Anoplocephala spp. and Paranoplocephala spp.

Ingest mite infected with cysticercoid

Grazing horse ingests mite infected with cysticercoid

Cystecercoid develops into a tapeworm in intestines

Gravid proglottids and embryonated eggs pass in horse feces

Egg is eaten by oribatid mite

larval tapeworm (cysticercoid) develops in mite body cavity

mite is ingested by horse

Pathogenesis of equine tapeworms

A. Magna and P. mamillana are well tolerated

Heavy infections (A. perfoliata) can interfere with function of ileocecal valve through ulceration and imflammation

Persistant diarrhea, intussusception, colic

Eggs in fecal float (unreliable)

Proglottids in feces

ELISA for a. perfoliata

Tapeworm segments in stool or perianal region

Eggs or egg packets on fecal flotation

4 suckers, no hooks

medial genital pores

paruterine organ

Club shaped proglottids in feces

Hexacanth embryo eggs

pseudophyllidean procercoid 

pseudophyllidea plerocercoid

Ingestion of procercoid larvae in crustacean

Ingestion of infected intermediate or paratenic host

Dorsoventrally flattened

Bilaterally symmetrical

Functional digestive tract

Hermaphroditic

Need atleast 2 hosts for LC completion

Egg

Miracidium

Sporocytes

Redia

Cercaria

Metacercaria

Adult

Unembryoned eggs shed in feces into water

Eggs embryonate, mircadia hatch and penetrate snail (IH)

Within snail miracidia --> sporocytes --> rediae --> cercariae

free swimming cercariae encyst on water plants

metacercariae on water plant ingeste by human, sheep or cattle

Plug feeders

Oral sucker (mouth)

Ventral sucker (acetabulum)

Full digestive tract

Vitelline gland - provide yolk for eggs

Hermaphroditic (contains 2 testes and 1 ovary)

one miracidium enters snail ---> becomes sporocysts then radiae and finally hundreds to thousands of cercariae come out

asexual reproduction occurs here at sporocysts and rediae stage

Every morning school really chafes my ass

Every man should remember cheating means alimony

Eggs on fecal sedimentation or fluke finder 

Adults at necropsy (up to 3 cm)

Adults at necropsy (up to 10 cm)

Egg from fecal sedimentation or fluke finder BUT patent infections only occur in the DH - in abhorant host, no connection of cysts with bile ducts so infections never become patent

adults at necropsy

eggs via fecal sedimentation or fluke finder

adults at necropsy in small intestines (2.5mm)

Eggs on fecal sediment or fluke finder

Dogs: 4-5 weeks

Cats: up to 10 weeks

adults cysted in lung parenchyma

eggs travel with mucus, swallowed and exit with feces

Enter water --> miracidia penetrate snail --> cercariae emerge and penetrate crayfish --> metacercariae form -> DH ingests RAW CRAYFISH

encystment in small intestine then migrate to lungs

Eggs in sputum or feces

Adults up to 2.5 cm 

pulmonary cysts on radiograph (R-caudal lobes)

eggs shed in feces of adults and swallowed by terrestrial snail (miracidium stays in egg)

cercariae exit snails in slime balls that get eaten by ants

metacercariae form within the ants which is infective to DH

parasite alters behavior in a way that alters IH2 in a way that favors transmission to DH

metacercariae form around central ganglia in ant and alters behavior; normal in day; at night infective ants go to the top of vegitation and waits instead of going down onto ground

occurs in dicrocoelium dentriticum

eggs containing miracidium in fecal sedimentation or fluke finder

adults at necropsy in gall bladder or bile ducts up to 10 mm

adults at necropsy

eggs containing miracidium on fecal sedimentation or fluke finder

Adults in small intestines eggs shed in feces and must enter water

eggs ingested by aquatic snails

cerciariae exit aquatic snails

mesocerciariae go into tadpoles and can survive through metamorphasis of tadpole to adult frog --> can be transfered to PH or DH via ingestion

eggs on fecal sedimentation or fluke finder

adults at necropsy (rare)

Eggs produced in DH veins and pass through intestinal wall to be shed into feces

Eggs hatch in water --> Miracidium penetrates snail --> cercariae emerge from snail and are infective where it penetrates through skin

NO METACERCARAE

Penetration of cercariae = dermatitis

eggs through intestinal wall = enteritis

organisms whose infective stage posses an apical complex - set of electron dense organelles at anterior ends

ALL ARE PARISITIC

Schizogony (merogony) prodouce merozoites (AS)

Gametogony produce gametozoites (S)

Sporogony produce sporozoites (AS)

can pass from one stage to another when host molts

larvae --> nips --> adult

transmission from adult to larvae within egg

occurs only in LARGE babesia spp.

size of piroplasm

>< 3 micrometers

B. canis vogeli

seen in GREY HOUNDS

DH: kennel tick, brown dog tick

most often seen in greyhounds

small babesia

most commonly seen in pitbulls or dogs fighting with pit bulls

primary transmission: blood to blood

more pathogenic than b. canis

all three stages (molts) occur on same host with several blood meals

ex: riphicephalus (boophilis) spp.

northeast and midwest

Transmitted by ticks or blood transfusion 

Tick transmitted (transtadial only)

