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57 Cards in this Set

  • Front
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Phylum Apicomplexa

All parasitic


No obvious motility structures


characterized by apical complex, rhoptries, micronemes, and micropores



apical complex

set of structures that are considered distinguishing characteristic of Apicomplexa


consists of:


- 1 or two polar rings immediately beneath cell membrane


- coniod - truncated cone of spirally arranged fibrillar structures within polar rings


- subpellicular microtubules - radiate from rings and run posteriorly, parallel to body axis



Function of apical complex

locomotion, structure

rhoptries and micronemes in apicomplexa

- rhoptries (2 to several) extend to cell membrane within polar rings - help with adhesion to and penetration of host cell

- micronemes - smaller, more convoluted bodies that also extend posteriorly from apical complex




Contents of these two organelles are enzymes that are released upon entry into the host cell

micropores

aid in food ingestion within host cell

Class Sporozoea

Subclass Coccidia


Family Sarcocystidae


Toxoplasma gondii


Sarcocystis spp.


Cryptosporidium sp.


Cyclospora cayentanensis


Pneumocystis carinii (actually in Fungi


Kingdom kind of?)

Toxoplasma gondii causes _____ , which is


asymptomatic in adult humans but causes major birth defects in fetuses.

toxoplasmosis

Toxoplasma gondii prevalence

parasite of many mammal species


intracellular in many tissues

Life cycle of T. gondii: cat's infection from rat -> merozoites/gamonts

- cats become infected by ingesting bradyzoites (within zooitocysts) in muscles of another host (ex rodent)


- released in intestine


- penetrate epithelial cells (enteroepithelial cycle)


- others can penetrate mucosa and infect other


organs (extraintestinal)


- in epithelial cells, trophozoites divide asexually (merogeny/schizogany)


- merozoites escape cell, initiate merogeny in other cells OR transform into gamonts and perform gametogony (separate note card)

Life Cycle of T. gondii: gametogenesis

- after merozoites escape from a host cell, they can continue to initiate merogeny in other host cells OR transform into gamonts


- Fertilization leads to formation of oocyst


-immature oocyst passes with feces


- sporulates when exposed to O2


contains 2 sporocysts (4 sporocysts each)


*next step on other card

Life Cycle of T. gondii: when mammal ingests oocyst

-when another mammal ingests oocyst

- sporozoites escape in small intestine



- enters host cells


- asexual reproduction occurs- produces


tachyzoites that reproduce rapidly


- host immune reaction slows divison and


tachyzoites become bradyzoites


- host forms wall around infected cell - zoitocyst


- remains viable in host for a long time

Humans can become infected by T. gondii by ingesting ____ or _____ in uncooked meat

oocyst or zoitocyst

Pathogenicity of T. gondii

usually asymptomatic in immunocompetent


many people have antibody virulence and susceptibility varies



Acute T. gondii

mainly intestinal involvment


flu-like symptoms, swelling of lymph nodes


more likely in immunosuppressed



Chronic T. gondii

kept in check by immune system

If immunosuppressed individual gets T. gondii or if a T. gondii cyst breaks

bradyzoites released, immune reaction occurs and can cause extensive tissue damage in NS,




can lead to blindness and brain/heart damage

Congenital toxoplasmosis

when a mother contracts T. gondii near conception or during pregnancy



T. gondii crosses placental barrier in ___% of mothers nfected and causes congenital toxoplasmosis.

____% of those infected will be asymptomatic


_____ % may be lethal


____ % severe pathogenesis - causes either hydrocephaly, brain damage/retardation, etc



45%




60%




9%




30%

Sexual/asexual reproduction of T. gondii

sexual reproduction occurs only in cats - in intestinal epithelial cells


(asexual reproduction occurs in cats as well. in intestinal and other tissues)




In other mammal hosts, asexual reproduction ONLY

Diagnosis of T. gondii

- parasite in tissue biopsy


- infection of mice with infected tissue


- ELISA - enzyme/antibody/color identification test



Treatment of T. gondii

- pyrimethamine and sulfonomides

____ % of the world pop. infected with T. gondii




___ million in US alone




In 1976, ____ cases of congenital toxoplasmosis.


In 1999, at least ______ cases.

13 % of world pop




60 million in US




3500 cases in 1976




400 cases in 1999



Pregnant women should not clean litter boxes, children's sandboxes should be covered.


Why?

Oocysts passing in cat feces (only occurs for a few days after infection of cat)



Major source of infection of T. gondii (besides cat feces) among humans is _____.

undercooked meat




Safe frozen ( -14 C)

Sarcocystis spp. intermediate host

herbivorous mammals

Sarcocystis spp. definitive host

carnivorous mammals



Life cycle of Sarcocystis spp.

- Int. host ingests sporocysts (sometimes in oocyst)


- sporozoites penetrate intestinal epithelium


- go to various body tissues


- invade endothelial cells of blood vessels


- merogeny (may be several generations)


- zoitocysts (also known as sarcocysts/Meischer's tubules) then form in skeletal and cardiac muscle and occasionally in the brain *separate notecard for these



zoitocysts of Sarcocystis spp.

