Protozoal Diseases Flashcards
What causes Toxoplasmosis? What is the intermediate and definitive host?
Toxoplasma gondii
mice, people, birds, fish
any felid/cat - only ones able to complete the life cycle
What life cycle of Toxoplasma is seen only in cats? How does it occur?
enteroepithelial life cycle
- bradyzoites are released into the stomach and GI from ingested tissue cysts
- oocysts form and are shed in the feces for 1-3 weeks
- oocysts are infective in the feces once they have been in the environment for 1-5 days —> MUST clean litter boxes on day one of feces release
(clinical disease with this lifecycle is rare)
What is the extraintestinal life cycle of Toxoplasma like? What does this result in?
- sporozoites from feces or bradyzoites in tissue cysts are ingested
- tachyzoites develop and disseminate into the blood or lymph during active infection
- bradyzoites develop as the host immune response attenuates tachyzoite replication
tissue cysts form readily int the CNS, muscles, and visceral organs, where they typically remain dormant and become infective if eaten
How is Toxoplasma transmitted? Cats especially?
ingestion of any of the 3 life stages of the organism or transplacentally
not coprophagic - ingest bradyzoites during carnivorous feeding and shed oocysts in feces from 3-21 days
How do sporulated oocysts and bradyzoites of Toxoplasma persist?
survive in the environment for months to years and are resistant to most disinfectants
may persist in tissues for the life of the host
What happens following Toxoplasma infection? What 2 stages are seen?
spread to any organs
- ACUTE - rarely fatal (unless immunocompromised)
- CHRONIC - body mounts an immune response and wall off bradyzoites into cysts (prefer skeletal muscle, myocardium, visceral organs, and CNS)
What does severity of Toxoplasma infection depend on?
location and degree of tissue injury
- often associated with FIP, FIV, FeLV, CDV, and steroids
What is the most common protozoan to infect the CNS? What signalment is most commonly affected?
Toxoplasma —> nonsuppurative, focal or multifocal meningoencephalitis
male cats and young or immunocompromised animals that develop overwhelming intracellular replication of tachyzoites after primary infection
What are the most common clinical signs associated with Toxoplasmosis?
- uveitis common incats
- pneumonia, dyspnea —> diffuse interstitial to alveolar patterns, pleural effusion
- neuro signs
other signs reflect necrosis in major organs
What signs are most commonly associated with rapid courses of Toxoplasmosis? What is seen with chronic disease?
respiratory and CNS disease
lifelong immunity possible, but recrudescence can occur with immunosuppression, which results in CNS disease, pneumonia, or pancreatitis
What is the best test for diagnosing Toxoplasmosis? What lab result is commonly elevated caused by bradyzoites?
antibodies can be found in normal animals since organism cannot be cleared —> IgM will be higher than IgG with recent infection
CK, AST
What are 3 other options for diagnosing Toxoplasmosis?
- FECAL - only able to be seen in cats, as dogs do not shed oocysts
- HISTOPATH - tachyzoites in infected tissues
- PCR - most reliable for definitive diagnosis, uses feces, tissues, CSF, aqueous humor, and respiratory secretions
blood causes false negatives, as the organism does not live in blood
What results are expected on serology with Toxoplasmosis?
high IgM with recent infections —> expect > 1:64-256 with active infection
high IgG with prior infection/exposure —> begins to rise 2 weeks following infection and persists for 3-6 months or more (most cats will be IgG+ for life)
(single high titer is not diagnostic, must show a 4 fold increase over 3 weeks)
What treatment is recommended for Toxoplasmosis? What are some alternates?
Clindamycin, discontinue any immunosuppressive drugs
- pyrimethamine + sulfonamide, TMS
- Azithromycin
- TMS may get to CNS better
What follow-up is recommended for patients with Toxoplasmosis?
- signs should resolve within 2 days of antibiotic treatment —> uveitis resolves in a week, neuro signs should resolve in 2 weeks
- EXAMINE 2 weeks into antibiotic treatment, if signs are gone, discontinue
PROGNOSIS is guarded in cats with signs still present after 2 weeks
How can Toxoplasmosis be prevented?
- prevent cats (and people!) from eating raw meat or vectors (cockroaches, flies)
- prevent cats from roaming to hunt prey
- pick up feces from litter box within 24 hours
healthy cats with positive IgG titer will not shed oocysts
What is the definitive host of Neospora caninum? Intermediate hosts?
dogs —> shed oocysts in feces/urine into water after ingestion of infected bovine placental tissue (vertical transmission possible!) and tissue from infected deer - able to complete the lifecycle
cattle, sheep, goats, horses, cats
What dogs are at higher risk of being infected by Neospora caninum?
those living amongst cattle —> farms, ranches, hunting dogs
How are most puppies infected by Neospora? What signs predominate? What is seen in the terminal stages?
congenitally —> vertical!
