Protozoal Disease Flashcards
Babesia -Transmission and pathogenesis
Spp in Aust
B canis vogeli and B gibsopni found in Aust
Transmitted by Rhipicephalus (and undergo transovarial and transtadial spread in tick)
Transmit after >36H feeding then enter RBC and undergo asexual reproduction until cell lyses then tachyzoites infect other RBC which can suibsequently reinfect tick (where they undergo saexual maturation).
Infected RBC are removed by RES, parasite antigens are incorporated into RBC membrane and also soluble antigens bind non-infected RBC membrane resulting in haemolysis of both. Resulting in positive DAT and spherocytosis as well as agglutination
RBC also become more fragile due to changed viscosity and oxidative damage.
Also causes hypercoagulability (gibsoni) due to activation of kallikrein and sludging of blood in small vessels - inparticular CNS
Clinical findings in Babesiosis
B vogeli - non-regenerative anaemia, leukocytosis
B gibsoni - moderate to severe regenerative anaemia. LN adn spleen enlargement, PLN, neutropaenia
Diagnosis and TReatment of Babesiosis
B vogeli : pairs of protozoa in RBC, increasing IFA Ab titres (need to test specifically for each species) Titre >1:64 thought to be diagnostic
B gibsoni: single small protozoa in RBC
PCR sens/spec is variable only way to differentiate different spp. . Serial sampling is recommended to improve sensitivity if strong suspicion.
Tx imidocarb for B vogeli +/- clinda and diminizene
Atovaquone and azithromycin for B gibsoni.
More difficult to clear this infection so recommend PCR at day 60 and 90 post treatment to confirm.
Treatment of immunocompromised patients needs to be longer, and splenectomised patients have poorer prognosis.
Atovaquone MOA, use
Inhibits protozoal mitochondrial ctyb –> unable to synthesise pyrimidines for DNA synthesis
Used in treatment of Babesia gibsoni
AEs rare/not well studied
Vomiting and allergic reactions reported in people
Imidocarb MOA, indications, AEs
MOA - interferes with protozoal nucleic acid synthesis/metabolism, causes denaturing of DNA. Inhibits cellular repair and replication.
Indication: Babesia vogeli treatment and prophylaxis.
AEs: mild cholinergic effects (salivation, lacrimation, defecation, urination), vomiting, injection site pain.
Toxoplasma Lifecycle and diagnosis
- Bradyzoite cysts are ingested i tissue of intermediate host
- Replicate in the enterocytes of SI and produce large numbers of oocysts
- oocysts shed in faeces for a few weeks, require 1-5d in env to sporulate and become infectious.
- Sporulated oocysts can be ingested in water/soil that is contaminated the tachyzoites emerge from cysts and invade GI mucosa of incidental/target hosts where they can migrate to various tissue (MSK, CNS, liver, lungs predilection) and form bradyzoite cysts which are resistant to immune clearance.
(NB: cats can also ingest oocysts and have this mode of infection as well)
Disease only really occurs in immunocompromised animals such as FIV/FeLV or use of cyclosporine in cats (documented in patients receiving renal transplant)
Disease is also seen in immunocompromised dogs.
Diagnosis - serology IgM to IgG conversion
or 4 fold titre increase
NB: healthy naieve cats also undergo seroconversion
All exposed animals will likely have seropositivity for life
CSF - PCR and Ig assays
Are cats seropositive to toxoplasma a zoonotic risk
No - highly unlikely to be shedding if seropositive.
May shed if become immunosuppressed.
Can do faecal PCR/oocyst on faecal float though has low sensitivity.
Lifecycle of neospora
Oocysts shed by adult dogs, can be for months after infection.
Sporulate rapdily in environment and infect intermediate cattle/herbivore hosts. in GIT tachyzoites enter tissues and encyst as bradyzoites in muscles and viscera as well as crossing placenta and causing abortion.
Transmission back to dog (definitive host) occurs by ingestion of aborted placenta or infected tissues
Tachyzoites can undergo sexual reproduction in DH GIT and continue oocyst shedding
In dogs the tachyzoites can also cross the placenta. Dogs also develop bradyzoite cysts that reactivate in times of stress/immunosuppression resulting in increased tachyzoites -> infection of pups in utero
Pathogenesis and clinical signs of Neospora and diagnostic tests
Pups infected in utero and tachyzoites have predilection for replication in nervous system tissue
Causes ascending paralysis with muscle atrophy and fibrous muscle contracture
CS: high stepping HL gait, urinary incontinence and muscle pain.
