ParasitologyTest2Apicomplexans

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ParasitologyTest2Apicomplexans
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  1. Babesia- spp, disease, vector,
    • *NOTE- related to Plasmodium
    • B. microti (American) and B. divergens (European)
    • Human babesiosis is rare
    • Causes Texas Cattle Fever and malignant jaundice in dogs
    • B. microti is found in rodents
    • B. microti vector is tick (Ixodes scapularis)
    • *NOTE- humans (dead-end hosts) infected when tick accidentally feeds on human
  2. Babesia life cycle (starting with vector infection)
    • Tick acquires infected blood, gametic fusion occurs within 24 hours
    • Zygote becomes cigar-shaped ookinete (8-10um), enters tick's gut, becomes encysted sporont and grows (16um) in 48 hours
    • Each sporont undergoes schizogony
    • Sporozoites migrate into hemocoel and then invade various tick tissues (esp. ovaries)
    • After undergoing more divisions the final generations of sporozoites migrate to salivary glands
    • Tick accidentally feeds on humans, sporozoites introduced to blood
    • Sporozoites enter RBC directly (no exoerythrocytic phase), become trophozoite, rapidly grow/multiply by binary fission, and produce numerous merozoites
    • Merozoites are released, infect other RBCs, cause fever and anemia (mimics mild malaria)
  3. Babesia- symptoms, treatment,
    • Symptoms mimic mild malaria
    • Erythrocytic stages in blood smears often mistaken for plasmodium
    • sometimes treated with chloroquine (accidentally), no real evidence that it is effective
    • Treatment of symptoms might be best way to manage disease (easy recovery from infection)
    • Transfusion recommended in rare cases if high parasitic density
  4. Toxoplasma gondii- discovery, disease, efficiency (why?), distribution, symptoms, typical means of infection
    • Discovered in African rodent (gondi) (1908)
    • Toxoplasmosis
    • Very successful (20-30% of US population is infected, 94% of Guatamalans)
    • *NOTE- very low host specificity
    • Globally distributed
    • Infection is typically asymptomatic or mild (same for cats)
    • Clinical toxoplasmosis is rare, but congenital toxoplasmosis is often fatal
    • May become infected by ingesting inadequately cooked meat of infected beef, pork, or lamb
    • More frequently by contact with domestic cats via infective oocyts in feces
  5. T. gondii- general overview of non-human life cycle (starting with infected cat)
    • Only known definitive hosts are domestic cats (family Felidae)
    • Cats shed large #s of unsporulated oocysts for 1-2 weeks after infection
    • Sporulation of oocysts takes 1-5 days in environment (become infective)
    • Intermediate hosts (birds, rodents) become infected after ingesting oocysts
    • Oocysts transform into tachyzoites shortly after ingestion
    • Tachyzoites localize in neural and muscle tissue and develop into tissue cysts (bradyzoites)
    • Cats infected after consuming intermediate hosts with cysts OR ingesting sporulated oocysts
  6. What are common ways that humans become infected with T. gondii?
    • Eating undercooked meat of animals harboring tissue cysts
    • Consuming food/water contaminated with cat feces
    • Blood transfusion
    • Organ transplantation
    • Transplacentally from mother to fetus
  7. T. gondii- what is the difference between tachyzoites and bradyzoites
    • tachyzoites: quickly dividing
    • found in various cells throughout the body, quickly replicating and destroying the cells to cause further invasion
    • bradyzoites: slowly dividing
    • found within pseudocysts in brain, heart, and skeletal muscles
    • *NOTE- both bradyzoites and tachyzoites can be infective
  8. T. gondii- generally describe the various stages in the lifecycle and where they occur
    • Enteric (enteroepithelial) phase: occurs only in felines
    • sporozoite containing oocysts is formed (primary source of human infection)
    • Tissue (extraintestinal) phase: takes place in many hosts, including felines
  9. Describe the anatomy of a sporulated oocyst and its importance in the T. gondii lifecycle
    • ~12um x 10um, roundish
    • Oocyst ontains 2 sporocyts
    • Each sporocyst contains 4 sporozoites
    • Ingestion of a sporulated oocyst is responsible for the development of either phase!
