Protozoa Flashcards
characteristics of protozoa
- eukaryotic - unicellular - contain nucleus, mitochonrdira, ER, golgi app. - and can be heterotrophic or autotrophic
protozoan organelles of locomotion
- flagella - cilia - pseudopods - undulating ridges, subpellicular microtubules
protozoan reproduction
- binary fission (asexual) - multiple fission or schizogony (asexual) - budding (asexual) - conjugation (asexual) - gametogony (sexual)
heterotrophs can be: holozoic or saprozoic
holozoic: ingest via mouth saprozoic: absorb nutrients thru cell membrane
phylum of protozoa
- sarcomastigophora - apicomplexa - ciliophora - microspora
phylum ciliophora characteristics and genera
- distinct nucleus - movement: cilia - direct life cycle (asexual or sexual) - most free-living (few parasitic) - diagnosis: direct smear, fecal - genera: balantidium and paramecium, rumen and cecla ciliates, many normal fauna
phylum microspora characteristics
- obligate, spore-formers - intracellular parasites of vertebrates & invertebrate - characteristic feature: polar filament or polar tube used to infiltrate host cells - close to fungi
phylum sarcomastigophora characteristics
- distinct nucleus - movement: most use flagella - ASEXUAL reproduction - life cycles: direct and indirect
giardia spp. characteristics
cysts: resistant, INFECTIVE STAGE Trophozoites: vegetative, reproducing stage, mucosal surface of small intestine
giardia lifecycle
- giarida is transmitted by ingesting the cyst stage - contaminated food or water, they can survive for months 2. excystation occurs in the duodenum 3. replication via BINARY FISSION 4. encystment occurs in the lower intestinal tract - infective cysts passed in feces - prepatent period ~ 1 week
Giardia spp. clinical signs, prevalence, and diagnosis
clinical signs: chronic infections (villus atrophy), intermittent diarrhea (loose, mucoid, not watery, can last weeks to months), majority asymptomatic
- prevalence: more common in younger animals
- diagnosis: flotation, direct smear, ELISA
Trichomonad characteristics
- 3 anterior flagella
- 1 posterior, recurrent flagellum
- axosytle -> a microtuble
- pseudocysts
- longitudinal binary fission
trichomonad structure:
pelta - support flagella
axostyle - support cell body
- parabasal body - golgi apparatus
- blepharoplast - origin of flagella
- costa - unique, support UM
- hydrogenosomes - ATP and H+ producer
Tritichomonas foetus
- causes Bovine Genital Trichomonosis
- venereal disease
- cows: vagina, cervix, uterus
- bulls: prepucial cavity
Bovine Genital Trichomonosis: clinical features
- early embryonic death and abortion, called “trichomonad abortion”
- insidious disease: estrus 60 days into breeding season
- 20-40% reduction in pregnancy rate
- spread out calving season
- varied weaning rates
Bovine Genital Trichomonsis: clinical features for cows and bulls
- bulls (chronic carriers) are aysmptomatic
- cows (clear 2-6 months): get vaginitis, cervicitis, endometritis, pyometra, mucopurulent discharge
Bovine Genital Trichomonosis: diagnosis
- recover organisms
- PCR
- direct smear
- culture organisms
Non-pathogenic Bovine Trichomonads
Pentatrichomonas hominis
- 3-5 anterior flagella
- 1 posterior flagellum
Tetratrichomonas spp.
