Parasitology Lab Review

Toxocara canis Life cycle: direct (paratenic host possible), L3 infective stage (right image) Host: dogs and wild canids (small intestine) Transmission: Ingestion – tracheal (usual) or somatic migration. Ingestion of paratenic host Transplacental – most important (tracheal migration in pup) Transmammory – least important PPP: 3-6 weeks Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick pitted shell wall, subspherical single dark cell 85-90 x 75 µm Pathogenesis: usually nonpath., ill thrift syndrome (pot belly), obstruction

(rare), death (neonate to 2-3weeks old). Zoonotic potential: visceral larva migrans Control: Sanitation, antihelmintics, preventative (2,4,6,8 weeks)

Toxocara cati Life cycle: direct (paratenic host possible), L3 infective stage Host: cats and wild felids (small intestine) Transmission: Ingestion – tracheal (usual) or somatic migration. Ingestion of paratenic host Transmammory – mucosal migration PPP: 5-8 weeks Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick pitted shell wall subspherical single dark cell 65-75 µm Pathogenesis: usually nonpath., ill thrift syndrome (pot belly) Zoonotic potential: visceral larva migrans (potentially) Control: Sanitation, antihelmintics, no hunting, preventative (3,5,7,9

weeks)

Toxocara leonina Life cycle: direct (paratenic host possible), L3 infective stage Host: dogs and cats (small intestine) Transmission: Ingestion – mucosal migration. Ingestion of paratenic host – mucosal migration PPP: 8-9 weeks Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick smooth shell wall elliptical single light cell 75-85 x 60-75 µm Pathogenesis: usually nonpath., fatal in puppies (extremely rare) Zoonotic potential: none Control: Sanitation, antihelmintics

Baylisascaris procyonis (left) Toxocara canis (right) Life cycle: direct (paratenic host possible) Host: raccoon and sometimes dogs (small intestine) Transmission: Ingestion of paratenic host – neuro-tropic migration Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick smooth shell wall elliptical brown coat may be present 62-79 x 52-68 µm Pathogenesis: severe central nervous system disease Zoonotic potential: visceral and ocular larva migrans Control: Sanitation, antihelmintics, avoid raccoon latrine areas

Ancylostoma caninum / Uncinaria stenocephala (bigger) Life cycle: direct (paratenic host possible), L3 infective stage (in 2-8 days) Host: small intestine of dogs, cats (A. braziliense), dog & cat (A. tubaeforme) Transmission: Ingestion of L3 – mature in gut or somatic migration (dominant) L3 skin penetration – tracheal or somatic migration. Transmammory – A. caninum only (dominant for A. c.) Ingestion of paratenic host – accumulate in lungs of rodents. PPP: 2-3 weeks Diagnosis: fecal float (preferred), clinical signs (peracute hookworm disease) Morphology: thin smooth barrel shaped wall, ellipsoidal, clustered cells

64 x 40 µm (A. c.), 70-90 x 40-50 µm (U. s.) Pathogenesis: chronic (anemia), acute & peracute (can be fatal), cutaneous

larva migrans Zoonotic potential: cutaneous larva migrans, eosinophilic enteritis Control: Sanitation, antihelmintics (2-12 wks e.o.w., then monthly to

6mths)

Taenia spp / Echinococcus spp. Life cycle: indirect (intermediate needed), eggs immediately infective Host: dogs, cats, humans (small intestine) Transmission: Carnivorism – predator (definitive host), prey (intermediate) Diagnosis: segments in feces, fecal float (if eggs free, but usually in segments), meat inspection (ruminants and swine) Morphology: adult – scolex w/ 4 suckers & rostellum +/- hooks egg – thick wall w/ radial striations, hooks present internally Pathogenesis: carcass condemnation, coernurus cerebralis (space occupying

lesion in brain of ruminants), pressure atrophy & allergic reactions (E. spp.)

Zoonotic potential: cysticercosis (often in CNS) Control: 3 steps – cestocide, stop hunting, prevent carnivore fecal

contamination

Trichuris spp. (whipworm) Life cycle: direct, L1 infective Host: dogs (T. vulpis), cats (T. campanula), ruminants (T. ovis), pigs (T. suis) Transmission: Ingestion of eggs – very resistant.

Larvae enter wall of sm. intestine. Emerge and mature in cecum of colon.

