Toxoplasmosis comprises a widespread parasitic illness that the parasite Toxoplasma gondii causes. The infection is mostly a relapse of a mild infection that can be subclinical as symptoms or signs may be unclear. This paper examines the various features of Toxoplasma gondii.
T.gondii Morphology
There are three forms of T.gondii, which include oocyst, tissue cyst, and trophozoite. The tissue cyst and trophozoite are asexual multiplication stages of the parasite (Schizogony). Sexual reproduction (Sporogony or gametogony) forms oocyst. All forms of T.gondii are found in domestic cats and other felines that are the definitive host and support both gametogony and schizogony. Only the tissue cysts, trophozoites and sexual forms are found in other animals, which includes birds and humans that act as intermediate hosts. Tissue cysts and oocyst infect through ingestion (Blader & Saeij, 2009).
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T.gondii Epidemiology
Worldwide, Toxoplasma gondii is the most dominant pathogen that affects about one-third of the entire global population. Infection occurs mostly in locations with warm elevation and warm climates (Blader & Saeij, 2009). Globally about 46 percent of people are infected with the parasite, even though infections vary for different countries. For instance, about 90 percent of people in France are T.gondii carriers. High incidences of the parasite are found in countries like Japan and France because of these countries’ habits of eating barely cooked or raw meats (Hall, 2017). High T.gondii rates are also found in South America due to an unusually high number of stray cats (Hall, 2017). Incidences in other countries include about 70 percent in Germany, about 70 percent in Brazil, and nearly 80 percent in the Netherlands. Besides, nearly 22 percent of people in the U.S and in the UK are carriers while the incidence in South Korea is about 4 percent (Hall, 2017).
T.gondii Cellular Characteristics
T.gondii comprises an obligate intracellular organism that fits into the coccidian sub-group and has a feline host specific sexual reproduction cycle. T.gondii belongs to the phylum Apicomplexa group of protozoa with characteristics such as complex organelles that help it to invade host tissue cells and complex life cycles that aid the parasites to be transmitted between different hosts (Blader & Saeij, 2009). T.gondii favors liver, muscle and neural tissues, even though it can affect other tissues.
Gram Stain Characteristics of T.gondii
T.gondii gram stain is negative and stains with safranin. Its structure is not well defined, but its nuclei and the sucking attachment trophozoite disk are identifiable (Blader & Saeij, 2009).
Virulence Factors of T.gondii
T.gondii can escape the phagosome prior to forming phagolysosome, can stimulate in a loose vacuole by readjusting the cytoskeleton, can stimulate phagocytosis, and can stimulate acceptance into a tight vacuole by invaginating the plasma membrane. It has a polymorphic development that enables it to be consumed in the abdominal expanse, as an oocyst in feces or as a cyst in meat and infect cells across the body with tachyzoites types that can be motile. The parasite can then develop new cysts that enable it to reproduce intracellularly. Its ability to alter host behaviour is its most outstanding virulence factor (Blader & Saeij, 2009).
Susceptibility of T.gondii to Antibiotics
T.gondii is susceptible to monensin (Lavine & Arrizabalaga, 2011). T.gondii is also susceptible to the synergistic and pyrimethamine antitoxoplasma effect caused by a combination of sulfadiazine and pyrimethamine (Grayson et al., 2017).
Host cells During T.gondii Invasion
Invasion of T.gondii is a sophisticated mechanism that consists of different and independent controlled stages. For instance, the parasite is first attached to the host cell’s surface loosely. The surface protein mediates this low-affinity interaction. The unique ability of the parasite to contaminate nearly most nucleated cells together with the many surface proteins that the parasite expresses suggests that more host molecules mediate the loose attachment (Blader & Saeij, 2009).
T.gondii Nutritional Needs
T.gondii cannot synthesize several nutrients but it has to search for nutrients. The nutrients include purine nucleosides, tryptophan, iron, arginine, and glucose that can diffuse freely throughout the PV and the membrane carriers propel them into the parasite (Blader & Saeij, 2009).
T.gondii Growth Conditions
T.gondii does not grow outside its suitable host. Oocysts can live in the environment. Oocysts live and stay ineffective in feces and water for several months at about 29 degrees Celcius. Oocysts are resistant to numerous disinfectant and detergent solutions and can stay viable in 2 percent sulphuric acid and about 3 percent potassium dichromate and sodium hypochlorite (Hall, 2017).
How T.gondii Evades the Immune System and Mode of Invasion into the Host
The parasite secretes three successive protein waves from its organelles that include rhoptries, dense granules, micronemes into the host cell. The protein that modifies the function of the host cell and prevents the immune reaction directed towards it. The proteins also alter the lipid membrane around the parasite to form parasitophorous vacuole (PV), which enable essential nutrients to be transported from the host cell to the parasite. The PV also hinders lysosomal fusion that would potentially kill the parasite (Blader & Saeij, 2009).
