Parasitology - Coccidia

What does the apical complex consist of?

Polar rings, conoids, subpellicular microtubules, rhoptry, and micronemes.

What are micronemes?

Small vesicles used for host cell recognition, attachment, and invasion.

What are rhoptries?

Club-shaped organelles with long necks that modify the host cell membrane and cytoskeleton to facilitate entry.

What are polar rings?

Cytoskeletal structures that help the internal architecture.

What are conoids?

Barrel-like structures that help with the internal structure and help the parasite penetrate the host cell.

What are subpellicular microtubules?

Long microtubes under the inner membrane that maintain the shape of motile stages.

What does the suffix “zoite” refer to?

Infective or invasive stages that invade cells and migrate in hosts.

What is a trophozoite?

The feeding stage that is usually intracellular.

What does the suffix “ont” refer to?

A bag of zoites that are doing intracellular replication.

What is schizogony/merogony?

Asexual reproduction by multiple fission/production of merozoites.

What is gametogony?

The production of gametes.

What is sporogony?

The production of sporozoites.

What happens during gametogony?

Merozoites develop into gametes.

What are the names for male and female gametes, respectively?

Microgametes and macrogametes.

What happens during sporogony?

The development of oocysts/sporozoites from zygotes.

How does the lifecycle of Apicomplexans go?

Oocysts go through sporogony to produce sporozoites, which go through merogony/schizogony to produce merozoites, which can either go through another round of merogony or become gamonts, which go through gametogony to produce gametes, which get fertilized and become zygotes, which go through meiosis to become oocysts.

What are some characteristics of gregarines?

They are monoxenous, parasites of invertebrates, most don’t do schizogony, and hosts become infected by swallowing spores/oocysts.

What are endopolygeny and endodyogeny?

Two types of asexual reproduction where multiple or two daughter cells are produced, respectively.

What is the course of infection of Cryptosporidium parvum? **

Host ingests water or food contaminated with thick-walled (sporulated) oocysts.

In the small intestine, the oocysts excyst.

Sporozoites are released, enter epithelial cells, and become trophozoites.

In the microvilli, the trophozoites undergo schizogony, the meronts burst and then the resulting merozoites undergo gametogony.

After fertilization of the macrogametes by the microgametes, oocysts develop.

Both thick-walled and thin-walled oocysts are created, and sporulated thick-walled oocysts are released in the feces, while thin-walled go through the autoinfective cycle.

Pathology includes damage to the small intestinal brush border, and symptoms include diarrhea, cramping, and fever.

How do you diagnose infection with Cryptosporidium parvum and how do you treat it?

Diagnosed by taking a fecal smear and looking for thick-walled oocysts, and treated with Nitazoxanide.

What are some factors of the epidemiology of Cryptosporidium parvum?

Cosmopolitan, it can be fatal and there can be invasion of secondary sites in immunocompromised people, method and manner of waste disposal, many animals serve as reservoirs, problematic in cattle industry, and most outbreaks occur in pools and daycare.

/What are any definitive, intermediate, or reservoir hosts of Cryptosporidium parvum?

Humans are the definitive host, and domestic animals like cattle can be reservoirs.

What is the course of infection of Toxoplasma gondii? **

Humans become infected by ingesting water or food contaminated with feline fecal oocysts or eating meat contaminated with bradyzoite cysts.

The bradyzoites or sporozoites infect macrophages in the small intestine mucosa.

Bradyzoites become tachyzoites and if sporozoites, the sporozoites go through schizogony and produce tachyzoites.

The tachyzoites reproduce asexually in cells and distribute throughout the body.

After a few weeks, the tachyzoites start dividing slower and produce zoitocysts filled with bradyzoites.

Acute pathology includes damage to small intestine, lymph node, and liver cells and inflammation.

Acute symptoms include swollen lymph glands, fever, headaches, and anemia.

Chronic pathology includes zoitocyst formation in brain, heart, and skeletal muscles.

Chronic symptoms include fever, weakness,

What is the difference between tachyzoites and bradyzoites?

Tachyzoites are the rapidly dividing stage responsible for the acute phase and bradyzoites are the dormant and slowly dividing form found in zoitocysts.

How do you diagnose infection by Toxoplasma gondii and how do you treat it.

Diagnosed by serodiagnosis and treated with Pyrimethamine and Sulfonamides.

What is congenital toxoplasmosis?

Disease caused by infection of Toxoplasma gondii while pregnant.

What are some characteristics of congenital toxoplasmosis?

Consequences are most serious in the 1st trimester and risk of transmission is highest in the 3rd trimester.

This can result in hydrocephalus, intracerebral calcification, and chorioretinitis.

What are any definitive, intermediate, and reservoirs hosts of Toxoplasma gondii?

Felines are the definitive hosts, many plant-eating mammals like humans are the intermediate hosts.