PPP: 11-12 weeks (T. vulpis), 7-9 (T. ovis), 6-7 (T. suis) Diagnosis: centrifugal fecal float (preferred), clinical signs (shedding sporadic), endoscope, necropsy/slaughter. Morphology: thick smooth shell wall, lemon shaped bipolar plugs w/ threading Pathogenesis: usually nonpath., severe disease rare, young pigs (diarrhea,

anemia), dogs – diarrhea and death (heavy infections) Zoonotic potential: Trichuriasis (T. suis) Control: Sanitation, antihelmintics, difficult to rid in dogs

Capillaria spp. Life cycle: direct or indirect, L1 infective Host: dogs, cats, ruminants, rodents, and birds Transmission: Indirect – earthworm (intermediate) Direct – Ingestion of egg Diagnosis: fecal float (preferred), nasal secretions, sputum or urine (spp. dependent), Morphology: thick smooth shell wall, ovoid to barrel shaped recessed bipolar plugs w/out threading Pathogenesis: rhinitis, tracheitis, bronchitis, cough, can be fatal in young

foxes, cystitis, hepatitis, enteritis. Zoonotic potential: none Control: Sanitation, antihelmintics, no hunting

Dipylidium caninum (flea tapeworm) Life cycle: indirect, flea/chewing louse (intermediate host) Host: small intestine of dogs, cats, foxes and humans Transmission: Flea/louse larva ingests egg from eating segment.

cystecircoid develops. dog/cat ingests flea.

PPP: 14-21 days Diagnosis: Segments in feces (rice grains), fecal float (less common) Morphology: Segments – bilateral genital pores Scolex – 4 suckers, armed rostellum Eggs – packets of 5-30 Pathogenesis: usually nonpath. Zoonotic potential: children infected if they ingest flea. Control: Treat for flea or louse infestation.

Diphyllobothrium spp. / Spirometra spp. (tapeworms) Life cycle: indirect, copepod (1st intermediate), fish (2nd intermediate – Diphy.), reptile/amphibian (2nd – Spiro.) Host: small intestine fish eating mammals and birds Transmission: coracidium hatches (ciliated), procercoid develops in copepod copepod ingested by fish, plerocercoid develops in muscles eaten by definitive host and matures. PPP: 21-28 days Diagnosis: Sedimentation technique, occasionally segments in feces. Morphology: Segments – genital and uterine (ventral) pores (Diphy.) Scolex – unarmed wi 2 bothria (slit like grooves) (Diphy.) Eggs – operculate, grey-green to brown Pathogenesis: usually nonpath., enteritis, can be severe in fish (Diphy.). Sparganosis – rare, fatal if proliferative (Spiro.) Zoonotic potential: infection with ingestion Control: Avoid raw fish, cestocides

Nanophyetus salmincola / Paragonimus kellicotti (flukes) Life cycle: indirect, snail (1st), crayfish (2nd Para.), salmonid (2nd Nano.) Host: small intestine fish/crayfish eating mammals Transmission: Eating intermediate PPP: 5-8 days (dogs – Nano.), 30-36 days (Para.) Diagnosis: Sedimantation technique (operculate eggs in feces),

Radiology – cysts in lungs (Para.) Morphology: Eggs – operculate Pathogenesis: Para. – chronic bronchiolitis, fatal pneumothorax (cyst rupture) Nano. – salmon poisoning disease (rickettsia) Control: Avoid raw fish/crayfish, anthelminitcs (little use)

Fasciola hepatica (Liver Fluke) Life cycle: indirect, snail (intermediate Host: bile duct of ruminants Transmission: ciliated miracidia infect snail metacercaria encyst on vegetation eaten by definitive host, penetrate gut & migrate to bile duct via the liver (6-8 weeks) PPP: 2-3 months Diagnosis: Sedimentation technique, find flukes postmortem. Morphology: Operculate eggs Pathogenesis: Cattle – chronic disease Sheep – acute to chronic. Secondary clostridial infections. Control: Pasture management (snails), flukicides (strategic deworming)

Giardia spp. Life cycle: direct Host: duodenum and upper small intestine of mammals and birds Transmission: Cyst (left) – ingested and excyst after exposure to stomach acid and alkaline duodenum. Trophozoite (right) – asexual repro., colonize sm. intestine. encyst with increasing bile, passed in feces. PPP: 7-10 days Diagnosis: ZnSO4 fecal float (gold standard – cyst cytoplasm collapses),

direct smear (trophs – falling leaf), ELISA. Morphology: Cyst – oval, 4 nuclei (2 trophs/cyst), axostyle, median bodies. Troph. – bilateral symmetry, pyriform, venral disk, axostyle, 2 median bodies, 4 pair of flagella, binucleate. Pathogenesis: Variable (host and parasite dependent), dose dependent,

malabsorption, increased intestinal motility. Control: Sanitation and hygiene, reduce stress, no licensed treatments.

