• Single celled, (multi)nucleated organism

Classification:

• Sarcodina
• Ciliates
• Flagellates
• Sporozoa

Asexual:

• Binary fission- one individual divides into two daughter cells
• Multiple fision- the nucleus and other organelles divide repeatedly before cytokinesis, leading to several daughter cells

Sexual:

• Haploid cells reulting from meiosis, followed by the union of 2 cells to restore diploidy

Encystment

•  secretion of a resistant covering and entrance into a resting stage
• Caused by adverse enviromental conditions: food deficiency, desiccation (extreme dryness), increased tonicity (osmotic pressure), decreased Oxygen, pH or temp change

Excystation

• Return to normal during favorable conditions

• Flagella-whip like structures
• Cilia-small whip like structures
• Pseudopodia-temporary extensions of the cell membrane
• No locomotor organelles

Move by means of pseudopodia

Diseases: Amebic dysentery, primary amebic

meningoencephalitis

Move by means of cilia

Diseases: Balantidiasis

Move by means of flagella

Diseases: Trichomoniasis, giardiasis, trypanosomiasis, leishmaniasis

• No organelles of locomotion, gliding movement
• Most are obligate intracellular parasites
• Apical complex
• Complex life cycle: 3 distinct processes- sporogony, gametogeny, schizogony

Diseases: Coccidiosis, toxoplasmosis, isosporosis, Malaria

• A network of circular DNA (called kDNA) inside a large mitochondrion that contains many copies of the mitochondrial genome
• An independently replicating structure lying near the base of the flagellum in certain protozoans

Leishmania and T. cruzi
intracellular replicative form

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Leishmania insect forms

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T. cruzi and
T. brucei insect form

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• Trypanosoma cruzi & Trypanosoma brucei mammalian forms
• T. brucei “procyclic” trypomastigote insect form

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Trypanosomatid

• Infected 16-18 million
• Disease Outcome (untreated): 10-30% die of complications after decades of infection
• Vaccine prospects: Poor, antigenic variation
• Available drugs: Toxic and ineffective in chronic infection
• Drug resistance: Suspected

Trypanosomatid

• Infected: 300-500 K
• Disease outcome (untreated): Uniformly fatal within 2 years
• Vaccine Prospects: Poor, antigenic variation
• Drug Resistance documented

Trypanosomatid

• Infected: 2 million
• Disease outcome (untreated): Viseral form is fatal
• Vaccine prospects: Poor, effective immune evasion
• Drug resistance documented

Cause: Leishmania spp.

• Annual incidence: 2 million
• Visceral Leishmaniasis is fatal, epidemics in India, Ethiopia, Sudan
• Vector: Sand flies
• No vaccine, drugs are toxic + resistance is mounting

1. Procyclic promastigote to metacyclic promastigote in the Sand fly (vector)
2. Amastigote-infected macrophage in the mammalian host
3. Cell Culure are lathargic and statioanry vs active In vitro

• Microscopic detection of parasites
• Culture and speciate parasites
• Serology (rarely used)
• DNA detection, PCR (rarely used)

• Pentavalent antimonials (stibogluconate)
• Miltefosine: Visceral Leishmaniasis
• Second line: Fluconazole, Amphotericin B, Itraconzole, Ketoconazole

Prevention

• Vector control (sand fly)
• Insect precautions
• Animal reservoir control

1. Metacyclic trypomastigotes infect cells and transform into amstigotes
2. Amastigotes multiply by fission in cells
3. Amastigotes transform into trypomastigotes and rupture the cell, entering the blood stream (diagnostic stage)
4. A kissing bug (reduviid) ingests a trypomastigote, it then transforms into a epimastigote in the midgut and multiplies
5. The epimastigote turns into a metacyclic trypomastigote, which is transmitted to a host through the bug's feces

Acute Chagas' disease

• Chagoma, Romana's sign
• Fever, anorexia, hepatosplenomegaly, adenopathy
• Resolves spontaneously (4-8 weeks)

Intermediate phase

• ~14 years
• No symptoms. low level parasitemia

Chronic Chagas' disease (10-30%)

• Cardiac disease - cardiomegaly, CHF, mural thrombus, arrhythmias
• Megadisease - megaesophagus, megacolon

Therapy suboptimal:

Benznidazole or nifutimox

• Direct demonstration best
• Serology can be helpful

• Suramin or Pentamidine when not in the CNS
• Melarsoprol or difluoromenthylornithine With CNS involvement
• Untreaed=fatal
• relapses are common after treatment
• >5% mortality with arsenical therapy

