|
Definition
most commonly transmitted through bites from infected animals (extensive viral shedding in saliva)
also through transplantation of tissues from an infected individual
*** potentially aerosolization is also a possible mode of transmission |
|
|
Term
| What viral antigen is used to create the rabies vaccine? |
|
Definition
| glycoprotein --> very highly antigenic results in a very effective vaccine that stimulates a robust and long lasting immune response |
|
|
Term
| What section of the brain provides the highest diagnostic yield for confirmation of rabies diagnosis? |
|
Definition
the hippocampus
*** rabies preferentially infects limbic system neurons |
|
|
Term
|
Definition
eosinophilic intracytoplasmic inclusions formed by aggregates of rabies virus nucleocapsids within neurons
*** negri bodies are not present in all rabid brains and there can also be false positives so confirm diagnosis with direct fluorescent antibody test |
|
|
Term
| What are the four clinical phases of rabies infection and what pathophysiology are associated with each phase? |
|
Definition
Prodromal phase: virus replicates and spreads throughout CNS --> behavior changes and pruitis at inoculation site
Furious phase: virus spreads into the forebrain -> aggression, hyperesthesia + virus spreads into peripheral and cranial nerves --> virus accumulates in salivary glands and other tissues
Paralytic phase: accelerated global apoptosis of neurons --> paralysis (inability to swallow results in accumulation of saliva with the appearance of frothing at the mouth)
Death: paralysis leads to respiratory failure |
|
|
Term
| T/F positive antibody titers for rabies DOES NOT correlate with protection from disease |
|
Definition
TRUE
*** other poorly understood immunologic factors play a role in prevent rabies, DO NOT use positive titers to determine when to booster vaccinations <--- animals should be boostered at least every 3 years for the MLV and every year for the recombinant vaccine (for cats, reduces prevalence of vaccine associated sarcomas) |
|
|
Term
| What protozoal life stage is resistant to chemicals, temperature extremes and can survive outside the host resulting in transmission to new individuals? |
|
Definition
|
|
Term
| What species is the definitive host for Toxoplasma gondii? |
|
Definition
cats
Why is this important?
cats are the only species that can secrete infective oocysts |
|
|
Term
| Which of the protozoal diseases we covered are zoonotic? |
|
Definition
Toxoplasmosis
Babesiosis
Leshmania
Chagas |
|
|
Term
| Although cats are the only species that can shed toxoplasma oocysts in their feces cats do not generally contract the disease from fecal oral exposure. What are the three methods of contracting toxoplasmosis? |
|
Definition
ingestion of an intermediate host <- rodents, birds, livestock (tissue cysts containing bradyzoites)
vertical (transplacental)
fecal-oral |
|
|
Term
| T/F toxoplasma tissue cysts can NEVER be cleared and will remain in an infected individual for life |
|
Definition
|
|
Term
| What clinical signs are associated with initial ingestion of toxoplasma tissue cysts or oocysts? |
|
Definition
most common is subclinical, can have mild diarrhea
**** neonates (transplacental infection) can have a more severe response due to reduced immunocompetence --> overwhelming tachyzoite replication especially affects liver, lungs and CNS |
|
|
Term
| T/F once infected all cats will shed infective toxoplasma oocyts for a maximum of 2 weeks post ingestion (this is occuring when most infected animals are asymptomatic!) |
|
Definition
FALSE
only about 20% of infected cats will shed oocysts |
|
|
Term
| Although older cats are often asypmtomatic when infected with toxoplasma gondii what tissues are most commonly affected by either acute exposure (tachyzoite replication) and recrudescence (bradyzoite release from tissue cysts) in symptomatic cats? |
|
Definition
