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Parasitology 6 - Phylum Apicomplexa - Coccidia, Eimeria, Toxoplasma, Cryptosporidium, etc.

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Some basic characteristics of Phylum apicomplexa - 1. All are x 2. All possess a structure called the x 3. Single x 4. No x., but 1 exception 5. Have x body 6. Motility
1. All are parasitic 2. All possess apical complex 3. Single nucleus 4. No cilia or flagella with exception of flagellated microgametes in some groups 5. Have cyst forms(in some the cyst wall has been eliminated) 6. GLIDING motility
What the heck is an apical complex?
Structure on end of apicomplexan that consists of 1. Polar ring at end 2. conoid 3. Subpellicular microtubules 4. Rhoptries (which release enzymes during cell invasion) 5. Micronemes (release contents during cell invasion
5 components of apical complex
1. polar ring 2. conoid 3. sub pellicular microtubules 4. Rhoptries 5. Micronemes
What originates from polar ring in apical complex?
sub pellicular microtubules
What releases enzymes during cell invasion?
Rhoptries
What releases contents during cell invasion. Involved in adhesion/invasion
Micronemes
Rhoptries
structures in apical complex that release enzymes during cell invasion
Micronemes
Releases contents during cell invasion. Involved in adhesion/invasion
Other apicomplexan structures are Golgi, RER, mitochondria, x and x
apicoplast and micropore
Apicoplast
vestigial plastid with 35kb genome that is needed for fatty acid synthesis in apicomplexans.
Micropore
Food uptake in apicomplexans
How do the apicomplexans reproduce?
Asexually or sexually Asexually like Binary fission, schizogony, sporogony, of endopolyogeny. Or sexually like Isogamous fusion or anisogamous fusion with microgametes and macrogametes
7 stages of Apicomplexans
1. Trophozoite 2. Merozoite 3. Sporozoite 4. Tachyzoite 5. Bradyzoite 6. Gametes(micro/macro) 7. zyogote 8. ookinete
Trophozoite
feeding stage
Merozoite
Daughter cell resulting from schizogony (exception is toxoplasma gondii)
Sporozoite
daughter cell resulting from sporogony and develops in an oocyst
Tachyzoite
ACTIVE daughter cell that develops by endodyogeny or endopolyogeny
Bradyzoite
RESTING daughter cell that develops by endodyogeny or endopolygeny. Form zoitocysts
Oocysts contain one or more x that develops into a x, each with one or more x
Oocysts contain one or more sporoblasts that develops into a sporocyst, each with one or more sporozoites. - Sporoblasts/sporocysts may be absent (development within oocyst).
Are apicomplexans monoxenous or heteroxenous?
both. Sporozoites released when a sporulated oocyst is eaten by host.
Some heteroxenous cycles in apicomplexan.
sporogony takes place inside an invertebrate - transmission by bite..
Sporulation
reaching end process with sporocysts form.
Apicomplexan oocysts features
Oocytes are often diagnostic, provided you identify the host. Large size. You can tell because of structures - count sporocysts, sporozoites in them, micropyle, and stieda body.
Sporocyst bigger than sporozoite?
Yep, sporocyst houses the sporozoites. Sometimes there is no sporocyst at all, just the sporozoites.
Eimeria tenella - 1. Definitive host is? 2. Lives in? 3. How much damage? 4. Loss of x?
1. Definitive host is chickens, host specific 2. Lives in epithelium and intestinal cecum of chickens. LETHAL 3. Results in over 300 million in loses/costs per year 4. Causes loss of birds - coccidiostats is the medicine.
Coccidiostats
Medicine to treat birds with Eimeria tenella, affects only the schizonts, so need continuous treatment to get everthing.
Life cycle of Eimeria tenella
1. Infection by eating sporulated oocytes 2. Sporozoites invade epithelium, become the trophozoite, and then a meront. Schizogony releases 1st generation merozoites that exit cell and invade new one. You have up to two more schizogony cycles. One oocyst can give rise to 2.5 million merozoites. In cycles 2-4 merozoites invade cell and develop into sexual stages - the micro and macro gametocyte. The microgametocytes leave cell and invade cell with macrogametocyte and fertilize. Forms oocyst and is released in feces.