May also have signs of infection in other organs: liver, lungs, CNS, heart
In adult dogs reactivation of cysts can occur with immunosuppression (although rare). Present with polymyositis or meningoencephalitis (predilection for cerebellum)
Dx - in pups is based on signalment, CS and demonstration of seroconversion or >1:800 serological titre (may be impeded by maternal Ab or cross reactivity with toxo at low levels)
PCR on tissues or CSF can be performed, but note that subclinical infection can occur.
Histopathology is also used in diagnosis - specialised IHC to differentiate from Toxo.
CSF - mixed inflammatory pleocytosis +/- eosinophilia
Sensitivity and specificity of CK and AST in differentiating protozoal from noninfectious MUO
NPV of both is 99% from recent JVIM study
CK Sens 95; Spec 96
AST Sens 94; Spec 84%
Recommended screening for Neosporosis following disease identified in pup
Dam should not be used for breeding again as no way to clear infection
Perform IFA on littermates and treat those positive.
Protozoal Causes of GI disease in dogs and cats
Giardia - brushborder destruction, hypersecretion of Cl, malabsopprtion, increased intestinal permeability.
Also present in healthy dogs
Isospora - often present in dogs without clinical signs but can cause diarrhoea in young dogs with poor husbandry
Dx on faecal float, large cysts
Tx not normally indicated unless severe infection
Resistant oocysts in env are difficult to disinfect in kennel/breeding situation. Prophylactic treatment of bitch may reduce coccidiosis in offspring
Cryptosporidium - again can be present in healthy dogs. Unclear significance in disease
Highly resistant in environment. Attach to brushborder of enterocytes and may cause disease by combination of malabsorption, and hypersecretion.
PPV of assays to detect infection is low due to high subclinical infection rate.
Tritrichomonas in cats - colonises the ileum and colon causing LP and neutrophilic inflammation. Chronic colitis. Has high prevalence, likely interaction with host biome and immune system play a role in disease development.
Detected on faecal exam of warm sample (die with refrigeration); PCR is most sensitive
Tx is with ronidazole, may resolve on own but can take long time. is emergence of resistance reported.
Only recommended to treat symptomatic cats. May remain asymptomatic shedder/carrier after Tx and intermittent relapses.
May be higher risk of disease in purebred cats
Tests for Giardia and interpretation
Microscopy/faecal float - low sensitivity, intermittent shedding and false positive misclassification of yeasts etc
Faecal immunofluorescence - needs specailised microscope, better than float but still not overly sensitive.
Faecal antigen ELISAs - high Sens and Spec
80 and 90% respectively compared to IFA. PPV of 51% and NPV of 97% in prevalence of 10%
PCR - highly sensitive but need to correlate with clinical signs
Not all dogs/cats with giardia have clinical signs. With treatment dont treat to clear but instead resolve CS. Failed Tx can be resistance to drug used or can mean other underlying disease causing diarrhoea (and giardia is bystander or 2ry)
Exotic Protozoal Diseases (location, vector if any, brief CS)
Hepatozoonosis - H americanum/canis
- transmitted by ixodes tick and dog ingestion of infected tick
- Rhipicephalus for americanum, Amblyoma for canis
- sporozoites infect macrophages and endothelial cells in liver, spleen, muscle, lungs and cause pyogranulomatous inflammation
+/- type III GN or amyloidosis
- disease most common in pups: anaemia and hyperaesthesia. Can be asymptomatic adults for H canis, H americanum much more pathogenic
- Dx with serology 93% sens, 96% spec
PCR on blood also used
- No Tx eliminates cyst stage of H americanum
Imidocarb for H canis
Leishmaniasis - transmitted by sandfly in Brazil, Africa, India, Europe
Dermatological and visceral lesions (LN, spleen). Causes a hyperglobulinemia and secondary HVS
Intracellular organism can cause severe immune response resulting in IMPA and ICGN
Dx - most dogs develop adequate CMI to infection, appears to be genetic basis for disease development.
Serology is strongly supportive of Dx. Cytology has reasonable sensitivity and high specificity
PCR on BM, LN spleen.
Tx limited options: allopurinol + meglumine antimoniate. Rarely curative.
Domestic cats may be a reservoir for L infantatum and this is spreading in Italy
Cytauxzoonosis - America and Europe cats
Cats are incidental host, commonly causes death.
- Dermacentor tick IH and Bobcat DH
- infect macrophages that line the veins then infect RBCs. Blood flow is obstructed by infiltrates and thrombosis leads to multiorgan failure.
- Rapid clinical progression, can occur prior to piroplasm appearance in RBC (can also look in LNs and spleen). PCR assay is most sensitive
Tx Atovaquone and azithromycin - up to 60% survival if given early in disease. Survivors remain carriers
