Parasites are of course “clever. ” yet insidious beings. You may hold a parasite inside you right now. without even cognizing it. An effectual parasite lives without being detected because if it is. so measures can be taken to eliminate it. One such parasite is known as Toxoplasma gondii. T. gondii is an obligate intracellular protozoon foremost discovered by Nicolle and Manceaux in 1908 ( Nguyen. 2006 ) . Since its find. T. gondii has been implicated as the causative agent of toxoplasmosis. an infective disease that may ensue in a spectrum of effects.

T. gondii continues to be an of import disease in the modern universe. particularly in pregnant adult females and immunocompromised patients. In order to better understand how T. gondii is able to infect its human hosts. we will research the parasite’s cellular belongingss and endurance schemes. Parasitic Characteristics Parasites are astonishing beings because they must develop and last in unusual and frequently hostile environments. In the face of such aggressive conditions. parasites have adapted assorted complex schemes that allow them to last.

Common features of successful parasitic beings include methods that allow easiness of entry into the host. methods to avoid sensing by the host immune system. the ability to develop eggs/cysts. the ability to turn up a new host. and turning away of killing the host ( Camus & A ; Zalis. 1995 ) . Toxoplasma gondii employs several of these schemes in order to finish its life rhythm. T. gondii is a one-celled eucaryotic protozoon parasite has a characteristic crescent form. This form serves a critical map in breeching host cells.

One terminal of the cell is more conelike and is believed to be the part that ab initio breeches the host’s cell membrane ( CDC. 2008 ) . The opposite terminal of the cell is more pointed and is responsible for keeping the cell organs that function in fond regard and infiltration of host cells ( Huynh. Rabenau. Harper & A ; Beatty. 2003 ) . Although it is non wholly understood how T. gondii crosses into its host cell. it has been hypothesized that cell organs called mirconemes provide adhesive protein look. The M2AP-MIC2 composite of proteins found in this cell organ appears to be responsible for these adhesive secernments ( Huynh et. l. 2003 ) .

In add-on to helping in adhesion and fond regard. this complex appears to ease the organism’s motility every bit good. particularly since no other agencies of motility such as scourge have been discovered ( Camus & A ; Zalis. 1995 ) . T. gondii besides has rhoptries. which are regulated secretory cell organs involved in the invasion of host cells. These rhoptry proteins secrete chemicals upon come ining the host cell to change the cell’s vacuole for maximal survival upon to help in the reproduction procedure ( Bradley & A ; Boothroyd. 2001 ) .

A site on the rhoptry protein ROP1 has been indicated as paving the pro part in rhoptry protein map ( Bradley & A ; Boothroyd. 2001 ) . This ROP1 site has been the mark of much research for possible vaccinums to T. gondii. which will be discussed farther in a ulterior subdivision. T. gondii besides employs several mechanisms to assist avoid its sensing by the host’s immune system. This being has the ability to sequester itself from the environment when stressed by immunologic factors. For illustration. the parasitic cell is able to infix and show specific antigens on its surface to hide it from immune onslaught ( Nguyen. 2006 ) .

Toxoplasma is besides able to occupy immunologically competent macrophages in order to “defuse” the killing mechanisms of these cells ( Camus & A ; Zalis. 1995 ) . Additionally. these parasites monopolize on the familial limitations of the immune response. In some strains of mice. T. gondii’s antigens do non let acknowledgment by the host’s defenses. finally forestalling the production of an immune response. The parasite receptors involved in the invasion of host cells can still work in the presence of antibodies.

This aid to explicate the failure of complete inoculation efforts to aim these molecules in T. ondii. The lifecycle of T. gondii besides conveys several advantages to its success as a parasite. This being chiefly exists in three signifiers: oocysts. tachyzoites. and bradyzoites ( Dubey & A ; Speer. 1998 ) . Oocysts are merely produced in the unequivocal hosts of these beings. members of the Felidae household ( including domestic cats and their close relations ) ( Torrey & A ; Yolken. 2003 ) . These hosts are termed “definitive” because it is in these hosts that T. gondii reaches sexual adulthood. In these hosts. the parasite will bring forth unsporulated oocysts into feline fecal matters.

After about five yearss. these oocysts gain the ability to sporulate in the outside environment. leting them to go infective. At this point. intermediate hosts such as birds. gnawers. or even worlds may go septic after consuming contaminated dirt. H2O. or workss ( CDC. 2008 ) . Following consumption. these oocysts transform into what are called tachyzoites. Tachyzoites are the motile signifier of T. gondii that quickly multiply and travel throughout the organic structure of the host. These tachyzoites divide quickly in host cells. doing cell devastation and the spread of infection ( Dubey & A ; Speer. 1998 ) .

