condensed protozoal diseases Flashcards
what is the etiology of toxo
Obligate intracellular coccidian parasite; infects virtually all sp of warm-blooded animals incl ppl
Domestic cats and other Felidae = definitive hosts → excrete oocysts in feces
All nonfeline hosts = intermediate hosts → harbor tissue cysts
what are the rule of 3’s for toxo
3 infectious stages
- Sporozoites in oocysts
- Tachyzoites (actively multiplying stage) - found in tissue
- Bradyzoites (slowly multiply stage) enclosed in tissue cysts
3 modes of transmitin
- Congenital infection
- Ingested of infected tissues
- Ingestion of oocyst-contaminated food or water
there are minor modes of transmission which are more improtant in human med
- Lactational
- Tranfusion of body fluids
- Transplantation of tissues or organs
summarise toxo life cycle?
Enteroepithelial life cycle:
Found only in the definitive feline host
Ingest infected int hosts → bradyzoites released in stomach and intestine → penetrate epithelial cells of SI and initiate the 5 types of predetermined asexual stages (A-E) → micro (male) and macro (female) gamonts formed → fertilization → oocyst → passed unspurulated in feces (uninfective) → exposure to room air and moisture 1-5 d → sporulate → sporozoites = infectious form of oocyst
Extraintestinal life cycle:
Same for all hosts (dog, rodent, cat, humans, etc.)
Ingest oocyst → sporozoites excyst in lumen of SI and penetrate intestinal cells (incl in lamina propria) → divide into 2 via asexual process (endodyogeny), become tachyzoites → multiply in almost any cell in body → cell ruptures → infects new cells OR multiply and eventually encyst (as bradyzoites)
Tissue cysts form in CNS, muscles, visceral organs - probably persist for life of host
Congenital transmission:
Parasitemia during pregnancy → placentitis → spread of tachyzoites to fetus
Humans and sheep; rare in dogs
Kittens born to infected queens become infected transplacentally or via suckling as tachyzoites shed in milk
May predispose to development of ocular toxoplasmosis
Clinical illness common’ some newborns shed oocyst
what is the clinical pathological findings for toxo in catS?
pretty much everything.
Weird things are;
- Neuro ->circling, behavior changes, seizures, twitching, tremors
- Ocular -> retinochoroiditis, retinal hemorrhages; optic neuritis; optic nerve atrophy; anisocoria; blindness; anterior uveitis, aqueous flare, hyphema, elvety iris; glaucoma; lens lux; retinal detachment
- neonatal -> stillbirth; fading kittens; organ dysfunction (liver: hepatomegaly, icterus, ascites; lung: dyspnea; CNS: sleep, crying)
- Arthritis; Arthritis, joint pain, shifting leg lameness
otherwise every other symptom known to man including icterus and abd effusion
what are toxo clinical signs with dogs?
CS may be resp, neuromuscular, GI, or generalized
Neuro form may last for several weeks
Generalized seen mostly in younger than 1 yr old dogs → fever, tonsillitis, dyspnea, diarrhea, vomiting
Myocardial involvement - subclinical (usually)
Occasionally dermatitis in immunosuppressed
Most dramatic CS in older dogs:
Neural and muscular systems
Seroprevalence in dogs w/polyradiculoneuritis for T. gondii = 55.8% vs control dogs (11.4%)
Clinically similar to neosporosis
Few reports of ocular lesions:
- Retinitis
- Anterior uveitis
- Iridocyclitis
- Ciliary epithelium hyperplasia
- Optic nerve neuritis
on histopath of dogs and cats infected with toxo, where are necrotic lesions most commonly found?
Cat
Necrosis predominantly in liver, mesenteric LNs, pancreas, and lungs
Dog
Necrosis = predom lesion; particularly in brain, lung, liver, mesenteric LNs; pulmonic lesions and enlarged/necrotic bronchial LNs; also see in pancreas, liver, kidneys, spleen
How do you diagnose toxoplasmosis
Tentative antemortem diagnosis if:
Serologic evidence exists of recent or active infection:
- high IgM titers, or 4x or >, incr or decr, IgG or other antibody titers (after treatment or recovery, or both)
- + other causes of CS excluded
- + beneficial clinical response to medications
How do you treat toxoplasma?
Clindamycin = drug of choice (BID for 4 weeks)
Drugs not effective at completely killing parasite -> suppress replication
How do you prevent toxo?
- Limit access of cats to hunting
- Feed commercial dry or canned food, not raw
- No vaccine commercially available currently
- Change litter boxes daily
- Unsporulated oocysts can survive at least 11 weeks at refrigerated temperatures so chilled meat is no protection
where is toxo the most prevalent in the USA
Highest seroprevalence in warm, moist, or tropical climates; lowest in arid and frigid regions
USA: highest in East and Appalachian Mountain region; lowest in SW arid regions and NW mountain regions
What is the etiology of neospora?
Neospora caninum
Protozoa (apicomplexa)
- Tachyzoites and tissue cysts resemble T. gondii under light microscope
- Definitive hosts: domestic dog, wild canids (coyote, Australian dingo) → shed oocysts after ingestion of infected tiss; red fox and wolf not confirmed
- Short shedding period (but up to 4 mos); few numbers
- Cats NOT def hosts → do not shed oocysts after consuming bradyzoites
- Herbivores become infected by eating oocysts shed by def hosts or by subclinical congenital infection (transplacental transmission; ingestion of milk by neonates)
Wild animal int hosts: white-tailed deer; water buffalo - Domesticated int hosts: cattle; sheep
Pups shed more oocysts vs adults; lower number shed on subsequent rechallenge/re-exposure - Naturally infected dogs: predominant route of transmission = transplacental
what is the pathogenesis of neospora
- Tachyzoites found w/in macrophages, PMN, spinal fluid, neural and other cells in body
- Cell necrosis after rapid intracellular replication of tachyzoites
- Widespread dissemination to many organs in acute phase; subsequent restriction by host’s immune response; to neural and muscular tiss in more chronically affected
- Nonseptate tissue cysts primarily in neural cells (brain, SC, peripheral nerves, retina); and occasionally in muscle
in what populations is neospora most commonly found?