Isospora spp. Life cycle: direct, host specific Host: intestinal epithelial cell of host (varies with species) Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront – asexual repro (merogony) ⇒ merozoites Burst out to infect other cells (2nd generation). Last generation ⇒ micro & macrogametocyte (gametogony) Sexual repro. ⇒ zygote ⇒ oocyst (w/in thick wall) Cell bursts ⇒ passed in feces ⇒ sporolates (right conditions) Diagnosis: fecal float, Hx & clinical signs, lesions at necropsy. Morphology: oocyst – round, unsporolated is single celled (A), sporolated has 2 sporocysts (B). Pathogenesis: Variable (host and parasite dependent), dose dependent,

malabsorption, villus atrophy, crypt hyperplasia, hemorrhage. Control: Supportive care, environ. management, prophylactic drugs.

A  

B  

Toxoplasma gondii (B) Life cycle: indirect, any warm blooded mammal (intermediate) Host: epithelial cells of small intestine of felids Transmission: Host ingests bradyzoite (tissue cyst) or sporolated oocyst.

excyst ⇒ merogony in epithelial cells ⇒ merozoites invade other cells ⇒ gametocytes ⇒ fuse into oocyst (zygote w/ capsule) ⇒ into feces ⇒ sporolate (viable 12-18 mths).

PPP: 3-10 days (bradyzoite), >18 days (oocyst) Diagnosis: Centrifugal fecal float (sugar or ZnSO4), serology (humans),

ELISA. Morphology: oocyst – small round 10-12 µm (A = Isospora sp.) Pathogenesis: Variable. No signs (intestinal phase), clinical signs to death

(extra-intestinal phase). Zoonotic potential: flu-like symptoms to severe disease (immunocomp.) Control: No hunting, no raw meat, drugs to reduce shedding.

Neospora caninum Life cycle: indirect, any warm blooded mammal (intermediate) Host: small intestine of canids Transmission: Congenital – predominant route. Ingestion of cysts – oocyst and tissue cysts (as in Toxoplasma) Diagnosis: fecal float (rare because sporadic), gross lesions,

immunohistochemistry, ELISA. Morphology: oocyst – small round 10-12 µm Pathogenesis: focal areas of necrosis (tachyzoites), non-suppurative

inflammation. Subclinical common (dog), abortion (cattle). Control: No hunting, no raw meat, drugs to reduce shedding, treat all

littermates. Cattle – cull abortive cows, protect feed and water, no dogs eating fetuses etc.

Sarcocystis spp. Life cycle: indirect, prey animal (intermediate) Host: goblet cells of small intestine of canids and felids Transmission: Asexual stages in intermediate host, sexual in definitive host. oocysts sporolate in lamina propria, pass in feces.

Ingested by intermediate ⇒ vascular endothelium (merogony) ⇒ myocytes invaded by merozoites ⇒ transform into metrocytes ⇒ bradyzoites.

PPP: 75 days (for sarcocyst to be infectious to definitive host) Diagnosis: Clinical signs, histology (sarcocysts), fecal float (definitive host) Morphology: sporocyst – small, ellipsoid, 7-22 µm, thin wall (A), 4 sporozoites (B), residual bodies (C). Pathogenesis: Most pathogenic to intermediate only. Variable disease Control: no fecal contamination, no raw meat (definitive), anticoccidials

(intermediate).

Trichostrongyle type egg Life cycle: direct, Host: small intestine, abomasums, gastri glands of ruminants Transmission: Eggs shed in feces ⇒ develop into L3 in environment (retain

sheath) ⇒ ingested. PPP: varies w/ species and host Genuses: Cooperia spp., Haemonchus spp., Ostertagia spp.,

Trichostrongylus spp. Diagnosis: fecal float. Morphology: thin smooth shell light brown segmented cluster of cells. 50 x 80 µm Pathogenesis: anemia (Haemonchus), green diarrhea, anorexia, weight loss. Control: Strategic deworming, pasture management.

