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Infectious Disease - Veterinary Internal Medicine > Protozoal disease > Flashcards

Protozoal disease Flashcards

1
Q

List and briefly describe the sensitivity and specificity of the diagnostic tests for giardia infection in dogs and cats

A
  • ELISA
    • Highly sensitive but false negatives can occur
      • Sensitivity of 71.9%
    • Assessment of centrifugal concentration sample also recommended to improve sensitivity
    • 99.6% specific
  • PCR
    • Detects nucleic acid - 97% sensitivity
    • Specificity 85.6%
  • IFA
    • More sensitive but slightly less specific than ELISA
      • Sensitivity 78.6%, Spp 96.9%
    • Requires external laboratory
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2
Q

Describe the treatment options for giardia

A
  • Febendazole: 50 mg/kg PO q 24 hours for 5 days
    • Effective in most cases at reducing oocyst shedding
  • Metronidazole
    • ~ 2/3 of cases will resolve
    • Optimal dose not know
    • 25 mg/kg q 12 has been recommended for 5-7 days
    • Neurotoxicity is a potential complication

No treatments are perfect and reassessment of faeces is required following treatment and especially if clinical signs persist.

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3
Q

Discuss the important measures for preventing Giardia infection in dogs and cats

A
  • The organise is transmitted via the faecal oral route so envirnmental contamination must be limited
    • Cleaning the environment is essential
      • Remove visible organic matter / faeces
      • Dilute bleach
      • Quaternary ammonium products
    • Bathing / decontaminating the pet’s coat
    • Treating all infected animals
    • Prevent re-introduction
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4
Q

Briefly describe the lifecycle of L**eischmania infantum

A
  • Multiple sandfly species are the major vector
    • Phelbotomus
  • The organism - promastigotes live and replicate within the sandfly gut
  • Transmitted to dog during feeding
  • The promastigote replicates within macrophages to form Amastigote
  • Amastigotes are ingested by the sandfly during feeding
  • Amastigotes transform into motile promastigotes within the sandfly gut
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5
Q

Briefly comment on the pathogenesis of L**eishmania infantum

A
  • Local replication in macrophages causes no apparent illness
  • Immune responses (predominantly T cell mediated) may initially clear the infection
  • If not cleared locally, amastigotes cause macrophage rupture and the organism can disseminate
    • Haemolymphoid organs most affected - spleen, liver, bone marrow, lymphoreticular system
  • Latency is common and clinical disease may not manifest for 3 months to 7 years after initial infection
  • Chronic disease is primarily associated with T cell depletion, and Ab producing B cell proliferation
  • Immune mediated diseases and immune complex diseases can be seen - IMT, GN, vasculitis
  • Immune complexe disease activating complement is an important pathological process
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6
Q

List the potential clinical signs in the non-self limiting severe illness causes by Leishmaniasis infantum in dogs

A
  • Visceral and cutaneous disease together in most dogs
  • Essentially a chronic systemic disease that may affect any organ, tissue or body fluid manifested by a plethora of clinical signs
    • Skin lesions
    • Local or generalised lymphadenomegaly
    • Weight loss / Inappetance
    • Exercise intolerance / lethargy
    • Splenomegaly
    • PU/PD
    • Ocular lesions
    • Lameness
    • Vomiting / diarrhoea
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7
Q

List the methods by which a diagnosis of Leishmaniases in a dog may be confirmed

A
  • Clinical signs are highly variable but need a high index of suspicion in endemic areas
  • Microscopic demonstration of the parasite in cytology or histopathology preparations
  • Serology
  • Culture of the organism (special media)
  • Genetic identification testing (PCR)
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8
Q

Describe the common clinical pathological abnormalities in dogs with severe leishmanases

A
  • Hyperglobulinemia (up to 100%)
    • Polyclonal
  • Hypoalbuminemia
  • Proteinuria - commonly present
  • Mild increases in ALKP / ALT
  • Mild azotemia may be present
  • Mild non-regenerative anaemia is frequently found (60-73%)
  • Leucocytosis or leukopenia
  • Thrombocytopathy / IMT
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9
Q

Describe the diagnostic algorithm recommended to confirm a diagnosis of Leishmania infantum infection