lungs, CNS, skeletal and cardiac muscle, liver, eyes <-- intracellular growth of ogranism causes necrosis
**** immunosuppression (ex. FIV) is often associated with more severe clinical signs in both adult cats and kittens |
|
|
Term
| What clinical signs are associated with toxoplasma gondii infection in dogs? |
|
Definition
respiratory, GI (associated with acutely decompensating disease in puppies)
neuromuscular (can be the only system affected <-- associated with protracted clinical course in older animals) |
|
|
Term
| reactivation of toxoplasma tissue cysts with subsequent release of bradyzoites is associated with what constellation of clinical signs in cats? in dogs? |
|
Definition
cats --> CNS +/- occular
dogs --> CNS + chronic polymyositis
*** mechanisms of reactivation is unknown but thought to be associated with immunosuppression (remember FIV + toxo = BAD), stress, and/or co-infections |
|
|
Term
| What type of sample is associated with the highest yield of toxoplasma tachyzoites for diagnostic purposes? |
|
Definition
cavitary effusions
*** can also look for them in tissue during acute stages of disease but they are more abundant in effusions |
|
|
Term
| Why is a fecal flotation not especially helpful for diagnosing toxoplasmosis? |
|
Definition
dogs will never shed oocysts
cats only shed oocysts during the first two weeks of infection (most commonly asymptomatic at this point) and only 20% of infected cats will shed oocysts |
|
|
Term
| What is the best way to diagnose toxoplasma gondii? |
|
Definition
serology!
+ IgM indicates active or recent exposure (remember, IgM is the first antibody produced in response to infection)
+ IgG -> chronic or reactivated infections
*** can also run titers on CSF and aqueous humor is suspecting CNS or occular involvement |
|
|
Term
| If testing cats for toxoplasma gondi exposure due to immunosuppressed or pregnant owners what test result offers the greatest sense of safety for the owner? |
|
Definition
| + IgG <-- this means that the cat is NO longer shedding oocysts (if it ever did, only 20% of infected cats shed) and if it does become reinfected it will most certainly NOT shed oocysts at that point <-- so the owner has really no chance of being exposed to infective oocysts from a IgG + cat |
|
|
Term
| If you suspect transplacental toxoplasmosis in a kitten when is the earliest you can confirm infection with serology? |
|
Definition
12 weeks
**** if you test before this serology will be negative due to maternal antibody interference |
|
|
Term
| What is the treatment for toxoplasmosis? What is the expected clinical course following initiation of therapy? |
|
Definition
clindamycin BID ---> suppresses tachyzoite replication and associated cell necrosis ---> patients should show clinical improvement within 24-48 hrs
*** NO therapy can clear tissue cysts |
|
|
Term
| What are some strategies for preventing toxoplasma gondii infection in cats? |
|
Definition
prevent cats from roaming and/or hunting
DO NOT feed raw meet to cats (can destroy cysts by freezing and irradiation) |
|
|
Term
| You can prevent zoonotic fecal-oral transmission of toxoplasma gondi by performing what housekeeping duty? |
|
Definition
clean litterboxes at least every 24 hours
**** although cats may be shedding oocysts, they require 24 hours to sproulate and become infective in the environment |
|
|
Term
| What is the definitive host for neospora? |
|
Definition
dogs
*** natural infection in cats has NOT been reported |
|
|
Term
| How is neospora transmitted? |
|
Definition
ingestion of tissue cysts in intermediate hosts
vetrical (transplacental infection) |
|
|
Term
| What organ systems are primarily affected by neospora? What is the pathophysiology of the lesions? |
|
Definition
primary affects CNS and skeletal muscle
ruptured tissue cysts induce granulometous inflammation --> multifocal CNS abnormalities and myositis |
|
|
Term
| How does neopsora present clinically in transplacentally infected puppies? |
|
Definition