Nematodirus spp. Life cycle: direct, L3 infective. Host: Ruminants Transmission: Ingestion – L3 larvated egg. Hypobiosis – resistant to desiccation (overwinter) PPP: 14-21 days Diagnosis: fecal float, clinical signs, herd flock history. Morphology: Thin smooth shell w/ thickened ends, ellipsoidal. Segmented brown nucleus (2-8 cells), wide clear area around. 200 x 95 µm (larger than trichostrongyles) Pathogenesis: Mixed. Diarrhea, anorexia, poor hair coat, etc. Control: Strategic deworming, pasture management.

Monezia spp. (tapeworm) Life cycle: indirect, orbatid mite (intermediate) Host: small intestine of ruminants Transmission: Ingestion of mite PPP: 28-42 days Diagnosis: fecal float (eggs), segments in feces, trailing from anus. Morphology: bicyle seat (M. expansa [both images]), square (M. benedeni) Embryo w/ hooks and pyriform apparatus. 56-75 µm Pathogenesis: usually nonpath., ill thrift in young lambs w/ heavy infections Zoonotic potential: none Control: cestocides (not economically worth it)

Dictyocaulus viviparous / filarial (lungworm) Life cycle: direct Host: bronchi of ruminants Transmission: L1 hatches from egg in lungs or intestines, passes in feces. Ingest L3 while grazing migrate to alveolar space via lymph/blood PPP: 4-5 weeks Diagnosis: Baermann technique (L1 in feces), nasal secretions, adult

worms in bronchi. Morphology: tail – straight, pointed or blunted intestinal granules. Pathogenesis: sheep – well tolerated to bronchitis or secondary infections. cattle – significant pathogen in young, atelectasis, emphysema Control: Anthelmintics

Strongyloides papillosus Life cycle: two cycles – homogonic and heterogonic (L3 infective) Host: small intestines of ruminants Transmission: Homogonic – occurs in host, autoinfection or eggs passed in

feces and ingested by new host. Tracheal and somatic migration of L3.

Heterogonic – in environment, eggs develop into male and female. female produces larvated eggs.

Routes – transmammory, skin penetration, ingestion Diagnosis: fecal float (larvated eggs in feces), Baermann technique (larva

in feces) Morphology: smooth thin membrane, ellipsoidal Colorless fully developed larva inside Pathogenesis: subclinical, foot rot w/ skin penetration Control: rarely needed, anthelmintics

Cryptosporidium spp. Life cycle: direct, immediately infective (sporolated) Host: microvilli of epithelial cells (GI & resp.) of ruminants (C. bovis), pigs (C.

suis), dogs/cats/cattle/horses/humans (C. parvum) Transmission: sporozoites ⇒meronts⇒merozoites⇒gamonts⇒oocysts. thick walled oocysts passed in feces, ingested by new host. thin walled oocysts – autoinfection cycle (same host). PPP: 4-6 days Diagnosis: Histopathology (microvilli), fecal float w/ sugar (eggs in feces) Morphology: smooth, round, small 4-8 µm., colorless to pinkish hue granular

nuclei. Staining to differentiate from yeast. Pathogenesis: Cryptosporidiosis – villous atrophy/fusion, malabsorptive

diarrhea. Zoonotic potential: Cryptosporidiosis Control: Sanitation, good management, no treatment available

Eimeria spp. Life cycle: direct (often mixed infections) Host: intestinal epithelial cell of host (varies with species) (not in dogs/cats) Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront – asexual repro (merogony) ⇒ merozoites Burst out to infect other cells (2nd generation). Last generation ⇒ micro & macrogametocyte (gametogony) Sexual repro. ⇒ zygote ⇒ oocyst (w/in thick wall) Cell bursts ⇒ passed in feces ⇒ sporolates (right conditions) Diagnosis: fecal float, Hx & clinical signs, lesions at necropsy. Morphology: oocyst – round, unsporolated is single celled, sporolated has 4 sporocysts. Micropyle cap may be visible (operculum) Pathogenesis: Variable (host and parasite dependent), dose dependent, Summer/winter/nervous coccidiosis Control: Supportive care, environ. management, prophylactic drugs.

Strongyle type egg Life cycle: direct, Host: cecum and large colon of equids Transmission: Eggs shed in feces ⇒ develop into L3 in environment (retain

sheath) ⇒ ingested. PPP: varies w/ species and host Genuses: Small strongyles – Cyathostomum sp., Petrovinema sp. Large strongyles – Strongylus vulgaris, S. edentatus Diagnosis: fecal float, clinical signs, deworming history. Morphology: thin smooth shell, ellipsoidal light brown segmented cluster of cells. 60-120 x 35-60 µm Pathogenesis: Larval Cyathostominosis, L4 emergence causes inflammation Control: Strategic deworming (timing), pasture management, choice of

anthelmintics.