Maintained in nature via sylvatic life cycle - wild canids and herbivores
Breed predilection(?) - GSHP, Labs, Boxers, Foldens, Bassets, Greyhounds
Feral dogs w/higher prevalence vs owned dogs in same geo area
Fed raw meat → higher prevalence
Greater in farm dogs vs urban dogs
Increase in seroprevalence w/age
Neospora caninum life cycle?
ingestion of tiss cysts, some bradyzoites transform to tachyzoites w/systemic spread resulting in encystment in neural and muscle tissues.
In the intestine, enteroepithelial replication also occurs w/merogony, leading to development of gamonts and a zygote.
Oocysts are shed unsporulated in the stool.
Once mature and infectious, sporulated oocysts are ingested by a variety of herbivores. Organisms spread from the intestine as tachyzoites and encyst in muscle and nervous tiss.
Spread to reproductive tissues often results in abortion.
The tiss of the fetus or infected int host are ingested by a new definitive host and the cycle continues.
what is the clinocopathology of neospora caninum infection in dogs?
Similar to toxoplasmosis BUT neurologic deficits and muscular abnormalities predominate
Pups and older dogs clinically affected -signs in pups begin at 3-9 wks old
Gradual muscle atrophy and stiffness; ascending paralysis; arthrogryposis
Older dogs ill d/t reactivation of chronic subclinical infection
what are the signs which suggest neospora infection in pups <6m old?
Disseminated infection in many tissues
- Variable CNS signs
- Mono, para, tetra paresis
- Progress to paralysis
Signs of myositis
- Muscle atrophy, rigid hyperextension, hyperesthesia, incontinence
- Resp muscle paralysis, cranial muscle paralysis (cranial myositis), dysphagia, trismus, glossal paralysis
what are clinical sings that suggest neospora infection in dogs >6m of age
LMN flaccid paralysis (regional or generalized myositis in older dogs)
- Lameness and focal hyperesthesia
- Acute flaccid LMN signs
- Paraparesis to tetraparesis
- Diffuse hyperesthesia
- Muscle hypotonia
CNS manifestations (meningitis, encephalomyelitis, cerebellitis)
- Para, tetraparesis; ataxia
- Tremors and ataxia (cerebellitis)
- Head tilt; seizures; bhvr changes; altered thirst
- Blindness, anisocoria (retinitis, choroiditis, optic neuritis); Horner’s syndrome; trigeminal neuropathy
Systemic signs
- Fever, dyspnea, cough (pneumonia)
- Cardiac arrhythmias, sudden death *myocarditis)
- Ulcerative, pruritic skin lesions (pyogranulomatous dermatitis)
- Regurgitation, megaesophagus (esophagitis, esophagomyositis)
- Fever, vomiting, icterus (pancreatitis, hepatitis)
what can be seem post mortem in neopsora infections?
Histology of gross lesions; multifocal streaks of necrosis, fibrosis, mineralization of striated muscle, esp diaphragm. Hepatomegaly, pneumonia, discoloration of brain or spinl cord tiss
Pups: disseminated infection can have parasitic stages in thymus, liver, kidney, stomach, adrenal, skin, etc.
Parasite containing lesions in muscles, heart, brain, spinal cord, nerve roots, retina
Histo staining : nonsuppurative encephalomyelitis, polyradiculoneuritis, ganglionitis, myositis (of all striated m), an myofibrosis
what antemortem diagnostics can be perfomed to identify a neospora infection?
- Faecal flotation -> oocysts. Dogs w/clinical neosporosis typically DO NOT shed oocysts → very low sensitivity; NOT used routinely for diagnosis.
- Fecal PCR assay on faeces (same a s
- Cytology -> insensitive unless they are skin lesions
- Serology -> Serum of CSF -> assay performance varies greatly. Dogs w/chronic neosporosis may NOT show a rise in titer; titers >1:800 + CS suggests neosporosis
- Histopathology -> can detect brady and tachyzoites -> f organisms detected in present of inflamm and necrosis → clinical neosporosis likely. May be difficult to differentiate from T. gondii. IHC can help in differentiation.
- PCR assey -> muscle/skin/body fluid (espc csf) -> Assay performance varies btwn labs; positive PCR can occur in healthy dogs; MUST interpret in light of CS and other findings.
How do you treat neopspora?
Prognosis?
Neurologic involvement - TMS or pyrimethamine and sulfonamide → penetrates CNS
No prevention for transmission from mother to pups
Clindamycin → suppresses replication and dissemination of tachyzoites; is not effective against encysted bradyzoites; clinical improvement but not complete elimination from body
Older (>16 wks) pups and adult dogs respond better to treatment
How to prevent neospora?
- Do not feed uncooked meat (esp beef); offal or aborted materials (esp on farms)
- Keep from defecating in troughs, water sources, pastures, livestock holding pens
- No vax available; no preventative for transplacental transmission
- Do not breed infected females
