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
- Highly sensitive but false negatives can occur
- 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
- More sensitive but slightly less specific than ELISA
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.
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
- Cleaning the environment is essential
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
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
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
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)
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
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
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
- Metabolises by the organism to produce an inosine analogue that is incorrectly incorporated into proteins
- Miltefosine
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
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
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
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
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
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
- Light microscopic examination of a blood smear
- Highly specific, poorly sensitive
- Low numbers especially in chronic carriers
- 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
- 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
Descirbe the diagnostic testing options for cats with suspected *Tritrichomonas foetus* infection
* 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
Briefly describe the aetiology of *Toxoplasma Gondii*
* 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
Briefly describe the epidemiology of *Toxoplasma gondii* infection in dogs and cats
* 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
Briefly describe the various modes of transmission for *Toxoplasma gondii* in dogs and cats
* Transplacental (congenital)
* Ingestion of infected tissues
* Tissue cysts present
* Ingestion of oocyst-contaminated food/water
29
Describe the extra-intestinal life cycle of *Toxoplasma gondii* that occurs in non-feline hosts
* 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
Briefly describe the pathogenesis of *Toxoplasma gondii* infection in dogs
* 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
Describe the findings of routine clinical laboratory tests in dogs and cats with acute *Toxoplasma gondii* infection
* 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
Describe the utility of serological testing for the diagnosis of *Toxoplasma gondii* infection in cats or dogs
* 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