Parascaris equorum Life cycle: direct, L3 infective stage Host: small intestine of equids Transmission: Ingestion of L3 in egg – tracheal migration. Viable in soil months to years. PPP: 72-110 days Diagnosis: fecal float. Morphology: thick pitted shell wall, subspherical single or binucleate granular nucleus Protein coat may or may not be present (dark brown) 90-100 µm Pathogenesis: foals susceptible (pot belly, enteritis) – age immunity after 6

months. Coughing from larva migration through lungs. Control: Sanitation, antihelmintics – 6 week intervals (6 weeks – 6

months).

Strongyloides westeri (threadworm) Life cycle: two cycles – homogonic and heterogonic (L3 infective) Host: small intestines of equids Transmission: Homogonic – occurs in host, autoinfection or eggs passed in

feces and ingested by new host. Tracheal and somatic migration of L3.

Heterogonic – in environment, eggs develop into male and female. female produces larvated eggs.

Routes – transmammory, skin penetration, ingestion Diagnosis: fecal float (larvated eggs in feces), Baermann technique (larva

in feces) Morphology: smooth thin membrane, ellipsoidal Colorless fully developed larva inside Pathogenesis: common in foals – mild diarrhea. Immunity after 15-35 weeks. Control: rarely needed, anthelmintics

Oxyuris equi (pinworm) Life cycle: direct Host: cecum and large colon of equids Transmission: Female deposits eggs on perineal area, infective in 3-5 days. Ingested, hatch in gut, mature in mucosal crypts of large

intestine. PPP: 4-6 months Diagnosis: Acetate tape technique, clinical signs (damaged tail), Hx, fecal

float usually negative (eggs not in feces). Morphology: Operculate, thick, smooth shell. One side flattened. Embryonated or not. 90 x 42 µm Pathogenesis: Stabled animal problem. Anal pruritis (itchy) Control: Sanitation, anthelmintics effective.

Anoplocephala spp. Life cycle: indirect, orbatid mite (intermediate) Host: Large and small intestine of equids Transmission: Adult⇒eggs⇒cysticercoid ingesting free living pasture mites. A. perfoliata common, A. magna - rare PPP: 28-42 days Diagnosis: fecal float (although eggs commonly not found), adults at

necropsy. Morphology: Thick grayish multilayered shell. Hooked embryo amid pyriform apparatus. “D” shaped 90 x 42 µm Pathogenesis: mucosal erosions, spasmodic colic, mild enteritis. Control: Sanitation, Cestocides.

Eimeria leukarti Life cycle: direct Host: intestinal epithelial cell of equids Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront – asexual repro (merogony) ⇒ merozoites Burst out to infect other cells (2nd generation). Last generation ⇒ micro & macrogametocyte (gametogony) Sexual repro. ⇒ zygote ⇒ oocyst (w/in thick wall) Cell bursts ⇒ passed in feces ⇒ sporolates (right conditions) Diagnosis: fecal float, sedimentation technique, Hx & clinical signs. Morphology: oocyst – tear drop shaped, thick brown shell, granular nucleus.

Micropyle opening at one end (B). Pathogenesis: Rare – diarrhea and weight loss Control: Supportive care, environ. management, prophylactic drugs.

Strongyle/Trichostrongyle type eggs Life cycle: direct, Host: large intestine (Oesaphogostomum dentatum) and stomach

(Hyostrongylus rubidus) of pigs Transmission: L3 Ingested – encysts in intestinal wall. PPP: 41 days Diagnosis: fecal float,

caseated nodular lesions (O. dentatum). Blood red worms in stomach (H. rubidus).

Morphology: thin smooth shell, ellipsoidal light brown segmented cluster of cells. 60-120 x 35-60 µm Pathogenesis: O. dentatum – Serious (breeding stock), enteritis, diarrhea. H. rubidus – suck blood, anemia, death loss (by gastric ulcers). Control: Sanitation, pasture management, anthelmintics.