A
  • Appropriate clinical signs - highly varied
  • Antibody titre
    • Numerous methods have been developed - ELISA, IFA, in-house tests, direct agglutination, Western blotting
    • A high antibody titre with appropriate clinical signs is confirmatory of disease
  • Low ab titre ⇒ Cytology or histopathology of lesion
    • Organism identified - positive
  • No organism identified ⇒ Need PCR
    • PCR positive confirms Leishmania diagnosis
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10
Q

Briefly discuss the treatment options for Leishmaniases in dogs

A
  • Cure is rare and repeat treatment is the normal
  • Clinical disease can often be resolved
  • Meglumine antimoniate
    • Given SC once daily for 4-8 weeks
  • Allopurinol
    • Metabolises by the organism to produce an inosine analogue that is incorrectly incorporated into proteins
      • Inhibits replication
    • Used in combination with meglumine antimoniate
  • Miltefosine
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11
Q

Describe the etiology of Babesia spp

A
  • Intraerythrocytic protozoan organism
  • Large numbers of genetically distinct Babesia organisms have been described
    • Generally divided into large and small babesia
  • Variable pathogenicity between species
  • The species have often been named based on the vertebrate host
  • They cause haemolytic anaemia, splenomegaly and fever and infection can vary from subclinical to life-threatening
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12
Q

Briefly describe the Babesia spp lifecycle

A
  • The sporozoites develop within the tick vector
  • They enter the host vertebrate during tick feeding
  • The sporozoites attach to the hist RBCs
  • The organism is endocytosed by the host RBC
  • Assexual reproduction within the RBC
    • Merogony can infect new erythrocytes
  • Tick ingests infected RBCs
  • Sexual reproduction in the tick gut with another asexual phase of reproduction in the tick gut epithelial cells
  • Transstadial and transovarial transmission occurs
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13
Q

Briefly describe the transmission of Babesia spp infection

A
  • The majority of transmission around the world is via a tick vector
  • The sexual phase of the life-cycle occurs only within the tick gut
  • Non-vector transmission likely occurs with fighting or via congenital transplacental infection is likely significant
    • This can lead to genetically identical clones
    • May lead to the development of widespread drug resistance
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14
Q

Briefly describe the pathogenesis of anaemia in Babesia spp infection

A
  • Pathogenesis varies widely depending on the babesia species and the host immune response
  • Infected RBCs express pathogen antigens on their surface and may be opsinised for removal
  • Soluble parasite antigens can adhere to RBCs and platelets also triggering immune responses
    • Haemolytic anaemia and thrombocytopenia in this instance does not necessarily allign with the degree of parasitaemia
  • Increased osmotic fragility reduced RBC life-span
  • Parasite may induce oxidative stress in the RBC
  • Lipid peroxidation of the RBC membrane occurs - membrane becomes more stiff
  • Parasite proteases stimulate the kallikrein system inducing fibrinogen life protein formation
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15
Q

Describe the pathogenesis of Babesia spp infection on cells other than the RBC

A
  • Immune mediated thrombocytopenia is common and may be only abnormality
  • Coagulation testing usually remains normal and DIC is uncommon
  • Tissue hypoxia mediates much of the tissue damage
    • anaemia, vascular stasis, shock, increased CO production, damaged Hb, reduced oxygen transport to tissue from Hb
    • Leads to lactic acid production and metabolic acidosis
  • Respiratory alkalosis to compensate for both metabolic acidosis and hypoxemia
  • SIRS, septic shock and MODS can be seen in rare cases
  • Membanoproliferative GN may be seen
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16
Q

Describe the clinical signs in dogs with Babesia spp infection

A
  • Wide degree of clinical severity
  • Fever
  • Haemolytic anaemia
  • Thrombocytopenia
  • Splenomegaly
  • Non-specific signs
    • Lethargy / weakness
    • Waxing and waning signs
    • Anorexia
  • Palour and icterus may be noticed by owners
17
Q

List organs and systems that may be affected by severe complicated babesia infection

Briefly note the changes that may be seen

A
  • Renal
    • AKI may be seen together with proteinuria
  • Neurological
    • Diffuse / widespread non-specific neurological signs
    • Caused by microvascular thrombosis / haemorrhages and sequestration of parasitized RBCs in the capillaries
  • Coagulation
    • Thrombocytopenia is common. DIC is rare
  • Liver
    • Most likely due to transient hypoxia.
    • Inflammation may be relevant also
  • Haemolytic anaemia
    • Hallmark feature is continual haemolysis despite successful antibabesia treatment
  • Lungs - ARDS
    • Common and typically catastrophic
    • Due to widespread microthrombi, hypoxemia and inflammation / oedema
  • Haemoconcentration, hypotension, cardiac arrhythmia, pancreatitis (with severe disease)
18
Q