- 4-5 anterior flagella
- 1 posterior flagellum
Bovine Genita Trichomonas: Control
- replace old bulls
- test new bulls and bulls after breeding : cull positives
- use AI
- cull open cows at pregnancy exam
- do not purchase open or bred cows
- limit breeding season to < 90 days
- avoid grazing in common lands (especially bulls)
Feline Trichomoniasis
large bowel disease:
- chronic diarrhea
- tenesmus
- flatulence
- irritated anus
- fecal incontience
transmission unknown
feline trichomoniasis: clinical features
- chronic diarrhea
- age of onset average 9 months
- diarrhea may relapse
- sponatneous resolution
- T. foetus lives in colon and adheres to epithelial cells
- feline hosts: male and female, domestic and purebred
feline Trichomoniasis: diagnosis
- direct fecal smear
- culture
- PCR
- colonic biopsy
Feline Trichomoniasis: Control
- keep infected cats away from other cats
- do not allow litter box sharing
Trypanosoma cruzi characteristics
- paraistes of all classes of vertebrates: blood and tissues, some intracellular
- majority transmitted by blood feeding invertebrates
- most do not cause disease
- kinetoplast
- pleomorphic
- cytoskeleton: microtubules
- single nucleus
Characteristics of Trypanosomes and their life stages
elongated cell body; single flagellum
- trypomastigote: blood stage, kinetoplast @ cell posterior
- promastigote: mainly insect vector, kinetoplast @ cell anterior
- epimastigote: some species, kinetoplast between and anterior
rounded cell body; short flagellum
- amastigote: some species, flagellum short if presented at all
Trypanosoma cruzi
- American Trypanosomiasis in dogs, cats, opossums, armadillos, reservoir hosts
- Chagas Disease in humans
- vector: reduviid bug aka assassin bug or kissing bug
- epidemiology: rare in US but 8-11 million cases in Mexico and South America
Trypanosoma cruzi: morphology
- trypomastigote will be found in circulating blood and will have a subterminal kinetoplast (the largest of all the trypanosomes)
- amastigote will be found in muscles and other tissues
Trypanosoma cruzi: lifecycle
- metacyclic trypomastigotes are the INFECTIVE STAGE; passed in feces of IH. they enter host via bite wound, scratch or mucus membrane
- trypomastigotes - found in blood, enter cells of spleen, liver, lymphatics and muscle
- amastigotes replicate via BINARY FISSION - form clusters in pseudocysts
- cells rupture and trypomastigotes remain in circulation or reinfect
- trypomastigotes transform into epimastigotes - they replicate via BINARY FISSION
Trypanosoma cruzi: Chagas Disease in Humans
Acute Chagas Disease
- weeks to months: asymptomatic
- parasites in circulating blood
- fever, swelling around site of parasite entry (Romana’s sign)
- rarely severe inflammation of heart or brain
Chronic Chagas Disease
- prolonged: asymptomatic
- NO parasites in circulating blood
- 20-30% develop severe disease: heart arrhythmia, dilated heart
- immunosuppression can lead to ‘reactivation’ of disease
Trypanosoma cruzi
American Trypanosomiasis in Dogs
- found most office in sporting dogs and working dogs, 50% acute death, < 1 year old
- clinical features: most diagnosed during chronic stage
- symptoms will include: dilated, enlarged heart, arrhythmia, lethargy, rspiratory difficulties, hepatomegaly, anemia
Trypanosoma cruzi diagnosis
serological testing including: TESA blot/Western blot, ELISA, IFA (indirect immunofluorescence assay), IHA (indirect hemagglutination assay)
- blood smear
- xenodiagnosis
Phylum Apicomplexa Characteristics
- distinct nucleus
- movement: subpellicular tubules
- apical complex
- Orders: Eucoccidiida, Piroplasmida
Order Eucoccidiida Characteristics
(Phylum Apicomplexa)
- Asexual & Sexual reproduction
- sporogony
- shizogony
- gametogony
- parasitic stages
- DH: primarily in inestinal epithelial cells
- IH: various locations
- oocysts
- life cycles: direct and indirect
- diagnosis: fecal float, serology, immunochemistry
Cystoispora (Isospora) and Eimeria spp.
