Toxoplasmosis Research Paper

Small birds and mammals because they forage for seeds. A tiny amount of the parasite needs to be ingest to begin causing problems and it can be found in raccoon feces.

The article seemed to imply that the parasite naturally occurs within the feline population. The article does not mention

Once inside the felid, T. gondii resides in the stomach area, eventually making its way into the cat’s intestinal wall, nesting within its epithelial cells. These parasites then undergo sexual reproduction and produce a large number of oocysts, thick zygote-containing masses within the intestine. Upon enlargement, the oocysts once connected to the felid’s small intestine are released into the digestional tract and excreted through the feces of the cat.

After the infecting agent gets into the human’s bloodstream they invade the liver within an hour; the parasite then takes about 15 days to mature(Collins, Jeffery, E.). The infecting agent divides and forms plasmodium merozoites which are then released into the bloodstream and infect red blood cells(“Plasmodium”). The plasmodium is an oval-shaped cell, measured at about .00006 inches long and .00004 inches wide. Plasmodium has a pellicular cisterna which makes up the golgi apparatus. The apparatus receives materials and sends them to other parts of the cell. The plasma membrane forms the external boundary and the merozoite coat acts like the cell membrane which lets things in and out of the cell. It has an apicoplast that allows the parasite to invade host cells, and microtubules that work with the inner membrane to give bulkiness to the cell. The micronemes help the cell invade the host, and the polar rings, apical end, rhoptries and dense granules all help it invade the cell. Plasmodium also has some things in common with animal or human cells: a nucleus, ribosomes, and a mitochondria(“Structure of Plasmodium

By direct contact with feces of infected pig or human, which can infect many tissues. If the larvae get in the nervous system and the brain, it can result in neurocysticercosis.

If possible it would be best to have someone else do the litter box cleaning, and this should be done daily, as the parasite is shed in the cat’s feces, but does not become infectious until 1 to 5 days after the cat has released, thus getting rid of all feces immediately is best. If you have no one to do this for you, then you can protect yourself by wearing disposable gloves, making sure to wash your hands after you’re done. If you don’t already own a cat do not get one while pregnant, and do not handle stray cats more specifically kittens.

The complexity of S. stercoralis’ life cycle begins with its alternation between free-living and parasitic cycles.1 When the soil is contaminated with the infective filariform larvae, humans get infected through the skin.1 The infective filariform larvae penetrate the human host and reach the small intestine, where they mature into adults and produce eggs through parthenogenesis.2 The eggs hatch in the small intestine and eventually become larvae that are passed in the stool.6 The rhabditiform larvae passed in the stool become either infective filariform larvae or into free-living adults that reproduce outside the host environment.6 Some rhabditiform larvae are not completely excreted in the host’s feces, and they reinvade the small intestine or perianal skin and cause autoinfection.6 With the ability to autoinfect the hosts, S. stercoralis is potentially dangerous and fatal. Most chronic infections remain

The acute infection is characterized by fast growing forms called tachyzoites, which lyse their host cells within 24–48 hours to release large numbers of progeny. In response to immune pressure, the parasite differentiates into a slow growing form called a bradyzoite, which resides within an intracellular cyst. Tissue cysts normally occur in long-lived cells such as muscle or neuronal cells. Ingestion of tissue cysts by members of the cat family results in sexual development within intestinal epithelial cells, culminating in the shedding of oocysts that undergo meiosis in the environment to form sporozoites.

It is second only to trauma in the leading cause of death in cats killing 85% of infected cats within the first three years that they become infected. In the United States, approximately 3% of all cats are infected with feline leukemia. That rate significantly rises to 13% or more in cats that were previously ill with ineffective immune systems that have a high risk of infection, young kittens, or male cats between the ages of one to six years old who are at the highest risk of becoming infected. It is often called the friendly cat disease because it is commonly spread from cat to cat through casual contact, such as grooming or sharing food or water. FeLv is spread through saliva and nasal secretions, urine, feces, and milk from infected cats. Cat-to-cat transfer of virus may occur from a bite wound, during mutual grooming, and can even be transferred through the shared use of litter boxes and feeding dishes. It can also be transferred from an infected mother cat to her kittens, either before they are born or through her milk while they are nursing. FeLV doesn't survive long outside a cat's body—probably less than a few hours under normal household

carboxyl terminus is necessary to recruit mitochondria, and the N terminus is anchored to the

Elephantiasis is a neglected tropical disease. Infection occurs when filarial parasites are transmitted to humans through mosquitoes. The mosquito grows into a adult worm and the worm lives in the lymphatic system. It is usually acquired in childhood causing hidden damage to the lymphatic system. There are 8 filariasis worms known to affect humans and these can be divided according to the body area they affect.

The paper Genetic mapping reveals that sinefungin resistance in Toxoplasma gondii is controlled by a putative amino acid transporter locus that can be used as a negative selectable marker identified a gene linked to drug resistance in the parasite Toxoplasma gondii (Behnke et al. 2015). T. gondii infects many mammals and birds worldwide. Humans can become infected through consumption of undercooked meat as well as ingestion of food or water contaminated with T. gondii oocysts. The disease caused by T. gondii in people with compromised immune systems can be fatal if left untreated. The drug sinefungin has been used to inhibit the growth of T. gondii for the past several decades, but resistance to sinefungin has occurred. Behnke et al. hypothesized that there was a gene associated with sinefungin resistance in T. gondii, so they performed QTL analysis to determine the genetic basis for sinefungin resistance (Behnke et al. 2015). Drug resistance is becoming a serious issue because the rate at which microbes are becoming resistant to antibiotics is faster than the rate at which we are developing new drugs. A better understanding of how genetics contributes to the development of drug resistance will allow scientists to manipulate a microbe’s genome to prevent development of resistance to a particular drug; ultimately leading to the microbe’s

Do I need to seek care if I think I might be infected with one or more of these parasites?

Many women who are expecting know there is a specific list of foods they can not eat, but they do not know the reasoning behind it. Mainly these foods can possibly contain parasites that are linked to diseases, which can affect the fetus developmentally. Toxoplasmosis is a disease carried by the parasite Toxoplasma gondii, and it is the most common parasite in humans (1,2). It has been linked to many brain disorders in humans, and even permanent changes in the way a person thinks and acts (1). Scientists have learned that it is hosted in cats and carried through other animals. The parasite can be carried in anything from vegetables to undercooked meat, which is why pregnant women cannot eat these foods.

     Transmission of the parasite can occur in several different ways. Direct transmission can occur by handling infected animal or human feces. One quarter of reported direct transmission infections occurred by direct contact with feces, while the rest were reported to have happened by person to person contact (Donnelly & Stentiford, 1997).