| ascending paralysis and myositis that doesn't respond to therapy --> death from respiratory failure |
|
|
Term
| How do you diagnose neospora antemortem? |
|
Definition
paired serology (>1:50 is positive)
maternal interference in pups up to 32 days of age
*** post mortem can look for tachyoiztes in many tissues (esp. muscle) and cysts in CNS |
|
|
Term
| How can you treat neospora? What is the prognosis? |
|
Definition
clindamycin or sulfadiazine/pyrimethamine (can be used in combo)
response to tx is variable in adults and grave in puppies (if one puppy is affected treat ALL pup is the litter <-- transplacental infection is likely) |
|
|
Term
| What can you do to prevent neospora infections in dogs? |
|
Definition
Do not feed raw meat
Clean up live stock abortive material expediently
keep dogs from defecating near live stock pens or feeders |
|
|
Term
| What are the two most significant species of babesia that infect dogs in the USA? |
|
Definition
B. canis vogeli --> large piroplasm (greyhounds)
B. gibsoni --> small piroplasm (Pit bulls) |
|
|
Term
| How is babesia transmitted? |
|
Definition
| ixodid ticks --> must remain attached to the dog for 2-3 days to transmit the disease |
|
|
Term
| What breeds are at increased risk for contracting babesia? |
|
Definition
greyhounds (B. canis)
Pit Bulls (B. gibsoni)
*** these breeds often have assymptomatic infections and are commonly used as blood donors <-- important to screen ALL blood donors for babesia |
|
|
Term
| What is the pathogenesis of babesia infection? |
|
Definition
parasite replicates within RBC eventually causing that cell to rupture --> clinical signs are similar to IMHA (regenerative anemia, pale/icteric MM, fever etc.)
*** many adult dogs remain subclinical with occasional bouts of disease associated with parasite replication |
|
|
Term
| Because babesia looks so similar to IMHA clinically it is important to distinguish it using what diagnostic test? |
|
Definition
PCR <-- very sensitive, even for subclinical infections (although false negative are possible with very low parasite burden)
*** can also do paired IFAT serology or look for the organism on blood smear (esp. capillary blood - ear tip, nail bed) but PCR is most sensitive test available |
|
|
Term
| What is the treatment for babesiosis? |
|
Definition
Imidocarb (more effective against B. canis than B. gibsoni)
**** SLUD side effects due to anticholinesterase activity (vomiting, diarrhea, salivation, lacrimation, PU) |
|
|
Term
| T/F vaccination is the best way to prevent babesiosis in the USA |
|
Definition
FALSE
**** tick prevention is best method in general, vaccination has been developed in Europe and is only effective against species found there |
|
|
Term
| What species can be infected by cytauxzoon? |
|
Definition
|
|
Term
| How is cytauxzoon transmitted? What is the pathogenesis of disease? |
|
Definition
dermacentor (american dog tick)
tissue phase --> merozoites invade and replicate within mononuclear cells resulting in large schizonts which occlude small vessles --> multiorgan failure and death
erythrocyte phase ---> macrophages rupture and release large numbers of merozoites (remember, they replicated in the macrophages) which now infect RBC --> hemolytic anemia and death |
|
|
Term
| What is the clinical presentation of cytauxzoon in cats? |
|
Definition
| rapid clinical course, signs are associated with specific organ failure and hemolytic anemia --> grave prognosis |
|
|
Term
| How do you diagnose cytauxzoon infection? |
|
Definition
antemortem is challenging, prioplasm in RBC can be confused with other parasites, PCR is sensitive and specific but not widely available
postmortem is relatively easy --> histology will demonstrate schizonts in many tissues (BM, LN, liver, spleen etc.) |
|
|
Term
| What treatment for cytauxzoon has resulted in better survival rates that the traditional therapy (imidocarb --> 20% survival)? |
|
Definition
atovaquone + azithromycin --> 60% survival!