Ascaris suum Life cycle: direct, L3 infective stage Host: small intestine of pigs Transmission: Ingestion of L3 in egg – tracheal migration. Viable in soil months to years. PPP: 60-620 days Diagnosis: fecal float, milk spots on necropsy. Morphology: thick pitted shell wall, subspherical, granular nucleus fills ova. Protein coat may or may not be present (dark brown). 88-90 x 66-68 µm Pathogenesis: Young pigs – milk spot liver, thumps or heaves in lungs

(predispose for secondary infection), intestinal obstruction. Zoonotic potential: Ascariasis Control: Sanitation, antihelmintics 2 weeks prior to farrowing & piglets

at 5-6weeks/repeat in 30 days.

Coccidial oocyst Life cycle: direct Host: intestinal epithelial cell of pigs (Isospora spp. or Eimeria spp.) Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront – asexual repro (merogony) ⇒ merozoites Burst out to infect other cells (2nd generation). Last generation ⇒ micro & macrogametocyte (gametogony) Sexual repro. ⇒ zygote ⇒ oocyst (w/in thick wall) Cell bursts ⇒ passed in feces ⇒ sporolates (right conditions) Diagnosis: fecal float, Hx & clinical signs. Morphology: oocyst – round, smooth refractile shell. pale granular nuclei. Pathogenesis: Severe in nursing piglets. “Sour milk” diarrhea. Control: Sanitation, supportive care, environ. management, drugs

ineffective.

A   B  

Balantidium coli (ciliate) Life cycle: direct Host: G.I. tract of pigs Transmission: Trophozoite – binary fission (asexual) or conjugation (sexual)

reproduction in large intestine. Encyst in response to dehydrated feces. shed in feces. Ubiquitous in pigs. Diagnosis: Trophs – wet mount. Cysts – wet mount, fixed smear, or fecal float Morphology: Troph (A) – Thick ovoid ciliated shell, central macronucleus

and micronucleus, funnel shaped cytosome (mouth). Cyst (B) – spherical, thick, refractile shell, no cilia. Pathogenesis: most asymptomatic, secondary infection from lesions. mild colitis, occasional severe dysentery. Zoonotic potential: Amoebic dysentery. Control: Pigs – Sanitation, hygiene, no drugs. Humans – tetracyclines

Leucocytozoon spp. Life cycle: indirect, intermediate vector – black fly (Simulium spp.) Host: various tissues of wild and domestic birds Transmission: Sporozoite transmitted when fly feeds.

enter cells⇒schizogony⇒merozoites emerge⇒infect circulatory cells and endothelium⇒develop into gametocytes and megaloschizonts⇒merozoites from megaloschizont released⇒develop into elongate gametocytes (image) ⇒ingested by fly⇒fusion and sporogony in gut & salivary gland of fly.

Diagnosis: gametocyte in blood smear, schizonts in tissue, clinical signs, Hx. Morphology: elongate, w/in leukocyte, cytoplasmic “horns”. Pathogenesis: anemia, leukocytosis, splenomegaly, hepatomegaly,

obstruction. Young most susceptible – death w/in 24 hrs. Control: Control fly, separate domestic and wild birds, preventative

medicine.

Babesia spp. Life cycle: indirect, intermediate vector – tick (host/tick specific [see notes

for details]) Host: bovine, equine, canine, feline, vole/mouse (human) Transmission: transmitted as tick feeds. Infect erythrocytes. Merogony & gametogony I occur in vertebrate. Gametogony II & sporogony in tick. Diagnosis: blood smear (trophs in erythrocytes), use capillary blood (⇑ #’s),

Hx, clinical signs. Morphology: piriform shaped merozoite/trophozoites within the erythrocytes.

Wright-Geimsa stain. Pathogenesis: rare disease – hemolytic anemia, capillary obstruction, anoxia,

organ failure. Control: tick control, diaminazene IM or phenamide SC.

A  

B   C  D  

Trypanosoma spp. Life cycle: indirect, intermediate vector – tsetse fly or triatomine bugs Host: dogs, humans Transmission: transmitted in feces of arthropod. Trypomastigotes enter body

through bite or scratch. Enter blood, then organs and muscle cells⇒amastigote⇒binary fission⇒release from cell⇒back into trypomastigote⇒ingested by bug with blood meal⇒epimastigote in gut of bug.

Diagnosis: blood smear or lymph (w/in 5 weeks), culture, IFA, xenodiagnosis. Morphology: slender, pointed posterior. kinetoplast at posterior (A),

flagellum at anterior (B), narrow undulating membrane (C), central nucleus (D).

Pathogenesis: cell distruction, necrosis. Chronic or acute disease. Control: control arthropod, avoid reservoir animals, drugs kill only

extracellular form.