African Sleeping Sickness

T. brucei gambiense (W Africa)

T. brucei rhodesiense (E Africa)

• Transmitted by Tsetse fly
• Evades immune response by antigenic variation
• Initial: chancre, lymph node enlargement, blood stage infections, fever
• Late: invasion of the CNS (weeks in rhodesiense, months in gambiense), neuropsych, somnulence, coma

African sleeping sickness (W/SW Africa)

• Tsetse Vector: Glossina palpalis group
• Ecology: Rainforest, riverine, lakes
• Transmission: Human-fly-Human
• No amimal reservoir
• Epidemology: Endemic, some epidemics
• Disease: Slow (~1yr) acute->chronic
• Low parasitemia
• Asymptomatic carriers are common

African Sleeping sickness (E/Central Africa)

• Tsetse vector: Glossina morsitans group
• Ecology: Dry brush, woodland
• Transmission: Ungulate-fly-Human
• Epidemiology: Sporadic, safaries
• Disease: Rapid progression to death
• High parasitemia
• Asymptomatic carriers are rare

Human stages

1. Injected metacyclic trypomastigotes transform into trypomastigotes in the bloodstream
2. Trypomastigotes multiply by binary fission in blood, lymph and spinal fluid

Tsetse fly stages

1. Fly takes blood meal, ingesting trypomastigotes
2. trypomastigotes transform into procyclic trypomastigotes in the fly's midgut and multiply by binary fission
3. Procyclic trypomastigotes leave the midgut and transform to epimastigotes
4. Epimastigotes multiply in the salivary glands and trans form into metacyclic trypomastigotes
5. Tsetse fly bites a human and completes the cycle

Unique

• no intermediate host is required
• transmission by direct sexual contact

Disease: Equine dourine

• Acute stage: swelling of the genetalia/ mucoid discharge
• Chronic stage: emaciation, paresis, fever and death
• Control: cull infected animals. Eradicated from N. America

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Disease: Trichomoniasis in cattle

• venereal disease, usually transmitted by bulls
• causes infertility and occasional abortions
• costly to eradicate
• organism lives in microscopic folds of skin bulls: penis (lifetime), cows: uterus or vagina until immune system eliminates it (repeat infection possible)

• Asymptomatic carrier: semen quality and sexual behavior normal
• Parasites live in the crypts inside the sheath
• older bulls have more crypts for T. fetus
• older bull is more likely to be chronically infected

• No clinical signs
• occasional vaginal discharge in 1-3 weeks
• Inflammatory response leads to aborstion
• inconsistant calving period

• 10-40% decrease in pregnant cows
• Spread out calving season

Bulls

• Best to test after 2 weeks sexual rest( 3 tests recomended for >99% sensitivity)
• Usually culture for 1 to 7 days;
• If even one bull is positive, assume the herd has been exposed
• Cows
  • Usually clear infection rapidly – often in one season
  • Test soon after embryo death
  • Months delay for suggestive history in a herd

• All breeds are susceptible
• ~⅓ purebred feline population may be
infected
• T. fetus can live for several days in wet
stools
• The primary route of infection is
probably the litter box
• Infected cats may be asymptomatic
• Symptomatic cats show diarrhea – cow
pie-like stools that are often gassy and
malodorous

Treatment: Ronidazole for 2 weeks

1. cysts ingest in food or water
2. Trophozoites multiply in the GI tract
3. cysts are shedd in the feces

• Transmission: fecal-oral route

G. doudenalis: Animals and humans

G. agilis: Amphibians

G. muris: Rodents

G. ardeae and G. psittaci: Birds

• Zoonotic A: humans, livestock, cats, dogs, beavers, guinea pig, slow loris
• Zoonotic B: humans, slow loris, chincillas, dogs, beavers, rats, siamang
• Dog C,D: Dogs
• Livestock E: Cattle, sheep, pigs
• Cat F: Cat
• Rat G: Domestic rats
• Muskrats Vole: wild rodents

• Cysts are immune to chlorinization
• Trophozoites reproduce in the small intestine
• Most human cases

• Attachment to the microvilli of the proximal small intestine to feed, occasionally this causes ulceration
• Malabsorption of nutrients is common

• Most animals are asymptomatic
• Diarrhea, with vomiting
• Normal appetite with body weight loss
• Grayish and greasy feces with bad odor

• Parasites in feces

1. Fecal smear: mobile trophozoites
2. Flotation: cysts

• Antigens in feces: ELISA

Antibiotics: Not safe in puppies or pregnant animals.