- neurologic: multifocal CNS disease, LMN ascending paralysis
- muscular: rigid hyperextension, incontinence
cervical weakness and dysphagia
How are older dogs most commonly infected by Neospora? What signs are most commonly seen?
recrudescence from cyst rupture, especially during pregnancy, stress, or immunosuppression
CNS involvement = seizures, tremors, myositis + myocarditits, dermatitis
What is the best diagnostic for Neospora?
SEROLOGY —> high IgM + expect 4 fold increase, early infection can cause false negatives, no cross-reactivity with Toxoplasmosis
What is treatment for Neospora like? What is used?
often ineffective —> improvement commonly partial or temporary, poor prognosis with muscle contracture
Clindamycin for at least 2 weeks after clinical signs plateau
What is the main difference between Neospora and Toxoplasma? How can it be prevented?
no zoonosis
prevent dog-cattle interactions, where the dog could eat cysts in placenta or aborted fetuses
What type of diseases are most commonly seen with Leishmania? What is the primary mode of transmission?
visceral, cutaneous (cat), mucocutaneous —> all 3 seen in dogs
certain female phlebotomine sand flies, most commonly found in tropical and subtropical environments —> affected areas tend to be remote and have limited resources for treatment
What increases risk of developing Leishmania?
- outdoor living
- high mean humidity
- low mean wind speed
- high total annual rainfall
If the USA is not an endemic area, why are cases of Leishmania rising?
dogs and cats are frequently imported to the USA from all areas of the world and are not screened for Leishmania
- Iraq, Afghanistan, Mediterranean
An outbreak of Leishmania was found in a breeding kennel of Foxhounds in the USA. At this point, autochthonous (native) leishmaniasis has not been reported in dogs, other animals, or humans. What was learned from this?
non-vector transmission can occur over many generations
- transplacental
- transmammary
- sexual transmission
- blood transfusions, shared needles
- bites/wounds associated with mixing blood
What is the characteristic sign of Leishmania in dogs?
skin lesions around noses/eyes and hyperkeratosis of paw pads
What is the pathogenesis of Leishmania? What are the most common clinical signs?
chronic inflammatory changes and immune complexes —> affinity for macrophages, immune complexes cause changes in vessels and kidneys
- papular dermatitis and ulcerations where flies bite, most commonly the nasal planum, ears, footpads, bony prominences, and mucocutaneous junctions
- generalized lymphadenomegaly
- polyarthropathy - joint swelling, pain
- splenomegaly
Leishmania:
Leishmania:
What unique laboratory results are seen with Leishmania?
CBC - thrombocytopenia
CHEM - hyperglobulinemia (polyclonal gammopathy), hypoalbuminemia, renal azotemia, proteinuria
(very common findings for any chronic inflammatory disease)
What is the ideal diagnosis for Leishmania? What is not commonly used?
antibodies able to differentiate exposure vs. infection, monitor titers
PCR - does not circulate in large numbers in the serum
What 3 treatments are recommended for Leishmania?
- Allopurinol - static
- Meglumine antimoniate +/- Allopurinol - injection
- Miltefosine impavido +/- Allopurinol - capsule, kills a lot of organisms (not all!)
treatment commonly needs to be repeated, since its not curable and symptoms commonly return
Is Leishmania zoonotic?
yes, but must have sandfly vector, which is uncommon in the USA
What 3 species cause Babesia? What is implicated for transmission?
- B. canis = dogs
- B. felis = cats
- B. gibsoni = dogs in most countries of the world (most common in the USA, but rarely causes clinical disease)
TICKS - Rhipicephalus, Ixodes, Dermacentor, Haemaphysalis, Hyalomma —> R. sanguineus most common in the USA
How does Babesia cause disease? What is illness dependent on?
merozoites (piroplasms) infect RBCs (intracytoplasmic)
severity and rate of development of anemia, strain of organism and age/breed of dog, immune status
How does Babesia cause anemia?
immune-mediated hemolysis and direct piroplasm damage to RBCs —> intravascular hemolusis
- reproduction and multiplication causes clinical signs
What are the 3 mods of transmission of Babesia?
- tick
- transplacental
- blood transfusion or transfer (dog bites)
What 2 breeds of dogs are overrepresented for developing Babesia?
- Greyhounds (B. canis)
- Pit Bulls (B. gibsoni)
Other than anemia, what other sign is indicative of Babesia infection? What are 3 causes?
thrombocytopenia
- immune-mediated platelet destruction
- platelet sequestration in the spleen
- DIC
What complications are associated with Babesia infection? In what patients is infection more severe?
- acute renal failure
- hepatic disease
- pancreatitis
- coagulopathies
- pulmonary edema
- neurological abnormalities
- DIC, IMHA
splenectomized or asplenic patients
What are the most common signs of Babesia?
- lethargy, anorexia, weight loss, fever
- pale MM, tachycardia/pnea
- icterus (hemolysis)
- petechiation
- azotemia
- hemoglobinemia/uria
- hyperbilirubinemia
- hyperglobinemia
- increased liver enzymes from anemia/hypoxia
REGENERATIVE ANEMIA, mild to severe
glucocorticoids and splenectomies can activate chronic disease
What is seen on blood smears in patients with Babesia?
stained with modified Wrights stain, better to use blood collected from ear tip
- large = B. canis
- small = B. gibsoni
How is Babesia diagnosed?