Schizogony occurs in lymphocytes prior to entering RBCs

NO vaccine

transmission via ticks

tick preventatives

vertebrates: cattle, sheep, goats, swine, horses, poultry

species not hot specific

Direct fecal-oral route

infective host --> unsporulated oocysts in feces --> one cell inside oocyst (sporot) --> develop within environment, sporulation --> 8 sporulozoites infective--> cow ingests sporulated oocysts while grazing --> sporulozoites enter epithilial cells of small intestine and under 1st round of schizogony --> schizot formation, host cell ruptures and releases merozoites --> enter large intestinal cells and undergo round 2 schizogony --> cell ruptures to release 2nd generation merozites --> reenter large intestinal epithilial cells --> undergo gametogany (microgametocytes and macrogametocytes)--> micro leave cells and find cell with macro --> sexual reproduction --> oocysts form --> lumen of small intestines --> secreted in feces

pathogenic species of cattle

12-14 days

operculated eggs in feces

can be found on fecal floatations OR sedimentation

neorickettsia risticii

equine monocytic erlichiosis

caused by ingestion of aquatic insects (caddisflies) infected with trematode species that use trout or bats as hosts

obligatory intracellular bacteria

trematodes are known vectors for rickettsial agents

neorickettsia risticii

neorickettsia helminthoeca

fecal-oral

sexual

vector-borne

mechanically through fomites

Axostyle down along middle

Flagellae

median body

direct fecal oral

resistant stage cysts passed with formed feces --> ingestion of cysts (food, water, hands, fomites-feed bucket, water trough) --> trophozoites

Antigen snap test

Trophozoite diarrhetic stool via direct saline smear of fresh feces

duodenoscopic aspirates 

Cyst in well formed feces via zinc sulfate centrifugal flotation

bull: venereal (bulls 6-8% infected)

cats: shred litter boxes, grooming with contaminated paws

saline fecal smear

observation of reproductive secretions

cultures

PCR

t. foetus = undulating membrane, forwardly progressive

giardia = concave ventral disc, sluggish, falling leaf

DH: turkeys, chickens, guinea fowl, phesant, birds

PH: heterakis gallinarum, earth worms

1. ingestion of trophozoites directly from feces (direct)

2. heterakis gallinarum in cecum of infective bird ingests trophozoites --> cross into ovaries --> leave bird in infected eggs; naiive bird ingests heterakis eggs in environment and becomes infected with heterakis and histamonis

3. infected heterakis egg in envoronment is ingested by earthworm which can be digested by bird

ingest cysts via water, food, fomites (hands) --> trophozoites in large intestine

lives indefinitely in host (only asexual reproduction

direct 

trophozoites on surface of fish in white pustules (1 trophozoite on pustules) --> punch out of pustule --> enter water --> form gelatinous capsule  around themselves and undergo asexual reproduction --> thousands are released in water and find new fish

infective stages: theronts, tomites, swarmers released from gel capsule

trophozoite from pustules on slide

ciliated with large horseshoe shaped macronucleus

direct

cecum and colon in trophozoites --> form cysts that come out in formed feces (infective stage) --> ingested via contaminated water, food, fomites

trypamastagote 

amastagote 

trypomastigotes enter host through:

Abrasion at bite site

Ingest triatomine bug = enter through mucosa of mouth

Transplacental

Blood transfusion

Acute phase: lethargy, arrhythmias, heart failure (2-4 weeks PE)

Latent phase: no clinical signs, normal ECG, possibly exercise induced arrythmias (1 month PE)

Chronic phase: trypanosoma cruzi will change its VSG coat to evade host immune system --> chronic imflammation, waxing and waning disease, muscle wasting, fever, right sided heart failure (8 months - 3 years PE)

acute phase --> trypomastagotes in blood or PCR

Serology + clinical signs

intermittant fever

anemia

swollen lymph nodes and spleen

CNS complications --> death

chagoma

intermittant fever

lymphadenopathy

anemia, anorexia

muscle tremors and wasting

CNS problems

irreversible coma

fatal

50% mortality rate - emaciation, paralysis, CNS complications

other animals can become chronic carriers (donkeys)

infected sand fly takes a blood meal and promastigotes enter at bite site (salivary transmission) --> transform into amastigotes --> phagocytysed and spread throughout body --> transmitted to other sandflies

transplacental

transmammary

blood transfusion

foxhounds

initial cutaneous leishmaniasis at bite site --- papule, nodule, ulcerations, spreads across body

viscerial leishmaniasis - depression, wasting, swollen lymph nodes, anterior uveitis, renal failure due to AgAb complexes

Cause of death: renal failure

suspicion, confirmed by serology, PCR

REPORTABLE

L. major, L. tropica

oriental sore, baghdad boil, deli sore

L. mexicana, L. braziliensis

Espundia

hepatozoon americanum

states along gulf coast; not yet in other areas of world

hepatozoon canis

worldwide 

all life cycles occur in the same host

zygote divides many times to produce sporozoites (sporogony) --> sporozoites become merozoites which undergo merogony/schizogony --> meronts form gametes (gametogony) --> gametes combine (sexual reproduction) to form zygote

sporogony occurs in tick host

merogony/schizogony occurs in IH (vertebrate host)

infection through ingestion of tick containing sporulated oocysts (oocysts full of sporozoites)

sporozoites disseminate through out body in IH (canid) and undergo shizogony/merogony in muscle - live in onion skinned cysts  --> breach cyst wall and incite imflammatory response --> granuloma formation

schizonts undergo gametogony --> gametocytes form in periphrial white blood cells and are infective to feeding ticks

gamonts found on blood smears in WBC

cbc-anemia only

pcr

muscle biopsy to see onion skinned cysts

cbc - neutrophilia, anemia

pcr

NOT a blood smear