Describe the common clinical pathological abnormalities present with canine Babesia spp infection

A
  • Thrombocytopenia
  • Haemolytic anaemia
    • The clinical picture is similar to all other causes of haemoytic anaemia (toxin, oxidative damage, IMHA, osmotic damage, microangiopathy)
    • Initially normochromic and normocytic, the anemia becomes macrocytic and hypochromic (regenerative)
  • Auto-agglutination in saline is present in a small number of dogs - ~21% in one study
  • No pathognomonic biochemistry changes
    • Changes relate to complications
    • Elevated bilirubin, liver enzymes, renal parameters may be seen with increased severity
    • Hyperglobulinemia seen with some strains
  • Bilirubinuria and proteinuria +/- haemoglobinuria and rare granular casts on urinalysis
19
Q

Briefly describe the three basic methods utilised to confirm a diagnosis of canine babesiosis

A
  1. Light microscopic examination of a blood smear
    • Highly specific, poorly sensitive
    • Low numbers especially in chronic carriers
  2. Serological testing
    • Indirect detecting of antibodies may be used for screening infected hosts
    • Negative results early in the disease or in very young animals
    • Knowledge of the likely species in the geographical region is essential
  3. Molecular genetic testing - PCR
    • Highly sensitive and specific
    • Broad range testing available - multiple babesia species at once
    • Muliplex testing is also available that detects other tick-borne pathogens
20
Q

Describe the treatment options for Babesia spp infection in dogs

A
  • Imidocarb dipropionate
    • Eliminates B. canis infection
    • Eliminates infectivity of feeding ticks for up to 4 weeks
    • Has protective effect for up to 6 weeks
  • Atovaquone (with fatty meal) and azithromycin
    • Most effective treatment for Babesia gibsonii
    • 80% of dogs reduced to undetectable or sterilised infection
  • Supportive care as necessary
    • Blood products (packed RBCs ideally)
    • IV fluids
    • Oxygen
  • Glucocorticoids
    • Likely to worsen the parasitemia due to suppression of the monocyte macrophage system
21
Q

Briefly describe the aetiology of trichomoniasis in cats

A
  • Spindle to pear shaped highly motile protozoan
  • Exist only as trophozoites (no cysts)
  • Divide by binary fission
  • Transmitted from host to host by direct contact and environmental contamination
  • Tritrichomonas foetus colonises the distal ileum and colon of cats and causes a foul-smelling chronic diarrhoea
  • Prevalence of infection in highest in young pure-bred cats (~ 8 months of age)
  • No clear environmental risks have been identified including proximity to farms, feeding raw meat, outdoor access or water source.
22
Q

What is the usual mechaism of transmission for Tritrichomonas foetus infection in cats?

A
  • Most likely transmitted directly faecal-oral transmission likely in shared litter box arrangements
  • Venereal transmission is not likely based on the absence of the organism in the reproductive tract of cats
  • Venereal transmission occurs in cattle
23
Q

Describe the pathogenesis of Tritrichomonas foetus infection in cats

A
  • Faecal-oral transmission with the resultant infection localising within the distal ileum and colon
  • Diarrhoea is the primary clinical sign due to the following:
    • Interaction with the host bacterial flora
    • adherance to host enterocytes
    • elaboration of cytotoxins and enzymes
  • Infection is associated with a lymphocytic plasmacytic infiltration of the underlying intestinal lamina propria
  • Sub-epithelial invasion is rare
  • Environmental stressors may enhance the susceptibility for infection
24
Q

Describe the clinical findings in cats with Tritrichomonas foetus infection

A
  • Chronic large bowel diarrhoea
  • Waxing and waning course
  • Variable fresh blood in the faeces
  • Illthrift with poor housing and other conditions
  • May see perianal oedema and prolapse in very young cats
25
Q

Descirbe the diagnostic testing options for cats with suspected Tritrichomonas foetus infection