X is exogenous and aerobic
sporulation (sporogeny)
This process requires 2 days and is self limiting
Sporulation
Sporogeny/sporulation is x and x
exogenous and aerobic
Sporulated oocyst is known as
sporont
In a sporulated oocyst, x sporoblasts develop into sporocysts, x sporozoites develop in each sporocyst giving a total of x sporozoites per sporont
4 sporoblasts develop into sporocysts, 2 sporozoites develop in each sporocyst which gives you 8 sporozoites for sporont
Why is the Eimeria tenella infection self limited?
Number of asexual replication cycles is limited, so if you survive the replication rounds, you can get some immunity.
Symptoms of Eimeria tenella
Blood, diarrhea, epithelial sloughing, and death.
Sluggishness results in
increased susceptibility to predation
Discovered in 1990 to cause diarrhea in humans as the definitive host
Cyclospora cayetanensis
Infection of this concentrated in the jejunum
Cyclospora cayetanensis
Oocyst contains 2 sporocysts with 2 sporozoites each
Cyclospora cayetanensis
Sporulation requires 5-11 days, oocysts fluoresce blue green under UV light
diagnostic of cyclospora cayetanensis
If you see oocysts fluoresce green under UV light what is it?
cyclospora cayetanensis
Sporulation requires how many days in cyclospora cayetanensis
5-11
Diarrhea from cyclospora cayetanensis is cyclical? in HIV?
Relapsing or cyclical, prolonged in HIV infected individuals
Cyclospora cayetanensis
Discovered in 1990 - gives you diarrhea, oocysts fluoresce blue green
Cryptosporidium parvum is
an opportunistic cosmopolitan parasite of the intestinal tract of humans and animals. Small as hell
Opportunistic cosmopolitan parasite of the intestinal tract of humans and animals
Cryptosporidium parvum.
Cryptosporidium parvum is zoonotic?
No, it's a zoonosis.
Cryptosporidium parvum has x distinct genotypes
8
Can be deadly in immuno comprimised host
Cryptosporidium parvum
How big is Cryptosporidium parvum?
1.5-6 micrometers
Is cryptosporidium parvum in U.S.?
yep
Life cycle of Cryptosporidium parvum
Sporulated oocysts are passed in the feces - they contain 4 sporozoites (no sporocysts) - the sporozoites invade intestinal epithelium and develop into trophozoites. The trophozoites develop into type 1 meronts which could turn into merozoites and can turn back into trophs or into type 2 meronts, which then enter the sexual cycle and turn into merozoites which turn into undifferentiated gamont -then micro/macro gamont, which release gametes and fertilize to form zygote, which turns into either Thin or thick walled oocyst. Thin walled return to body and autoinfect. Thick walled leave body. Both sporulate inside of you.
How to transmit Cryptosporidium parvum?
1. Ingest oocysts (fecal oral, infectious when they leave body) 2. Contaminated drinking water 3. Swimming pools (resistant to chlorine) 4. One of the most common causative agent of chronic diarrhea in humans. 5. ZOONOSIS!
One of the most common causitive agents of chronic diarrhea in humans
Cryptosporidium parvum
Is cryptosporidium parvum carried in animals?
yep.
serious problem in warm region, as oocysts are long lived outside of the host in aquatic environments
Cryptosporidium parvum - remember that the oocyst dies if it dries
Can you catch Cryptosporidium in cold weather?
Yep Milwaukee 1993 outbreak. ***ed *** up
Describe the symptoms of Cryptosporidium parvum in immunocompetent vs. immunocomprised individuals
Immunocompetent - Usually self limiting diarrhea, abdominal cramps, dehydration , fevers - roughly 1-2 weeks of illness. In immunocomprimised individuals - profuse, watery diarrhea - 1-17 liters/ day. Several months of illness because of autoinfection / can be deadly.
How to diagnose and treat Cryptosporidium parvum?
Light and fluorescence microscopy or molecular tests and treat with Nitazoxanide, but only for immunocomprimised peeps
Nitazoxanide
drug give to immunocomprimised hosts when they have Cryptosporidium parvum
Cosmopolitan intracellular parasite of many kinds of tissues
toxoplasma gondii
DH host specific but not IH host specific
toxoplasma gondii
DH and IH of toxoplasma gondii
DH=felines IH = Felines/warm blooded animals
Toxoplasma gondii is particularly pathogenic in x and x
developing fetus and immunocomprimised hosts.
Fetus came out with a big ass head, what happened?
hydroencephaly from toxoplasma gondii
Prevalence of toxoplasma gondii in U.S. and worldwide
In U.S - 22.5% and worldwide = 42%.
