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Small Animal Medicine > Protozoal Diseases > Flashcards

Protozoal Diseases Flashcards

1
Q

What causes Toxoplasmosis? What is the intermediate and definitive host?

A

Toxoplasma gondii

mice, people, birds, fish

any felid/cat - only ones able to complete the life cycle

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2
Q

What life cycle of Toxoplasma is seen only in cats? How does it occur?

A

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)

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3
Q

What is the extraintestinal life cycle of Toxoplasma like? What does this result in?

A
  • 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

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4
Q

How is Toxoplasma transmitted? Cats especially?

A

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

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5
Q

How do sporulated oocysts and bradyzoites of Toxoplasma persist?

A

survive in the environment for months to years and are resistant to most disinfectants

may persist in tissues for the life of the host

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6
Q

What happens following Toxoplasma infection? What 2 stages are seen?

A

spread to any organs

  1. ACUTE - rarely fatal (unless immunocompromised)
  2. CHRONIC - body mounts an immune response and wall off bradyzoites into cysts (prefer skeletal muscle, myocardium, visceral organs, and CNS)
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7
Q

What does severity of Toxoplasma infection depend on?

A

location and degree of tissue injury

  • often associated with FIP, FIV, FeLV, CDV, and steroids
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8
Q

What is the most common protozoan to infect the CNS? What signalment is most commonly affected?

A

Toxoplasma —> nonsuppurative, focal or multifocal meningoencephalitis

male cats and young or immunocompromised animals that develop overwhelming intracellular replication of tachyzoites after primary infection

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9
Q

What are the most common clinical signs associated with Toxoplasmosis?

A
  • uveitis common incats
  • pneumonia, dyspnea —> diffuse interstitial to alveolar patterns, pleural effusion
  • neuro signs

other signs reflect necrosis in major organs

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10
Q

What signs are most commonly associated with rapid courses of Toxoplasmosis? What is seen with chronic disease?

A

respiratory and CNS disease

lifelong immunity possible, but recrudescence can occur with immunosuppression, which results in CNS disease, pneumonia, or pancreatitis

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11
Q

What is the best test for diagnosing Toxoplasmosis? What lab result is commonly elevated caused by bradyzoites?

A

antibodies can be found in normal animals since organism cannot be cleared —> IgM will be higher than IgG with recent infection

CK, AST

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12
Q

What are 3 other options for diagnosing Toxoplasmosis?

A
  1. FECAL - only able to be seen in cats, as dogs do not shed oocysts
  2. HISTOPATH - tachyzoites in infected tissues
  3. 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

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13
Q

What results are expected on serology with Toxoplasmosis?

A

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)

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14
Q

What treatment is recommended for Toxoplasmosis? What are some alternates?

A

Clindamycin, discontinue any immunosuppressive drugs

  • pyrimethamine + sulfonamide, TMS
  • Azithromycin
  • TMS may get to CNS better
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15
Q

What follow-up is recommended for patients with Toxoplasmosis?

A
  • 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

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16
Q

How can Toxoplasmosis be prevented?

A
  • 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

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17
Q

What is the definitive host of Neospora caninum? Intermediate hosts?

A

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

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18
Q

What dogs are at higher risk of being infected by Neospora caninum?

A

those living amongst cattle —> farms, ranches, hunting dogs

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19
Q

How are most puppies infected by Neospora? What signs predominate? What is seen in the terminal stages?

A

congenitally —> vertical!

  • neurologic: multifocal CNS disease, LMN ascending paralysis
  • muscular: rigid hyperextension, incontinence

cervical weakness and dysphagia

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20
Q

How are older dogs most commonly infected by Neospora? What signs are most commonly seen?

A

recrudescence from cyst rupture, especially during pregnancy, stress, or immunosuppression

CNS involvement = seizures, tremors, myositis + myocarditits, dermatitis

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21
Q

What is the best diagnostic for Neospora?

A

SEROLOGY —> high IgM + expect 4 fold increase, early infection can cause false negatives, no cross-reactivity with Toxoplasmosis

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22
Q

What is treatment for Neospora like? What is used?

A

often ineffective —> improvement commonly partial or temporary, poor prognosis with muscle contracture

Clindamycin for at least 2 weeks after clinical signs plateau

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23
Q

What is the main difference between Neospora and Toxoplasma? How can it be prevented?

A

no zoonosis

prevent dog-cattle interactions, where the dog could eat cysts in placenta or aborted fetuses

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24
Q

What type of diseases are most commonly seen with Leishmania? What is the primary mode of transmission?

A

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

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25
Q

What increases risk of developing Leishmania?

A
  • outdoor living
  • high mean humidity
  • low mean wind speed
  • high total annual rainfall
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26
Q

If the USA is not an endemic area, why are cases of Leishmania rising?

A

dogs and cats are frequently imported to the USA from all areas of the world and are not screened for Leishmania

  • Iraq, Afghanistan, Mediterranean
27
Q

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?

A

non-vector transmission can occur over many generations

  • transplacental
  • transmammary
  • sexual transmission
  • blood transfusions, shared needles
  • bites/wounds associated with mixing blood
28
Q

What is the characteristic sign of Leishmania in dogs?

A

skin lesions around noses/eyes and hyperkeratosis of paw pads

29
Q

What is the pathogenesis of Leishmania? What are the most common clinical signs?