- stenoxenous: meaning narrow host range
- worldwide distribution
- organ specificity depending on species: sm. or lg intestine, cecum, rarely liver or kidney
- monoxenous: paracitize only one host
characteristics of sporulated oocysts in CystoIsospora and Eimeria
- Isospora: 2 sporocysts, 4 sporozoites each
- Eimeria: 4 sporocysts, 2 sporozoites each
host types for Cystoisospora and Eimeria
- cystoisospora: dogs, cats, pigs, humans
- Eimeria: birds, cattle, small ruminants, horses, rabbits, rodents, pigs
Cystoispora and Eimeria life cycle
- Sporogony:
- resistant, thick-walled oocyst released via feces - sporulates
- sporulated oocyst ingested by host via contaminated soil, food, water, bedding or litter
- excysting sporozoites
- trophozoite undergoes shizogony (asexual repro via binary fission which produces merozoites)
- produces type 1 schizont
- devlops into tpe 2 schizont via epithelial cells
- merzoites form gametocytes
- gametocytes form zygote which develops into oocyst and the cycle starts all over again
Eimeria bovis & Eimeria zuernii characteristics
- host: cattle
- resistant oocyst
- development in terminal ileum and colon
- intracellular
Eimeria bovis & Eimeria zuernii and their effect on calves: susceptibility and clinical signs
susceptibility:
- calves 3 weeks - 6 months of age
- more problematic in confinement rearing
clinical signs: diarrhea, anorexia, dullness, dehydration, weight loss, fever, dysentery, tenesmus, intestinal lesions, death possible
Eimeria bovis characteristics
- easier to diagnose
- oocysts present when disease begins
- pre-patent period 5-15 days
- gametogony causes majority of damage
- type 1 schizonts are macroscopic
- cause mucosal damage:
- becomes edematous, congested
- petechiae (small purple/red spot that causes bleeding into skin)
- diffuse hemorrhages
- blood may fill lumen
- mucosa/submucosa lost
Eimeria zuernii characteristics
- more severe
- SCHIZOGONY produce most damage
- bloody diarrhea
- lumen may fill with blood, possible clotting
- tenesmus
- coughing can cause blood to squirt out anus 2-3 meters
- calves become anemic & emaciated
Eimeria zuernii acute phase vs. chronic phase
Acute Phase
- 7-10 days PI, death common
- much of mucosa destryoed
- prepatent period 15-17 days damage occurs much earlier
Chronic Phase
- survive acute phase
- diarrhea remains, blood loss abates
- emaciated, weak, rough coat, sunken eyes
- catarrhal enteritis develops in termina SI and colon
- neurological signs possible
Isospora suis characteristics as seen in pigs
- primary disease in suckling piglets (frequently between 8-15 days old
- contaminated feces: oocyst sporulates 1 - 3 days
- sporozoites penetrate villous epithelium
= greatest concentration jejunum & ileum
= cecum & colon involved if severe infection
- prepatent: 5 - 7 days
- patent: 5 - 16 days; peak when piglets 12 days old
Isospora suis clnical signs
- pasty/liquidy diarrhea (white/yellow in color, can be brownish gray)
- NO BLOOD in feces
- rough hair coat
- dehydaration
- low weight gain
- low mortality
- microscopically can see villous atrophy, fusion, necrotic enteritis, crypt hyperplasia, lesions encourage invasion of secondary pathogen
Coccidiosis prevention
- use feed bunkers to reduce fecal contamination
- use automatic watering systems to help with hygiene
- keep area dry - let oocysts desciate
- separate older and younger stock
- clean pens with high pressure hot water
- piglets: separate from feces, farrowing pens with slatted floors
Cryptosporidum Life Cycle
- resistant, thick-walled oocyst released via feces and ingested (may have thin-walled oocyst which is autoinfection)
- sporozoite is excysted.
- trophozoite undergoes schizogony
- Type 1 schizont with 8 merozoites and Type 2 schizont with 4 merzoites availble for reinfection
- merozoite undergoes gametogony which develops into a zygote and then another oocyst
cryptosporidum patent period
- 1 - 12 days for calves
- will be seen in microvillus border of intestine
cryptosporidium transmission
- direct contact with infective oocyst
- mucosal scrapings or tissue homogenates
- contaminated food or equipment
- water
factors that increase waterborne outbreak of cryptosporidium
- close association between animals and humans
- large numbers oocysts ecreted
- low infective dose
- small oocyst size and oocyst resistance
Cryptosporidium spp. oocyst resistance: physical disinfection vs. chemical disinfection
physical disinfection:
- heat to 64-72C for 1-5 minutes
- freezing down to -20C, -70C no survival
- UV radiation (high doses render oocysts noninfectious)
Chemical disinfection:
- chlorine, hypochlorite, hydrogen peroxide (for 30 minutes), iodine (30 - 60 minutes)
- the following does not work: ethanol, isopropanol, lysol, pine-sol, formaldehyde, betadine
is water processing effective against cryptosporidium?
not necessarily!