Panacur: safe in puppies older than 6 weeks

Drontal: safe in puppies over 3 weeks and more than 2 lbs

Preventing pets from infection:

• Avoid contact with animal feces
• Clean and kill the protozoa in environment: Lysol, bleach, and quaternary ammonium compounds

Control giardiasis once infected:

•Treat infected animals
•Decontaminate the environment: Lysol, bleach, and quaternary ammonium compounds
•Clean animals
•Prevent reintroduction

Schizogony -> Gametogony inside the host

Sporogony outside the host

Sporozoa

• Intracellular asexual reproduction
• Monoxenous (one host) or digenetic (two hosts)
• Parasites of vertebrates and invertebrates
• Life cycle: Merogony, gametogony, and sporogony
• Infective stage: rod- or banana-shaped sporozoites
• Emeria spp., Cryptosporidium spp., Cystoisospora spp.

• Requiring one host
• Often restricted to a certain host species
• Most are gastrointestinal parasites of
  vertebrates
• A given species may be limited to a
  narrow zone, specific kind of cells in a
  zone, even specific locations within the
  cells
• Number of Eimeria species numerous
• Merogony and gametogony within a host,
  sporogony typically outside of hosts

• Parasite of chickens
• Living in epithelium of intestinal ceca
• High mortality rate in young birds
• An estimate of $80M annual loss-Mid-1980s
• Annual expenditures for coccidiostates worldwide are estimated to be $250-300M

Pathogenesis

• Bloody diarrhea
• Sloughing of epithelium
• Plugged cecum due to clotted blood and cell debris, causing necrosis, No Effective Treatment

Prevention

• Prophylaxes using coccidiostats in food or water
• Vaccines, effective with species specificity

Eimeria bovis, E. auburnensis, E. zuernii: Cattle

E. faurei, E. intricata, E. ovina, E. ovinoidalis: Sheep

E. tenella, E. maxima: Chickens

E. arloingi, E. ninakohlyakim ovae, E. christensen: Goats

E. scabra, E. suis: pigs

E. intestinalis, E. perforans, E. stiedai (bile ducts): rabbits

• Prophylaxis of anticoccidian can help control disease outbreak
• No effective treatment

• Cryptosporidium parvum
• All  stages of the life cycle occur in the small intestinal epithelial cells
• Reservoir: farm animals, kittens, humans
• Cysts are resistant to chlorination
• Common in developing countries
• Causes watery diarrhea ~2 weeks
• Diagnosis: stool sample antigen test

A. Mammalian host: asexual cycle
• Cyst
• Tachyzoite (fast rate of proliferation)
• Tissue cyst with bradyzoite (slow rate of proliferation)

B. Definitive host (cat family)
• Sexual (enteroepithelial ) cycle

• Fetus may contract toxoplasmosis from the mother
• Mother may be infected from handling cat litter
• Can cause stillbirth, nuerological disease

• Distribution: cosmopolitan, most common protozoan infection
• Risk factors: host age, virulence of strain
• Transmission: transplacental, raw undercooked meat (Pork, lamb > beef), Cat feces, transfussion
• Leads to chronic infection with no symptoms most of the time

• Parasites of RBC of vertebrate hosts
• Ticks as vectors – sporogony within the epithelium of the intestinal wall
• Many species: B. microti, B. divergens important
• Human=deadend host, natural reservoir is ticks and mice

Epidemiology:

• Acquired from the bite of an Ixodes sp. tick
• Erythrocytic cycle only

Disease Manifestations:

•  Flu-like symptoms: Fever, hemolysis, anemia, hepatomegaly, splenomegaly
• B. divergens – severe, often fatal in splenectomized patients
• B. microti – milder, persists weeks to months normal hosts

Diagnosis:

• Blood smears

• Canine definative host
• Ruminant intermediate host
• Causes (+10-30%) aborstions in cattle
• livestock contract it by soil, food, water contamination with oocysts
• Canines eat bradyzoits in meat and become infected

• Sarcocystis nuerona
• Definitive host: Opossum
• Aberrant host: Horse
• Intermediate host: cat, skunk, coon, sea otter
• Causes ataxia and atrophy of hind quater 
• A progressively debilitating disease
  affecting the CNS, brain, brainstem, and
  spinal cord of horses
• Treat as quick as possible once diagnosed
  A successful recovery in 70-75% horses

• Close contact between pigs and humans
• tropical climate, poor waste disposal

Disease

• Asymptomatic
• Chronic infection - nonbloody diarrhea, cramping, halitosis, and abdominal pain
• Fulminating balantidiosis - mucoid, bloody stools with 30% fatality

Diagnosis: wet mount, trophozoite and cyst

Treatment:

• Tetracycline: 500mg. Qid, 10d
• Metronidazole: 750 mg, tid, 5d

• Cause of primary amebic meningoencephalitis
• Rare, world-wide, southern US
• Warm fresh water (dust-bourne in Africa)
• Reaches CNS by the nasal mucosa though the cribiform plate
• Death in 5-6 days