A

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
30
Q

Leishmania:

A
31
Q

Leishmania:

A
32
Q

What unique laboratory results are seen with Leishmania?

A

CBC - thrombocytopenia

CHEM - hyperglobulinemia (polyclonal gammopathy), hypoalbuminemia, renal azotemia, proteinuria

(very common findings for any chronic inflammatory disease)

33
Q

What is the ideal diagnosis for Leishmania? What is not commonly used?

A

antibodies able to differentiate exposure vs. infection, monitor titers

PCR - does not circulate in large numbers in the serum

34
Q

What 3 treatments are recommended for Leishmania?

A
  1. Allopurinol - static
  2. Meglumine antimoniate +/- Allopurinol - injection
  3. 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

35
Q

Is Leishmania zoonotic?

A

yes, but must have sandfly vector, which is uncommon in the USA

36
Q

What 3 species cause Babesia? What is implicated for transmission?

A
  1. B. canis = dogs
  2. B. felis = cats
  3. 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

37
Q

How does Babesia cause disease? What is illness dependent on?

A

merozoites (piroplasms) infect RBCs (intracytoplasmic)

severity and rate of development of anemia, strain of organism and age/breed of dog, immune status

38
Q

How does Babesia cause anemia?

A

immune-mediated hemolysis and direct piroplasm damage to RBCs —> intravascular hemolusis

  • reproduction and multiplication causes clinical signs
39
Q

What are the 3 mods of transmission of Babesia?

A
  1. tick
  2. transplacental
  3. blood transfusion or transfer (dog bites)
40
Q

What 2 breeds of dogs are overrepresented for developing Babesia?

A
  1. Greyhounds (B. canis)
  2. Pit Bulls (B. gibsoni)
41
Q

Other than anemia, what other sign is indicative of Babesia infection? What are 3 causes?

A

thrombocytopenia

  1. immune-mediated platelet destruction
  2. platelet sequestration in the spleen
  3. DIC
42
Q

What complications are associated with Babesia infection? In what patients is infection more severe?

A
  • acute renal failure
  • hepatic disease
  • pancreatitis
  • coagulopathies
  • pulmonary edema
  • neurological abnormalities
  • DIC, IMHA

splenectomized or asplenic patients

43
Q

What are the most common signs of Babesia?

A
  • 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

44
Q

What is seen on blood smears in patients with Babesia?

A

stained with modified Wrights stain, better to use blood collected from ear tip

  • large = B. canis
  • small = B. gibsoni
45
Q

How is Babesia diagnosed?

A
  • 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
46
Q

What supportive treatment is recommended for Babesia? How are the different species treated? What is not commonly recommended?

A

blood transfusion and aggressive fluid therapy

  • B. canis = Imidocarb (painful injection)
  • B. gibsoni = Azithromycin and Atovaquone

prednisone - can worsen things

47
Q

What species is responsible for severe cases of canine hepatozoonosis? How is it transmitted?

A

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)

48
Q

What dogs are most at risk for developing hepatozoonosis?

A

hunting, rural, and outdoor dogs

49
Q

What is the pathogenesis of Hepatozoon americanum? What does clinical disease result from?

A

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

50
Q

What are the most common signs associated with Hepatozoonosis?

A
  • 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
51
Q

What is the most common red flag on CBC in cases of Hepatozoonosis?

A

severe neutrophilic leukocytosis (20000-200000) and a left shift —> most inflammatory protozoan

(+ chronic, nonregenerative anemia due to chronic infection)

52
Q

How does the periosteal involvement of Hepatozoonosis affect biochemistry results?

A

increased ALKP

53
Q

What is characteristic of Hepatozoon americanum infection on histopathology? What definitive diagnostic is used? 2 others?

A

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

54
Q

What is treatment like for Hepatozoonosis?

A

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
55
Q

How is Heptaozoonosis prevented?

A
  • aggressive tick control measures to prevent reinfection of susceptible dogs
  • prevent dogs from hunting and ingesting prey in high-risk areas
56
Q

What is Cytauxoonosis? Where in the USA is it most commonly seen? What are the 2 most common vectors?

A

Bobcat fever caused by Cytauxzoon felis (usually fatal!)

south and central USA

Dermacentor variabilis (American dog tick) or Amblyomma americanum (Lone Star)

57
Q

What is the pathogenesis of Cytauxoonosis? What does this result in?

A

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

58
Q

What are the most common signs of Cytauxoonosis?

A
  • 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

59
Q

How is Cytauxoonosis diagnosed?

A
  • suspected in moribund cats in endemic areas
  • blood smear: piroplasms in RBC phase
  • PCR
  • postmortem pathology
60
Q

What treatments have success reported in treating Cytauxoonosis?

A
  • Atovaquone + Azithromycin
  • Diminazeneacetate
  • Imidocarb
  • aggressive treatment for DIC - fluids, heparin, plasma
61
Q

What causes Trypanosomiasis (Chagas’ disease)? What vector is responsible for transmission?

A

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)

62
Q

What is characteristic of Trypanosomiasis (Chagas’ disease)? How is it diagnosed?

A

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

63
Q

What may have some use for treating Trypanosomiasis (Chagas’ disease)?

A

NONE APPROVED FOR COMPLETE TREATMENT

  • Allopurinol = static
  • glucocorticoids may improve survival
  • treat arrhythmias and heart failure as indicated

Small Animal Medicine (52 decks)

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