water processing methods that are effective against cryptosporidium
- reverse osmosis
- distilled
- filtered using a filter <1 micron
- canned/bottled soda
- steaming hot (175 F) drinks
- pasteruized drinks
cryptosporidiosis susceptibility and clinical signs
susceptibility in calves <3 weeks old
clinical signs:
- acute onset
- profuse, watery diarrhea often yellow in color
- anorexia, dehydration, wegith loss
- duration: oocyst shedding: 12 days, diarrhea: avg 8 days
- villous atrophy, enteritis, fusion of villi (biopsy)
Toxoplasmosis: taxonomy, host, transmission
taxonomy: order Eucoccidiida, phylum apicomplexa
IH: most mammals
DH: members of felidae family
transmission:
- acquired: oocysts, raw/undercooked meat
- congenital: transplacental
toxoplasma gondii life cycle
- cat and/or IH ingests either the sporulated oocyst, the tachyzoite (congenital), or bradyzoite (IH - infective stage
- schizogony (asexual repro) + gametogony (sexual repro in cat intestine)
- oocysts in feces
- tachyzoites develop in any cell except RBC
- placenta - fetus
- immunity develops - bradyzoites develop as cysts in host tissue
(cycle may reinitiate after decline of immunity cycle)
toxoplasma gondii:
intermediate host
- tachyzoites develop after 12 hour PI
- bradyzoites and tissue cysts develop by 6 days PI
toxoplasma gondii effect on cats including clinical signs
- no confirmed oocyst shedding in clnically ill cats
- seroconvert 2-3 weeks PI
- studies indicate cats shed once
- relapse shedding (concomitant infections with I. felis, immunosuppression)
- clinical signs in cats: fever, anorexia, jaundice, abdominal pain, pancreatitis, neuro problems, respiratory interference, death
toxoplasma gondii: cattle, dogs, sheep, goats
- cattle: not good IH, can’t support parasite for > 30 days
- dogs: sero+ dogs
- sheep: main cause of infective ovine abortion, inflammation fetal cotyledons ‘hallmark’
- goats: abortions, more susceptible to clinical toxoplasmosis, fever, lethargy, diarrhea, decreased appetite
Toxoplasma gondii diagnosis
- fecal flotation
- serological examination (IFA, ELISA)
- one positive sample only indicates past infection
- 16-fold rise in titer in serum taken 2-4 weeks after 1st indicates acute acquired infection
- histological examination (biopsy)
- PCR
Toxoplasma gondii control
- cats: do not feed raw meat, keep cats indoors to prevent hunting
- humans: cook meat, change litter box daily, wear gloves while gardening
- other IH hosts: remove dead animals or aborted fetuses promptly, limit cat access to avoid water/food contamination
Neospora caninum: hosts and transmission
- IH: cattle, sheep, goats, deer
- DH: mainly dogs and coyotes
- transmission:
acquired: oocysts, consumption of raw infected meat, fetus, placenta
congenital: transplacental
Neospora caninum: life stages
- Bradyzoite
- slowly dividing, tissue cyst
- usually in CNS
- can remain viable in tissue (dead animals) 7 - 10 days
- Tachyzoite: rapidly dividing, any tissue
- oocyst
- sporulates within 24 hours
- prepatent period (dogs): approx 5 days
- patent period: varies, can be months
Neospora caninum life cycle
- dog ingests bradyzoites - invade intestinal epithelium
- schizonts develop - schizogony occurs
- merozoites released - reinvade - 2nd schizont OR gamont develops
- gamonts undergo gametogony - zygote - unsporulated oocyst passed in feces
- IH: bradyzoites or sporozoites (oocyst) invade intestinal epithelium - tachyzoites
- tachyzoites encyst mainly in muscle, CNS or travel to placenta
Neospora caninum and its effect on puppies
- neosporosis most severe in congenitally infected puppies.
- it causes limb paralysis - hind limb hyperextension
- occurs 3-6 weeks after birth, not all littermates affected equally or simulatenously
- generalized disease in some pups and older dogs: there is usually CNS involvement, myocarditis, hepatitis, pneumonia
- if untreated, dogs with clinical neosporosis usually die & prognosis with treatment is variable
Neospora caninum effect on cattle
- abortion only clinical sign in adults - usually occurs 3 months in gestation to term
- fetuses born alive remain chronicall infected
- in sheep and goats it causes abortions, neonatal paralysis
neospora caninum: horses
- neospora hughesi
- clinical signs resemble EPM (equine protozoal myeloencephalitis)
- most EPM cases are sarcocystis neurona
neospora caninum: diagnosis
- fecal float
- blood tests: IFA, ELISA
- rise in titer in serum takes 2-4 weeks after 1st indicates acute acquired infection
- diagnosis in conjunction with clinical signs
- titer > 1:50 suggestive of infection
- titer at least 1:200 - most dogs with clinical infection, careful of cross-reactivity with toxoplasma
- histological examination
- PCR
Neospora caninum: control
- limit canine exposure to animal housing facilities ie limit oocyst examination
- remove dead animals or aborted fetuses
- do not breed bitches infected with N. caninum
- do not feed dogs raw meat
- don’t know if zoonotic
Basics on sarcocystis: taxonomy, distribution, hosts, transmission
- phylum apicomplexa
- distribution: worldwide
- hosts: predator-prey relationship
- DH: carnivore
- IH: herbivore
transmission: DH = consuming sarcocysts IH = ingesting sporocysts
sarcocystis life cycle
- schizonts form in endothelial cells of blood vessels of brain, liver, kidney - sarcocysts form in skeletal and cardiac muscle of IH
- gametogony occurs in the intestine of the DH
- sporocysts released in feces.