  10. Where is T. gondii found (general answer)
    • Intracellular parasite (intestinal epithelia, lymph nodes, muscles)
    • Can be found free in blood during heavy infections
  11. T. gondii- lifecycle in detail (infection of cat)
    • Cat ingests sporulated oocyst
    • Sporozoites released from oocyst in lumen of small intestine
    • Sporozoites enter intestinal epithlia and begin enteric phase (3 stages)
    • schizogony: results in merozoites
    • sporozoites become trophozoites and undergo schizogony
    • # of cycles varies, but ~2-40 merozoites arise from each trophozoite
    • gamogony: results in gametes
    • 3-15 days after infection, some merozoites invade new host cells and develop into micro/macrogametocytes
    • sporogony: results in oocysts containing infective sporozoites
    • fertilization is intracellular
    • resulting zygote develops into oocyst that breaks of cell into the lumen of feline intestine (the passed in feces)
    • Oocyst undergoes sporogony in the presence of oxygen and warm temperatures after 1-5 days
    • Oocyst forms 2 sporocysts, w/ 4 sporozoites each
  12. T. gondii- lifecycle in detail (non-feline host)
    • *NOTE- can also occur in felines
    • Host ingests sporulated oocyst which infect cells other than the intestinal epithelium (extraintestinal phase)
    • After sporozoites infect extraintestinal cells they reproduce and form rapidly dividing merozoites (tachyzoites)
    • 8-16 tachyzoites are produced within a parasitophorous vacuole in the host cell causing cell to disintegrate and releasing parasites
    • group: an accumulation of tachyzoites in a host cell
    • as disease becomes chronic infection of brain, heart, and skeletal muscles occurs by slowly-replicating bradyzoites
    • pseudocysts: bradyzoites accumulate in large numbers and are surrounded by thick walls (survive for months to years)
    • *NOTE- pseudocyst formation indicates host immunity and reinfection of same host is unlikely unless immunity is disturbed
    • *NOTE- all animals (besides cats) can be considered paratenic hosts (delicious food)
    • *NOTE- both bradyzoites and tachyzoites can be infective
  13. T. gondii- toxoplasmosis classifications w/ symptoms
    • acute: parasitic invasion of lymph nodes and liver parenchyma
    • painful swollen lymph glands
    • fever
    • headache
    • anemia
    • muscle pain
    • sometimes lungs, retinal, and brain cells develop serious lesions
    • Chronic: depends on host immune response
    • 1) tachyzoites may destroy cells producing lesion in lungs, heart, liver, brain, eyes, and CNS damage
    • 2) Host immunity successfully prevents formation of tachyzoites and limits bradyzoites to pseudocysts
    • *NOTE- ruptured pseudocysts are usually irrelevant to those with immunity (except AIDS)
    • Congenital: result of fetal transplacental infection
    • 1/1000 births are affects this way
    • Infant may be deformed or quickly die
    • symptoms appear in triad
    • 1. Hydrocephalus (skull enlargement due to increase in CSF)
    • 2. Intracranial calcification
    • 3. Chorioretinitis (retina infected leading to blindness)
    • subclinical infection- no symptoms at birth w/ late onset of symptoms (mostly chorioretinitis)
    • no symptoms whatsover
    • *NOTE- timing of acquisition affects severity
  14. Give specific percentages and effects of a mother contracting T. gondii at various stages of pregnancy
    • 1st trimester: 17% infection - spontaneous abortion
    • 2nd trimester: 25% infection - spontaneous abortion or severe disease
    • 3rd trimester: 65% infection - subclinical disease
    • *NOTE- only an issue if T. gondii is acquired DURING pregnancy, previous infection has no effect on future pregnancy (except immunocompromised)
    • *NOTE- infection of fetus can only occur with chronic infection of mother (still during pregnancy)
  15. T. gondii- diagnosis, treatment, control
    • Diagnosed by isolation of parasite in tonsil/lymph gland biopsy and inoculation into mice (xenodiagnosis)
    • Treated with pyrimethamine and sulfadiazine (inhibit reproduction)
    • *NOTE- treatment must begin ASAP and be continued for several days after symptoms disappear
    • No vaccine is available (for any host)
    • Prevention requires avoiding oocysts (good luck)
    • avoid undercooked meat, wash hands and instruments thoroughly after meat prep, avoid cats
  16. Pneumocystis carinii- taxonomy, location in host, disease, high risk groups
    • Confusing taxonomy, technically a fungus it is an "oppotunistic parasite" that causes severe disease in immunocompromized
    • Found in interstitial issues of lungs and alveoli
    • Causes pneumonia (esp. in immunocompromised)
    • AIDS patients are highly susceptible (major cause of death)
    • Malnourished or immunocompromised children commonly infected
    • Organ transplant patients commonly infected (immunosuppresents)
  17. Pneumocystis carinii- morphological stages w/ description
    • Trophic: (2-8um) has small filopodia
    • Precystic: (2-3um) oval in shape
    • few filopodia
    • 1-8 nuclei (rarely seen)
    • Pellicle thickens as nuclei divide (can get as large as 40-120um thick)
