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Parasitology > Protozoa > Flashcards

Protozoa Flashcards

1
Q

characteristics of protozoa

A
  • eukaryotic - unicellular - contain nucleus, mitochonrdira, ER, golgi app. - and can be heterotrophic or autotrophic
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2
Q

protozoan organelles of locomotion

A
  • flagella - cilia - pseudopods - undulating ridges, subpellicular microtubules
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3
Q

protozoan reproduction

A
  • binary fission (asexual) - multiple fission or schizogony (asexual) - budding (asexual) - conjugation (asexual) - gametogony (sexual)
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4
Q

heterotrophs can be: holozoic or saprozoic

A

holozoic: ingest via mouth saprozoic: absorb nutrients thru cell membrane

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5
Q

phylum of protozoa

A
  • sarcomastigophora - apicomplexa - ciliophora - microspora
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6
Q

phylum ciliophora characteristics and genera

A
  • 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
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7
Q

phylum microspora characteristics

A
  • obligate, spore-formers - intracellular parasites of vertebrates & invertebrate - characteristic feature: polar filament or polar tube used to infiltrate host cells - close to fungi
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8
Q

phylum sarcomastigophora characteristics

A
  • distinct nucleus - movement: most use flagella - ASEXUAL reproduction - life cycles: direct and indirect
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9
Q

giardia spp. characteristics

A

cysts: resistant, INFECTIVE STAGE Trophozoites: vegetative, reproducing stage, mucosal surface of small intestine

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10
Q

giardia lifecycle

A
  1. 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
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11
Q

Giardia spp. clinical signs, prevalence, and diagnosis

A

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
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12
Q

Trichomonad characteristics

A
  • 3 anterior flagella
  • 1 posterior, recurrent flagellum
  • axosytle -> a microtuble
  • pseudocysts
  • longitudinal binary fission
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13
Q

trichomonad structure:

A

pelta - support flagella

axostyle - support cell body

  • parabasal body - golgi apparatus
  • blepharoplast - origin of flagella
  • costa - unique, support UM
  • hydrogenosomes - ATP and H+ producer
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14
Q

Tritichomonas foetus

A
  • causes Bovine Genital Trichomonosis
  • venereal disease
  • cows: vagina, cervix, uterus
  • bulls: prepucial cavity
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15
Q

Bovine Genital Trichomonosis: clinical features

A
  • 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
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16
Q

Bovine Genital Trichomonsis: clinical features for cows and bulls

A
  • bulls (chronic carriers) are aysmptomatic
  • cows (clear 2-6 months): get vaginitis, cervicitis, endometritis, pyometra, mucopurulent discharge
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17
Q

Bovine Genital Trichomonosis: diagnosis

A
  • recover organisms
  • PCR
  • direct smear
  • culture organisms
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18
Q

Non-pathogenic Bovine Trichomonads

A

Pentatrichomonas hominis

  • 3-5 anterior flagella
  • 1 posterior flagellum

Tetratrichomonas spp.

  • 4-5 anterior flagella
  • 1 posterior flagellum
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19
Q

Bovine Genita Trichomonas: Control

A
  • 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)
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20
Q

Feline Trichomoniasis

A

large bowel disease:

  • chronic diarrhea
  • tenesmus
  • flatulence
  • irritated anus
  • fecal incontience

transmission unknown

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21
Q

feline trichomoniasis: clinical features

A
  • 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
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22
Q

feline Trichomoniasis: diagnosis

A
  • direct fecal smear
  • culture
  • PCR
  • colonic biopsy
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23
Q

Feline Trichomoniasis: Control

A
  • keep infected cats away from other cats
  • do not allow litter box sharing
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24
Q

Trypanosoma cruzi characteristics

A
  • 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
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25
Q

Characteristics of Trypanosomes and their life stages

A

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
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26
Q

Trypanosoma cruzi

A
  • 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
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27
Q

Trypanosoma cruzi: morphology

A
  • 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
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28
Q

Trypanosoma cruzi: lifecycle

A
  1. metacyclic trypomastigotes are the INFECTIVE STAGE; passed in feces of IH. they enter host via bite wound, scratch or mucus membrane
  2. trypomastigotes - found in blood, enter cells of spleen, liver, lymphatics and muscle
  3. amastigotes replicate via BINARY FISSION - form clusters in pseudocysts
  4. cells rupture and trypomastigotes remain in circulation or reinfect
  5. trypomastigotes transform into epimastigotes - they replicate via BINARY FISSION
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29
Q