A
  • Faecal smear
    • Insensitive - 14% detection rate in natural infection
    • Can be performed direct (in saline) or after a colonic wash/flush
  • Faecal culture
    • Ideally performed in clinic with TF pouch
      • takes 3-12 days to obtain result dependent of ambient temperature
    • Oragnisms are fragile and they do not survive refrigeration
    • Adhered litter and desication can lead to organism death and false negative culture results
  • Faecal PCR
    • Highly sensitive and specific
    • Not affected by death of organisms in transit to the lab
26
Q

Briefly describe the aetiology of Toxoplasma Gondii

A
  • Obligate intracellular protozoan parasite
  • Can infect virtually all warm-blooded mammals
  • Domestic cats a Felidae are the natural / definitive host
    • Can shed oocysts in the faeces
  • Three infectious stages
    • Oocysts (sporozoites within) in faeces
    • Tachyzoites (actively multiplying stage)
    • Bradyzoites (slowly multiplying stage
      • Tachy- and bradyzoites are found in tissue cysts
  • Three isolates that can cause variable patterns of infection
27
Q

Briefly describe the epidemiology of Toxoplasma gondii infection in dogs and cats

A
  • Increased risk of infection or seropositivity with
    • Age
    • Rural or feral environment
    • Raw meat diet
  • Outbreaks have been associated with contaminated water sources
  • T gondii can survive in seawater and can infect marine mammals
  • Viable in the environment from 4-24° C for 6 months
28
Q

Briefly describe the various modes of transmission for Toxoplasma gondii in dogs and cats

A
  • Transplacental (congenital)
  • Ingestion of infected tissues
    • Tissue cysts present
  • Ingestion of oocyst-contaminated food/water
29
Q

Describe the extra-intestinal life cycle of Toxoplasma gondii that occurs in non-feline hosts

A
  • Ingested oocysts excyst in the small intestine
    • Sporozoites penetrate into the cells of the intestine including through the lamina propria
    • Sporozoites divide and become tachyzoites
  • Tachyzoites can replicate in almost any cell of the body
    • They multiple and eventually encyst
  • Cysts grow intracellularly and contain numerous bradyzoites
  • The cysts are encased by a thin elastic wall and can persist in tissues for the life of the host
    • Muscle, CNS, visceral organs
  • Note: tachyzoites are destroyed by the digestive process
    • Only tissue cysts and oocysts are infective
30
Q

Briefly describe the pathogenesis of Toxoplasma gondii infection in dogs

A
  • Tachyzoites are the rapidly replicating intracellular form.
  • They can cause cell necrosis by growth - no toxin is produced
    • Initial signs are caused by intestinal cell death and infection of the local lymphoid tissues
  • T. Gondii can then spread to distant organs via the blood or lymphatics
    • Brain, liver, lungs, muscle, eye and heart are all potential targets of infection and cyst formation
  • By ~ third week, host immune response clears the tachyzoites and they may encyst as bradyzoites
  • Cysts may rupture with clinical relapse during period of immunosuppression
  • Concominant infection and immunosuppression may increase the incidence of clinically significant infection
31
Q

Describe the findings of routine clinical laboratory tests in dogs and cats with acute Toxoplasma gondii infection

A
  • Non-regenerative anaemia
  • Variable leukocytosis with all cell lines affected
    • Including eosinophils
  • Leukopenia may be seen with severe infection
  • Hypoproteinemia and hypoalbuminemia
  • Marked increases in ALT and AST with acute liver/muscle necrosis +/- bilirubin increase
    • Less frequently seen and to a lesser degree in cats
  • CK increases with muscle involvement
  • Pancreatic lipase may become elevated
  • Cats may develop hypocalcaemia
32
Q

Describe the utility of serological testing for the diagnosis of Toxoplasma gondii infection in cats or dogs

A
  • Once infected, tissue cysts stay with animals for life
  • Long-term humoral responses occur
  • ~30% of dogs and cats in the USA have T gondii Abs
    • Seropositivity increases with age

Indirect fluorescent antibody testing

  • Adapted to detect IgM, IgG, IgA
  • Sensitive but false positives can occur

Agglutination testing

  • Tests IgG which is not elevated during acute infection

ELISA

  • As sensitive as IFA but less specific
  • Can detect IgM, IgG and IgA

Infectious Disease - Veterinary Internal Medicine (9 decks)

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