Older you are, more likely you are to get infected from
toxoplasma gondii
Life cycle of toxoplasma gondii- big MOTHER****ER
Summary - Invades muscle,epithelium,CNS. Has 2 stages, enteroepithelial in felines and extraintestinal in IH animals. 1. Begin in Feline DH by ingestion of zoitocysts, and tachyzoites and oocysts can also infect. 2. Things invade into epithelium and develop into trophozoites 3. Endopolyogeny or endodyogeny produces 2-40 merozoites, cycles for 3-15 days. The merozoites undergo gametogenesis similar to Eimeria with the macro and micro gametocytes. Oocysts is formed with 2 sporocysts w/ 4 sporozoites per cysts. Sporulates in 1-5 days. Then onto the IH animal - where they ingest oocysts from feces, or zoitocysts or bradyzoites from tissues. The sporozoites cross epithelium and multiply in lymph nodes and tissues via endodyogeny. Then tachyzoites form, disseminate, and quickly replicate via endopolyogeny. Slower developing and replicating bradyzoites develop and encase themselves in a tough wall called a zoitocyst and can live years, which can rupture in many bradyzoites
Zoitocyst
tough wall covering bunches of replicating bradyzoites.
If a pregnant woman becomes infected, x can infect the fetus via the bloodstream
tachyzoites can infect the fetus.
How do you acquire Toxoplasma gondii?
1. Ingest sporulated oocyst 2. Ingest bradyzoites 3. Transplacental
Most infections of Toxoplasma gondii are x because
asymptomatic or mild because virulence is strain specific and host specific.
Virulence is strain specific for Toxoplasma gondii because of
secreted kinases
virulence is host specific for Toxoplasma gondii because
age (older peeps more resistant) and degree of acquired immunity - premunition
Premunition -
Parasite induces a strong suppressing level of immune activity, but not enough to kill parasite, but enough to fight off severe case.
T. gondii tachyzoite proliferation in tissue results in
host cell death
T. gondii intracellular or extracellular?
intracellular, but extraintestinal stages in areas like the retina or brain cause more serious damage.
T. gondii infections most serious in
unborn and immunocompromised hosts.
Describe the various symptoms of T. gondii
1. Acute infections are first sign of the infection, you will get flu and coldlike symptoms. Painful swollen lymph nodes in the cervical, supraclavicular, and inguinal regions. Then the subacute infections: lesions in lung, liver, heart, brain, and eyes. Most damage occurs in CNS - ESPECIALLY TO IMMUNOCOMPROMISED. Then you can have Chronic infection: immunity builds up sufficiently to depress tachyzoite proliferation. Bradyzoites develop and form zoitocysts - which live for years and can rupture. Death of released bradyzoites result in localized hypersensitivie inflammatory responses. Nodules form and can lead to encephalitis, blindness, myocarditis
Congenital toxoplasmosis
Transplacental transmission if mother acquires infection while pregnant. - t. gondii.
Transplacental transmission if mother acquires infection while pregnant
Congenital toxoplasmosis
Describe congenital toxoplasmosis
1st 3 months most important to proper development. 45% transmission rate, and of those that get it 60% show no symptoms, 30% suffer severe damage like hydrocephaly, mental retardation, retinochoroiditis. 9% die
If you are a fetus in a mom with t. gondii, what are your chances to live?
60% you will show no symptoms. 30% you will get ****ed up defects 9% die of stillbirth
In immunocompromised individuals what happens when you get t. gondii?
Rapid dissemination of tachyzoites, leads to blindness, encephalitis, CNS damage.
How to diagnose t. gondii?
Light microscopy from biopsy, ELISA, PCR.
How to treat t. gondii?
When appropriate pyrimethamine and sulfonamides
Neospora caninum is
a toxoplasma like pathogen that is the major cause of abortion of dogs.
DH in Neospora caninum and IH is
DH is dogs, IH is cows,sheep, cats, etc.
Tranmission of Neospora caninum?
Oocyst ingestion, bradyzoite ingestion, Predation, transplacental
Many infection of Neospora caninum are
asymptomatic.
This causes Neurological damage especially in developing fetus
Neospora caninum
May cause abortions in succeeding pregnancies, cell death following multiplication of tachyzoites
Neospora caninum
Diagnosis of Neospora caninum
Diagnosis by combination of histological, serological and molecular techniques
Treatment of Neospora caninum mimics
Toxoplasma gondii treatment, but not very effective.
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