Trypanosoma cruzi: Chagas Disease in Humans

A

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
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30
Q

Trypanosoma cruzi

American Trypanosomiasis in Dogs

A
  • 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
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31
Q

Trypanosoma cruzi diagnosis

A

serological testing including: TESA blot/Western blot, ELISA, IFA (indirect immunofluorescence assay), IHA (indirect hemagglutination assay)

  • blood smear
  • xenodiagnosis
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32
Q

Phylum Apicomplexa Characteristics

A
  • distinct nucleus
  • movement: subpellicular tubules
  • apical complex
  • Orders: Eucoccidiida, Piroplasmida
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33
Q

Order Eucoccidiida Characteristics

(Phylum Apicomplexa)

A
  • 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
34
Q

Cystoispora (Isospora) and Eimeria spp.

A
  • 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
35
Q

characteristics of sporulated oocysts in CystoIsospora and Eimeria

A
  • Isospora: 2 sporocysts, 4 sporozoites each
  • Eimeria: 4 sporocysts, 2 sporozoites each
36
Q

host types for Cystoisospora and Eimeria

A
  • cystoisospora: dogs, cats, pigs, humans
  • Eimeria: birds, cattle, small ruminants, horses, rabbits, rodents, pigs
37
Q

Cystoispora and Eimeria life cycle

A
  1. Sporogony:
  • resistant, thick-walled oocyst released via feces - sporulates
  • sporulated oocyst ingested by host via contaminated soil, food, water, bedding or litter
  1. excysting sporozoites
  2. trophozoite undergoes shizogony (asexual repro via binary fission which produces merozoites)
  3. produces type 1 schizont
  4. devlops into tpe 2 schizont via epithelial cells
  5. merzoites form gametocytes
  6. gametocytes form zygote which develops into oocyst and the cycle starts all over again
38
Q

Eimeria bovis & Eimeria zuernii characteristics

A
  • host: cattle
  • resistant oocyst
  • development in terminal ileum and colon
  • intracellular
39
Q

Eimeria bovis & Eimeria zuernii and their effect on calves: susceptibility and clinical signs

A

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

40
Q

Eimeria bovis characteristics

A
  • 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
41
Q

Eimeria zuernii characteristics

A
  • 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
42
Q

Eimeria zuernii acute phase vs. chronic phase

A

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
43
Q

Isospora suis characteristics as seen in pigs

A
  • 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
44
Q

Isospora suis clnical signs

A
  • 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
45
Q

Coccidiosis prevention

A
  • 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
46
Q

Cryptosporidum Life Cycle

A
  1. resistant, thick-walled oocyst released via feces and ingested (may have thin-walled oocyst which is autoinfection)
  2. sporozoite is excysted.
  3. trophozoite undergoes schizogony
  4. Type 1 schizont with 8 merozoites and Type 2 schizont with 4 merzoites availble for reinfection
  5. merozoite undergoes gametogony which develops into a zygote and then another oocyst
47
Q

cryptosporidum patent period

A
  • 1 - 12 days for calves
  • will be seen in microvillus border of intestine
48
Q

cryptosporidium transmission

A
  • direct contact with infective oocyst
  • mucosal scrapings or tissue homogenates
  • contaminated food or equipment
  • water
49
Q

factors that increase waterborne outbreak of cryptosporidium

A
  • close association between animals and humans
  • large numbers oocysts ecreted
  • low infective dose
  • small oocyst size and oocyst resistance
50
Q

Cryptosporidium spp. oocyst resistance: physical disinfection vs. chemical disinfection

A

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
51
Q

is water processing effective against cryptosporidium?

A

not necessarily!

52
Q

water processing methods that are effective against cryptosporidium

A
  • reverse osmosis
  • distilled
  • filtered using a filter <1 micron
  • canned/bottled soda
  • steaming hot (175 F) drinks
  • pasteruized drinks
53
Q

cryptosporidiosis susceptibility and clinical signs

A

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)
54
Q

Toxoplasmosis: taxonomy, host, transmission

A

taxonomy: order Eucoccidiida, phylum apicomplexa

IH: most mammals

DH: members of felidae family

transmission:

  • acquired: oocysts, raw/undercooked meat
  • congenital: transplacental
55
Q

toxoplasma gondii life cycle

A
  1. cat and/or IH ingests either the sporulated oocyst, the tachyzoite (congenital), or bradyzoite (IH - infective stage
  2. schizogony (asexual repro) + gametogony (sexual repro in cat intestine)
  3. oocysts in feces
  4. tachyzoites develop in any cell except RBC
  5. placenta - fetus
  6. immunity develops - bradyzoites develop as cysts in host tissue

(cycle may reinitiate after decline of immunity cycle)

56
Q

toxoplasma gondii:

intermediate host

A
  • tachyzoites develop after 12 hour PI
  • bradyzoites and tissue cysts develop by 6 days PI
57
Q

toxoplasma gondii effect on cats including clinical signs

A
  • 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
58
Q

toxoplasma gondii: cattle, dogs, sheep, goats

A
  • 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
59
Q

Toxoplasma gondii diagnosis

A
  • 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
60
Q

Toxoplasma gondii control

A
  • 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
61
Q

Neospora caninum: hosts and transmission

A
  • IH: cattle, sheep, goats, deer
  • DH: mainly dogs and coyotes
  • transmission:
    acquired: oocysts, consumption of raw infected meat, fetus, placenta
    congenital: transplacental
62
Q

Neospora caninum: life stages

A
  • 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
63
Q

Neospora caninum life cycle

A
  1. dog ingests bradyzoites - invade intestinal epithelium
  2. schizonts develop - schizogony occurs
  3. merozoites released - reinvade - 2nd schizont OR gamont develops
  4. gamonts undergo gametogony - zygote - unsporulated oocyst passed in feces
  5. IH: bradyzoites or sporozoites (oocyst) invade intestinal epithelium - tachyzoites
  6. tachyzoites encyst mainly in muscle, CNS or travel to placenta
64
Q

Neospora caninum and its effect on puppies

A
  • 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
65
Q

Neospora caninum effect on cattle

A
  • 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
66
Q

neospora caninum: horses

A
  • neospora hughesi
  • clinical signs resemble EPM (equine protozoal myeloencephalitis)
  • most EPM cases are sarcocystis neurona
67
Q

neospora caninum: diagnosis

A
  • 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
68
Q

Neospora caninum: control

A
  • 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
69
Q

Basics on sarcocystis: taxonomy, distribution, hosts, transmission

A
  • phylum apicomplexa
  • distribution: worldwide
  • hosts: predator-prey relationship
  • DH: carnivore
  • IH: herbivore
    transmission: DH = consuming sarcocysts IH = ingesting sporocysts
70
Q

sarcocystis life cycle

A
  1. schizonts form in endothelial cells of blood vessels of brain, liver, kidney - sarcocysts form in skeletal and cardiac muscle of IH
  2. gametogony occurs in the intestine of the DH
  3. sporocysts released in feces.
71
Q

sarcocystis cruzi: cattle

A
  • causes Dalmeny disease
  • symptoms include: intermittent fever, diarrhea, vaginitis, abortion, mild nervousness, decreased milk yields, anemia, death
72
Q

sarcocystis spp: sheep and goats

A

in sheep:

usually causes acute disease, anemia, anorexia, fever death

in goats:

weakness, anorexia, fever, death, abortion

73
Q

sarcocystis spp.: pigs, humans

A

_ in pigs:_

  • mild infection is asymptomatic
  • poor growth, meat quality and weight gain reduced, abortion

in humans:

  • anorexia, abdominal pain, diarrhea
74
Q

sarcocystis spp: in horses

A

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
75
Q

sarcosporidiosis: diagnosis and control

A
  • 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
76
Q

Order Piroplasmida

(phylum apicomplexa)

A
  • develop in erythrocytes
  • indirect life cycle (ticks used as vectors)
  • diagnosis: blood smears, serology
  • genera: cytauxzoon, babesia, thelieria
77
Q

Cytauxzoon felis: taxonomy, distribution, hosts

A
  • 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
78
Q

Cytauxzoon felis: epidemiology

A
  • usually found in feral/farm cats
  • most often seen in summer
  • reservoir host found in bobcats
79
Q

Cytauxzoon felis: life cycle

A
  1. tick feeds on infected host - ingests piroplasms in erythrocytes
  2. piroplasms travel to the salivary glands of the tick
  3. 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!

80
Q

cytauxzoon felis: 2 forms of pathogenicity

A

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

81
Q

cytauxzoon felis: details on pathogenicity

A
  • 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
82
Q

cytauxzoon felis: diagnosis and control

A

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

Parasitology (6 decks)

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