T.gondii evades the immune system by interfering with the signalling pathways of the host according to virulence founded on the genotype of the parasite and the infected cell type (Blader & Saeij, 2009). The parasite can also trigger different reactions depending on the recruited inflammatory cells, the burden of the parasite and the molecular organization of the parasite. It can develop a coadaptation with the host cell, which allows it avoid exterminating the host and thus evade from immune reactions at various levels.
Interaction with the Host, Disease caused, and affected Body Systems
Excysted sporozoites are found in the small intestines’ epithelial cells within 2 hours postinoculation in the intermediate host infected by T.gondii oocysts. Sporozoites differentiate into tachyzoites within 12 hours within the intestinal epithelium, and a rapid replication occurs by 48 hours and the parasite can be identified in the lymph nodes. After infecting traveling cells, for instance, dendritic cells and macrophages, tachyzoites disseminate quickly across the host. They are then converted to bradyzoites, which cause toxoplasmosis. Bradyzoites cyst can persist for a long time within the striated muscle and central nervous system tissue (Pittman & Knoll, 2015).
Symptoms after infection of the Host
While T.gondii infection is mostly asymptomatic, particularly in individuals with a healthy immune system, symptoms in newly infected people are flu-like and include headaches, fatigue, fever, and body aches. Among people with a compromised immune system, for instance, HIV/AIDS patients, symptoms may include confusion signs, headaches, behavior change, and seizures due to neural tissue invasion by the parasite. Among some infected hosts, ocular toxoplasmosis occurs and it affects retina of the host, which causes impaired vision. Congenital infection signs in newborn infants entail enlarged spleen and liver, jaundice, signs identical to T.gondii infection in immune-suppressed people and eye lesions due to ocular toxoplasmosis. Serious infections may result in mental retardation, epilepsy, and blindness (Hall, 2017).
Diagnosis and Therapeutic Intervention Required
There are different ways of detecting T.gondii parasite. They include T.gondii separation from amniotic fluid, blood and spinal fluid. T.gondii can also be identified using biopsies and histology of the affected tissues of a person, which includes lymph tissue. Polymerase chain reaction can be used to recognize the occurrence of the genetic material of the parasite.today, diagnosis of infection is mostly done by detecting antibodies of the parasite in the serum of a patient (Hall, 2017).
A majority of individuals with a strong immune system will not need T.gondii treatment. Exceptions include healthy mothers who are infected by the parasite for the first time after becoming pregnant since the parasite can enter the fetus. Antibiotic spiramycin can be given in such instance to decrease the chance of the parasite infecting the baby. Spiramycin treatment mostly lasts about three weeks, after which the condition of the patient will be reevaluated. If infection signs occur in the infant born, antibiotic treatment should continue. For patients with a weak immune system, daratrim, folic acid, sulfadiazine and anti-malarial drugs are used to treat T.gondii (Hall, 2017). Treatment may last for about five weeks, even though individuals with severely compromised immunity may require medication for life.
Article summary
Based on the article by Pittman and Knoll (2015), Toxoplasma gondii has two cycles, the sexual cycle and the asexual phase. The sexual phase is limited to catlike animals while the asexual phase occurs in humans. Acquisition of the parasite in humans occurs through ingestion of tissues cysts in raw or undercooked meat and consumption of water and food contaminated with oocysts. During acute infection, rapid asexual replication occurs after ingestion across the body. The parasite separates into a slow-developing, asexual growth structure after stimulating the host immune reaction, which causes chronic infection. T.gondii cysts are dangerous for people with a compromised immune system and severe complications may emerge in healthy people if they are infected with specific strains of the parasite or if they acquire infection congenitally. The article demonstrates the complexity of T.gondii infection once in humans, which ought to be understood to develop measures to target the different developmental stages of the parasite.
In conclusion, T.gondii is found across the world even though few people show symptoms of Toxoplasmosis as the healthy immune system in people prevents T,gondii from causing the disease. Nevertheless, people with a compromised immunity system and pregnant mothers ought to be careful since the parasite can cause severe infections for them.
References
Blader, I. J., & Saeij, J. P. (2009). Communication between Toxoplasma gondii and its host: impact on parasite growth, development, immune evasion, and virulence. Apmis , 117 (5 ‐ 6), 458-476.
Grayson, M. L., Cosgrove, S. E., Crowe, S., Hope, W., McCarthy, J. S., Mills, J., ... & Paterson, D. L. (2017). Kucers' The Use of Antibiotics: A Clinical Review of Antibacterial, Antifungal, Antiparasitic, and Antiviral Drugs, -Three Volume Set . CRC Press.
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Hall, S. L. (2017). Toxoplasma gondii: Dangers, life cycle and research . New York: Nova Science Publishers.
Lavine, M. D., & Arrizabalaga, G. (2011). The antibiotic monensin causes cell cycle disruption of Toxoplasma gondii mediated through the DNA repair enzyme TgMSH- 1. Antimicrobial agents and chemotherapy , 55 (2), 745-755.
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Pittman, K. J., & Knoll, L. J. (2015). Long-term relationships: the complicated interplay between the host and the developmental stages of Toxoplasma gondii during acute and chronic infections. Microbiology and molecular biology reviews , 79 (4), 387-401.