- each cyst has 2 distinct regions:

peripheral region is occupied by globular metrocytes.


after several divisions the metrocytes give rise to more elongated bradyzoites.





only _________ are infective to definitive host of Sarcocystis spp.

bradyzoites

(Sarcocystis spp Life Cycle)




What occurs when a definitive host (carnivorous mammal) ingests a zoitocyst?

- its wall is digested away


- bradyzoites penetrate the lamina propria of the small intestine


- there they undergo gamogony without intervening merogenic generation


male gametes penetrate female gametes - resulting oocysts sporulate in the lamina propria.


-oocyst walls are thin and usually break open during passage through intestine, therefore sporocysts are usually passed in feces.

Sporocysts of Sarcocystis spp. can infect ______ hosts but not _______ hosts.

(first blank) intermediate




(second blank) definitive

Are humans definitive hosts of Sarcocystis spp?

Only in a couple species.

often asymptomatic





Cryptosporidium spp.

- 6 valid species


- very small, 2-6 um

Cryptosporidium parvum

can be parasitic to humans, but not very host specific

Life cycle of Cryptosporidium sp.

-live in brush borders of intestines


- intracellular/extracytoplasmic


- oocysts in feces ingested


- excyst of sporozoites when exposed to bile salts, acidity, and temperature of digestive


system


- sporozoites invade cells and become trophozoites


- merogeny


-produces trophs and gametes


-fertilization -> zygote -> sporogony -> 4 sporozoites -> oocyst

Life Cycle of Cryptosporidium sp.


- live in brush borders of intestines


- intracellular/extracytoplasmic


- _______ in feces ingested


- excyst of _______ when exposed to bile salts, acidity, and temperature of digestive system


- sporozoites invade cells and become ________


- ______ occurs and produces trophs and gametes


-fertilization -> ______ -> sporogony -> 4_______ -> oocyst

- live in brush borders of intestines

- intracellular/extracytoplasmic


- oocysts in feces ingested


- excyst of sporozoites when exposed to bile salts, acidity, and temperature of digestive


system


- sporozoites invade cells and become trophozoites


- merogeny occurs and produces trophs and gametes


-fertilization -> zygote -> sporogony -> 4 sporozoites -> oocyst

Two types of cysts in Cryptosporidium life cycle

Thick walled - passes out with feces


Thin walled - excyst and can cause autoinfection (remains in host and can cause reinfection)

Symptoms of Cryptosporidum infection

diarrhea, abdominal pain, nausea & vomiting,


fatigue, fever




major cause of persistant diarrhea in developing countries

Cryptosporidium identified as a human pathogen in _____ (year)

1976

Treatment of Cryptosporidium

As of now, none.


Nitazoxinide may be effective.


self limiting in most (1-10 days)


very dangerous in immunosuppressed

Immunosuppressed people with


Cryptosporidium

symptoms much more severe


often fatal


6-25 profuse watery stools/day

Oocysts of Cryptosporidium not resistant to _______ but remain viable in ______ for a long time. They are highly resistant to chlorine.

desiccation, water

1993 Milwaukee outbreak of Cryptosporidium

largest outbreak of water born illness ever in US


403,000 people ill


4,400 people hospitalized


took 2 weeks to ID cause.

_______ reservoir.


This reservoir may be important source of


infection of Cryptosporidium in humans (zoonosis).


may be very common cause of short term


diarrhea in general population, and persistent diarrhea in developing countries.

cattle

1998 Texas outbreak of Cryptosporidium

Brushy Creek, near Austin.


lightning struck sewage station


170,000 galloons spilled, ran into wells of water system.

Cyclospora cayentanensis first isolated ?

-relatively new parasite


-first isolated in Peru in 1979



C. cayentanensis first outbreak in US

Chicago 1990, several cases reported since.

Symptoms of Cylospora cayentanensis similar to ________________.

Cryptosporidiosis

Oocyst of C. cayentanensis is similar to Cryptosporidium sp but __________ .

larger - 8 - 10 um.




(Cryptosporidium oocyst is 2-6 um)

Pneumocystis carinii taxonomic status?

Not agreed upon. Some place it in fungi, some in apicomplexa.

P. carinii

very common parasite of mammalian lungs - usually harmless

P. carinii causes ______ in immunosuppressed

pneumonia

_________ leading cause of death in individuals with AIDS.


(60 % of patients infected)

Pneumocystis carinii

Biology of P. carinii: 3 stages in lung

- Trophozoite


- Pre-cyst


- Cyst surrounded by membrane




enter air spaces


may pass out in aerosol droplets or direct contact

Pathogenesis of P. carinii in immunosuppressed

- damage to lung epithelium


- alveoli fills with foamy exudate (full of parasites)


- death by asphyxiation


- mortality near 100%

Symptoms of P. carinii

fever, cough, difficulty breathing, cyanosis

Diagnosis of P. carinii and treatment

diagnosis: sputum sample or biopsy




treatment (usually not effective because immune system is not functioning):




Combination Trimethoprim-sulfamethoxazole


or inhaled pentamidine isethionate