- cytology of peripheral blood to identify organisms (definitive)
- serology (IFA) - false negatives in young dogs common
- PCR on EDTA blood can differentiate between species (most sensitive)
- Coombs’ test - will need to distinguish from IMHA
What supportive treatment is recommended for Babesia? How are the different species treated? What is not commonly recommended?
blood transfusion and aggressive fluid therapy
- B. canis = Imidocarb (painful injection)
- B. gibsoni = Azithromycin and Atovaquone
prednisone - can worsen things
What species is responsible for severe cases of canine hepatozoonosis? How is it transmitted?
H. americanum
Amblyomma maculatum tick (Gulf Coast) ingests the organism from an infected dog during a blood meal and another tick ingests the infected tick, which releases sporozoites
(dogs ingesting tick infected carcasses)
What dogs are most at risk for developing hepatozoonosis?
hunting, rural, and outdoor dogs
What is the pathogenesis of Hepatozoon americanum? What does clinical disease result from?
after the dog ingests an infected tick, sporozoites are released and infect mononuclear phagocytes and endothelial cells of the spleen, liver, muscle, lungs, and BM —> ultimately form cysts in skeletal muscle > cardiac
chronic infection causes pyogranulomatous inflammation, glomerulonephritis, or amyloidosis secondary to immune-complex disease
What are the most common signs associated with Hepatozoonosis?
- fever
- inflammatory reactions directed at tissue phases in skeletal muscle result in periosteal reactions (not seen in the skull)
- osteoproliferative lesions and myositis cause gait abnormalities
What is the most common red flag on CBC in cases of Hepatozoonosis?
severe neutrophilic leukocytosis (20000-200000) and a left shift —> most inflammatory protozoan
(+ chronic, nonregenerative anemia due to chronic infection)
How does the periosteal involvement of Hepatozoonosis affect biochemistry results?
increased ALKP
What is characteristic of Hepatozoon americanum infection on histopathology? What definitive diagnostic is used? 2 others?
large, onion skin cyst, which provides protection from host’s immune system
identification of gamonts in neutrophils or monocytes in specially stained blood smears or demonstration of organism on muscle biopsies
serum antibodies against H. americanun or PCR from blood
What is treatment like for Hepatozoonosis?
clinical signs can resolve with drug therapy, but no therapeutic regimen has been shown to eliminate the organism from tissue
- TMS
- Pyrimethamine
- Clindamycin
- Decoquinate
- Imidocarb dipropionate
- NSAIDs and antiinflammatories to lessen discomfort
How is Heptaozoonosis prevented?
- aggressive tick control measures to prevent reinfection of susceptible dogs
- prevent dogs from hunting and ingesting prey in high-risk areas
What is Cytauxoonosis? Where in the USA is it most commonly seen? What are the 2 most common vectors?
Bobcat fever caused by Cytauxzoon felis (usually fatal!)
south and central USA
Dermacentor variabilis (American dog tick) or Amblyomma americanum (Lone Star)
What is the pathogenesis of Cytauxoonosis? What does this result in?
infects macrophages, which line the lumen of veins throughout the body and merozoites are eventually released and infect RBCs
occludes venules within the liver, brain, spleen, lungs, and LNs —> clinical disease results from blood flow obstruction and hemolytic anemia
What are the most common signs of Cytauxoonosis?
- venous congestion with secondary ischemia
- extravascular hemolysis - icterus
- organ failure
- release of pro-inflammatory mediators
- DIC
- fever, lethargy, pale MM
must be differentiatef from other causes of acute anemia in cats, like Mycoplasma haemofelis
clinical disease is short and typically results in death
How is Cytauxoonosis diagnosed?
- suspected in moribund cats in endemic areas
- blood smear: piroplasms in RBC phase
- PCR
- postmortem pathology
What treatments have success reported in treating Cytauxoonosis?
- Atovaquone + Azithromycin
- Diminazeneacetate
- Imidocarb
- aggressive treatment for DIC - fluids, heparin, plasma
What causes Trypanosomiasis (Chagas’ disease)? What vector is responsible for transmission?
Trypanosoma cruzi, primarily seen in Southern USA and Central America, with rising numbers in Texas
kissing bugs pass the parasite to the host by biting and then defecating near the site
(+ ingestion of the vector, rare through blood transfusion and shared needles)
What is characteristic of Trypanosomiasis (Chagas’ disease)? How is it diagnosed?
acute myocarditis with progression to DCM in dogs that is not expected —> acute onset murmurs and right sided CHF
finding organism on cytology, serology, or PCR —> LN aspirates or effusions
What may have some use for treating Trypanosomiasis (Chagas’ disease)?
NONE APPROVED FOR COMPLETE TREATMENT
- Allopurinol = static
- glucocorticoids may improve survival
- treat arrhythmias and heart failure as indicated