**** much better to prevent the disease with tick control |
|
|
Term
| What species of hepatozoon is present in the US? How is it transmitted? |
|
Definition
Hepatozoon americanum (present in southern US) and transmitted by the gulf coast tick (ambylomma)
*** dogs INGEST infected ticks |
|
|
Term
| What is the pathophysiology of hepatozoonosis? |
|
Definition
dog ingests infected tick (amblyomma) --> sporozoites penetrate gut and invade macrophages which transport organisms to skeletal and cardiac muscle --> onion skin cysts form between myocytes and intermittently rupture --> pyogranulometous myositis
*** chronic infection --> persistent antigenic stimulation --> vasculitis, GN, amyloidosis |
|
|
Term
| What clinical signs are associated with hepatozoon americanum? |
|
Definition
unresponsive fever and hyperesthesia
hind limb ataxia and generalized paresis
mucopurulent occular discharge
***if kidneys are secondarily affected PU/PD |
|
|
Term
| What is the histologic appearance of H. americanum in muscle biopsies? |
|
Definition
'onion skin cysts' <-- forms layers of mucopolysaccharides
+ pyogranulometous myositis (occurs secondary to cyst rupture, happens intermittently so clinical signs may wax and wane) |
|
|
Term
| What laboratory abnormality is highly supportive of H. americanum? |
|
Definition
MARKED neutrophillia (+ marked leukocytosis) and normal CK
*** in association with suggestive clinical signs: pelvic limb ataxia and generalize paresis + unresponsive fever |
|
|
Term
| What radiographic changes can sometimes be appreciated in young dogs infected with H. americanum? |
|
Definition
| periosteal proliferation associated with muscular attachments (resembles HO) |
|
|
Term
| How can you diagnose Hepatazoon americanum? |
|
Definition
muscle biopsy (biceps and semimembranosus) with onion skin tissue cysts (remember, cyst is surrounded by layers of mucopolysaccharides) and pyogranulometous myositis ELISA
*** HO-like lesions on radiographs are supportive |
|
|
Term
| What is the treatment and prognosis for hepatozoon americanum? |
|
Definition
| NSAIDs for pain and fever long term decoquinate (2yrs) can reduce relapses as NO therapy will eliminate tissue cysts *** for all tick borne diseases consider concurrent doxycycline, if they have one tick borne disease they likely have others |
|
|
Term
| What breed is associated with leishmania in the US? |
|
Definition
|
|
Term
| How is leishmania transmitted? |
|
Definition
| promastigotes mature within the female sandfly and are transmitted to dogs during a blood meal --> promastigote transformes into an amastigote within host macrophages which disseminate the organsism throughout the body |
|
|
Term
| What is the pathogenesis of leishmaniasis? |
|
Definition
Most dogs are initially asympotomatic (some can clear inital infection and become clinically resistant)
---> throughout the course of infection T-lymphoid organs are destroyed resulting in progressive immunosuppresion and B cell proliferation --> hyperglobulinemia causes extensive antigen antibody complex deposition --> vasculitis, polyarthritis, uveitis, glomerularnephritis and IMHA/ITP |
|
|
Term
| How do you diagnose leishmania? |
|
Definition
definitive DX via identification of amastigotes on cytology or histopath (difficult)
IFAT serology (>1:64) however, may cross react with trypanosoma (chagas)
PCR to screen asymptomatic animals |
|
|
Term
| How do you treat leishmaniasis? What is the prognosis? |
|
Definition
allopurinaol + pentavalent antimonials-
relapse is common so often need to tx life long
prongosis is based on severity of disease at time of diagnosis as treatment does not resolve ab-ax complex lesions <-- if you can begin treating before this better prognosis |
|
|
Term
| What strategies can be used to help prevent leishmania? |
|
Definition
k9 advantix repels sandflies
deltamethrin impregnated collars also work well |
|
|
Term
| How is chagas disease (trypanosoma cruzi) transmitted? |
|
Definition
| kissing bug defecates at the same time as a blood meal --> dissemination hematogenously within macrophages primarily to cardiac and skeletal muscle |
|
|
Term
| What clinical signs are associated with acute chagas (trypanozoma)? |
|
Definition
| right sided heart failure (trypomastigotes rupture from host cells --> myocardial degeneration and DCM) |
|
|
Term
| How do you diagnose chagas disease? |