    • Cyst: (4-6um) spherical and has thick pellicle
    • 8 intracystic bodies (sporozites) arranged in rosette pattern
    • *NOTE- formed meiotically during sporogony
    • each intracystic body ruptures from cyst and each develops into trophic stage
    • *NOTE- all 3 stages live in interstitial tissue of lungs
  18. How is Pneumocystis carinii transferred between hosts?
    • Human-to-human transmission is by aerosol droplets and direct contact
    • Congenital infection is possible (found in stillborns, newborn rats, 3 day old children)
  19. Pneumocystis carinii- symptoms
    • Asymptomatic in normal individuals
    • Immunocompromised individuals have...
    • Fever
    • cough
    • breathing difficulty
    • cyanosis
    • death in 100% of untreated cases (asphyxia)
  20. Pneumocystis carinii- diagnosis, treatment
    • Identification of organism from lung biopsies
    • Treated with TMP-SMA, but mortality rate is still high due to problematic immunity in the affected hosts
    • treatment is unsuccessful in a majority of AIDS patients
  21. Cryptosporidium parvum- cases and reason for modern infamy
    • 1st case (1976) involved 3 year old from Rural TN who suffered severe gastroenteritis for 2 weeks
    • EM exam of mucosa confirmed infection
    • (early 80s) strong association between immunodeficient individuals and Cryptosporidium
    • Recently infamous due to large water-born contamination (via oocysts)
  22. Cryptosporidium parvum- classification, pathogenicity, disease, specificity, durability, geographical distribution, size
    • Apicomplexan (sporozoa) since oocyst releases 4 spores upon excystation BUT unlike other apicomlexans it is monoxenous (only 1 host)
    • Little is known about its pathogenicity
    • causes cryptosporidiosis
    • No safe and effective treatment has been developed
    • Can infect several different hosts (not specialized), ubiquitous
    • cysts can survive most environments for long periods of time
    • Inhabits all climates and locales (6 continents)
    • small parasite (~3-5um) cannot be filtered by standard water filters
  23. Cryptosporidium parvum- life cycle (detailed)
    • Monoxenous: completes entire life cycle within a single host (sexual and asexual)
    • Orally ingested oocyst excysts in the gut, releasing 4 spindle-shaped motile sporozoites
    • Sporozoites invade intestinal epithelia and asexually reproduce
    • Some sporozoites differentiate into microgametes and macrogametes which fuse during fertilization (Oocysts develop)
    • Infectious sporozoites form within the oocyst, which is excreted in feces and await ingestion by a new host
    • *NOTE- transmission is usally fecal-oral from water contaminated with livestock feces
  24. Cryptosporidium parvum- symptoms
    • Cryptosporidiosis
    • immunocompetent patients: acute diarrhea (1-2 weeks)
    • frequent watery diarrhea
    • nausea
    • vomiting
    • abdominal cramps
    • low-grade fever
    • immunocompromised: debilitating diarrhea
    • cholera-like diarrhea (up to 20 liters/day)
    • intense abdominal cramps
    • malaise
    • low-grade ffever
    • weight loss
    • anorexia
    • *NOTE- has been associated with infection of respiratory system and of biliary tract (leading to thickening of gallbladder wall)
  25. Describe the historical epidemoiology of Cryptosporidium parvum
    • Often strikes communities that previously had enjoyed safe water and high filtration standards
    • Carollton (1987) 13,000/65,000 fell ill even though town's filtration system followed national standards
    • Milwuakee (1993) 400,000 residents fell ill and >4000 hospitalized, estimated cost $54 million
  26. Why is Cryptosporidium parvum referred to as the "nightmare bug"
    • tough oocyst membrane grants resistance to traditional treatments (including chlorination)
    • hard to detect
    • able to live for long periods in reservoirs/pipes
    • strikes 1000s
    • presents great threat to immunocompromised
  27. Who are at high risk of Cryptosporidium parvum infeciton? (long list)
    • infants and younger children in daycare centers
    • drinkers of unfiltered/untreated water
    • farmers involved with calving, muck-spreading, etc
    • enging in sexual practices involving fecal-oral contact
    • nosocomial infections
    • veterinarians examining infected animals
    • travelers without filtered water
    • living in densely populated urban areas

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