sarcocystis cruzi: cattle
- causes Dalmeny disease
- symptoms include: intermittent fever, diarrhea, vaginitis, abortion, mild nervousness, decreased milk yields, anemia, death
sarcocystis spp: sheep and goats
in sheep:
usually causes acute disease, anemia, anorexia, fever death
in goats:
weakness, anorexia, fever, death, abortion
sarcocystis spp.: pigs, humans
_ in pigs:_
- mild infection is asymptomatic
- poor growth, meat quality and weight gain reduced, abortion
in humans:
- anorexia, abdominal pain, diarrhea
sarcocystis spp: in horses
true IH: sarcocystis bertrami, S. fayeri, s. equicanis
aberrant/dead-end host: sarcocystis neurona
DH: opossum; IH: otter, racoon, seal, skunk, armadillo
causes EPM (equine protozoal myeloencephalitis)
- CNS disease
- lesions in spinal cord, brain, meninges
- clinical signs: head tilt, drooping eyelids, facial paralysis, circling, stumbling, falling
- schizonts develop in neural cells and destroy them; process repeated by merozoites released by lysed cell
- no sarcocysts develop
sarcosporidiosis: diagnosis and control
- fecal flotation
- biopsy (looking for schizonts [IH] “rosettes” or sarcocysts)
- western blot (looking for Ab in serum or CSF)
- PCR
control: bury/incinerate dead livstock, cover stored grain, keep carnivores out of animal housing facilities
Order Piroplasmida
(phylum apicomplexa)
- develop in erythrocytes
- indirect life cycle (ticks used as vectors)
- diagnosis: blood smears, serology
- genera: cytauxzoon, babesia, thelieria
Cytauxzoon felis: taxonomy, distribution, hosts
- order piroplasmida, phylum apicomplexa
- among emerging infectious disease in N. America
- Hosts: DH: domestic cats, IH: dermacentor variabilis, amblyomm americanum, reservoir host: N. American bobcat
Cytauxzoon felis: epidemiology
- usually found in feral/farm cats
- most often seen in summer
- reservoir host found in bobcats
Cytauxzoon felis: life cycle
- tick feeds on infected host - ingests piroplasms in erythrocytes
- piroplasms travel to the salivary glands of the tick
- infected tick feeds on DH (cat) - schizogony occurs in macrophages. merozoites released when macrophage ruptures then enter erythrocytes and develop into piroplasms
and then it starts all over.
transstadial transmission can occur!
cytauxzoon felis: 2 forms of pathogenicity
there are two forms: a fatal form and a non-fatal form.
fatal form: fever, depression, lethargy, anorexia, jaundice, death in less than 1 week
non-fatal form: similar signs as “fatal’ form, may be asymtomatic, persistent parasitemia
cytauxzoon felis: details on pathogenicity
- schizogenous phase most destructive because macrophages infected with schizonts block blood vessels with multi-organ failure
- clinical signs appear approximately 10 days PI (post infection). severe cases can be rapidly progressive with PI in 6 days
- postmortem will find: dark, enlarged spleen, lungs, lymph nodes reddened and petechiated, pericardial sac may contain gelationus, icteric fluid
cytauxzoon felis: diagnosis and control
diagnosis: blood smears, PCR, biopsy/necropsy visceral organs (histiocytes - will have displaced nucleus, and cytoplasm filled with granules)
control: keep cats indoors, use acaricides for tick control, promptly remove ticks