|
Definition
identify organisms on cytology of LN or blood
serology (cross reaction with leishmania) |
|
|
Term
| What treatment can be used during the acute phase of chagas disease? |
|
Definition
benzinidazole
*** not effective for chronic stage, euthanasia is recommended due to zoonotic risk of infective blood |
|
|
Term
| When should kittens be vaccinated for rabbies? |
|
Definition
12 weeks
*** maternal antibodies persist up to 12 weeks of age and may neutralize vaccine antigens (glycoprotein) before an active immune response can be incited |
|
|
Term
| Why is Rabies invarriably fatal in unvaccinated animals displaying clinical signs? |
|
Definition
because the rabies virus is not especially cytopathic outside of the CNS little immune response will be illicited during the initial incubation period. Once the virus is in the CNS and causes clinical signs the immune system will begin responding with antibodies, but not quickly enough to neutralize the infection
*** vaccinated animals neutralize the virus quickly during the initial incubation period (at the site of the bite) |
|
|
Term
| What test is used to definitively diagnose rabies? |
|
Definition
| Immunoflorescence antibody test (FAT) on fresh brain tissue |
|
|
Term
| T/F If you are presented with a cat where Rabies is a differential expedient administration of post-exposure vaccine is indicated. |
|
Definition
FALSE
**** Post-exposure vaccination of cats depends on national public health regulations. It is forbidden in many countries and usually not authorised in cases of clinical suspicion. Supportive or specific treatment is ineffective in rabid cats, and treatment is not considered, likewise for public health reasons. |
|
|
Term
| serum neutralization tests are used to assess anti-rabies antibodies in vaccinated animals. Although protection from Rabies virus is multifactorial, what serology value correlates strongly with protection against the virus? |
|
Definition
| cats and dogs with neutralization values higher than 0.5 IU/ml – regardless of the time elapsed since vaccination – have a high probability of surviving a rabies virus infection. |
|
|
Term
| T/F rabies virus can easily be destroyed by sunlight, heat, drying, and antiseptics |
|
Definition
|
|
Term
| Which species is the major vector for rabies in Minnesota? Why? |
|
Definition
Skunks <--
Excrete high quantities of virus in saliva
Prolonged incubation periods and long-term subclinical infections
Very aggressive when signs develop |
|
|
Term
| What factors influence the length of incubation period for rabies? |
|
Definition
Age of bitten
Degree of innervation at the bite site
Distance from bite to spinal cord or brain
Virus variant
Amount of virus inoculated
Post-exposure prophylaxis |
|
|
Term
| What should be the course of action for an animal with up-to-date rabies vaccination that is exposed to Rabies (ie. any bite or scratch from wildlife that cannot be tested and confirmed negative) but presents healthy? |
|
Definition
| re-vaccinate and observe for 45 days --> if the animal becomes sick with Rabies-like symptoms during this period of time report to local health department, euthanize and submit fresh brain tissue for testing |
|
|
Term
| What should be the course of action for an animal that has never received rabies vaccination and becomes exposed to Rabies (ie. any bite or scratch from wildlife that cannot be tested and confirmed negative) but presents healthy? |
|
Definition
| vaccinate and observe for 180 days. If animal becomes sick with rabies-like symptoms during this time period notify local health department, euthanize, and submit fresh brain for testing |
|
|
Term
| What should be the course of action for an animal with up-to-date rabies vaccination that is healthy and WANTED but bites a human? |
|
Definition
DO NOT VACCINATE (vaccine reactions manifest as neurologic signs which can be confused for actual disease)
observe for a 10 day period ---> if the dog bit the human because it was rabid clinical signs would progress over this period ---> if the animal remains healthy it can be released |
|
|
Term
| What should be the course of action for an unwanted animal with unknown Rabies vaccination status that bites a human? |
|
Definition
| notify local health department, euthanize and submit tissue for diagnostics. |
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