Finally. these tachyzoites localize in nervous or musculus tissue where they develop further into tissue cysts known as bradyzoites ( Dubey & A ; Speer. 1998 ) . These bradyzoites are non-motile. slow-growing versions of the T. gondii that are finally responsible for the physical manifestations of the parasitic infection. The development of bradyzoites is thought to be an version of T. gondii in response to the host immune reaction. These bradyzoites constructions are more resilient to inauspicious conditions. similar to the manner endospores convey endurance for some Gram ( + ) bacterium ( Huynh et. l. 2003 ) . An endospore for bacterium is an utmost endurance scheme utilized when the bacteria is faced with unfavourable conditions.

In this sporulated province. these bacterial cells become more immune to environmental alterations. Once favourable survival conditions return. the bacteriums can return back to its normal bacterial signifier. Both bradyzoites and endospores allow the parasite or bacteria to last in a hibernating province from which they can reemerge and originate a latent infection in the host cell. Another unique and challenging endurance scheme employed by T. ondii is its ability to bring forth behavioural alterations every bit good as impair acquisition and memory in mice ( Wang et. Al. 2006 ) .

The current literature in this country suggests that Toxoplasma-infected rats have a decrease in their natural antipathy to the olfactory property of cats. The ensuing behavioural alterations in these rats increase the opportunities that they will be eaten by a cat. therefore enabling Toxoplasma to finish its life rhythm ( Wang et. Al. 2006 ) . This is a clear illustration of an evolutionarily goaded use of host behaviour by a parasite. Numerous surveies besides look towards the possibility of similar effects happening in septic worlds.

Among such common subjects that are being investigated is the relationship between T. gondii infection and acquisition. memory. depression. anxiousness. and schizophrenic disorder ( Torrey & A ; Yolken. 2003 ) . Transmission Toxoplasma can be transmitted in legion ways. Among the most common methods of transmittal are through vehicles ( such as the ingestion of contaminated nutrient and H2O ) and through vectors ( such as vertebrate animate beings like cats ) . For illustration. cats can go septic after devouring an intermediate host ( gnawers or birds ) that seaport these tissue cysts. or go infected straight by consuming sporulated oocysts ( Dubey & A ; Speer. 1998 ) .

Worlds may go infected by T. gondii in similar ways. This may happen by eating the undercooked meat of septic animate beings. devouring nutrient or H2O contaminated with cat fecal matters. blood transfusion or organ graft. passed from female parent to child across the placenta. or merely by cleaning the litter box of a favored cat ( Torrey & A ; Yolken. 2003 ) . When worlds do go septic with T. gondii. the parasites form tissue cysts in the same manner that they would in an intermediate host. Upon come ining a new host. the bradyzoites will transform back to their infective signifier as tachyzoites.

Common topographic points for the formation of these bradyzoites are in skeletal musculus. myocardium. nervous tissue. and the eyes ( Dubey & A ; Speer. 1998 ) . These cysts may stay in these parts throughout the lifetime of the human host and do a status known as toxoplasmosis. Taxoplasmosis Once a human ingests a substance contaminated with T. gondii. the ensuing infection by the motile tachyzoites and formation of bradyzoites is referred to as toxoplasmosis. This infection will show itself otherwise. depending on the current wellness and immune map of the host.

Most healthy persons that become infected with T. gondii do non show symptoms because their immune system is better equipped to forestall the parasite from doing unwellness. When symptoms do occur. they are largely mild “flu-like” symptoms such as stamp lymph nodes fever. and musculus achings that last for a few hebdomads and so travel off ( Jones. Kruszon-Moran & A ; McAuley. 2001 ) . However. even though the symptoms may vanish. the parasite remains within the host in an inactive province. If the host becomes immunosuppressed. it is possible for symptoms to re-emerge and decline ( Jones et. Al. 2001 ) .

If a adult female becomes infected during or merely before gestation. it is possible for her to go through the infection to her unborn babe. This is a procedure known as inborn transmission—the passing of pathogens from female parent to fetus via the placenta. This may potentially take to miscarriage. spontaneous abortion. or a child born with marks of toxoplasmosis such as unnatural expansion of the caput. Septic babies may demo no symptoms at birth. but may develop them subsequently in life in the signifier of vision loss. mental disablement. and ictuss ( Jones et. Al. 2001 ) . The clinical class in immunocompromised patients can be much more terrible.

Persons that are immunocompromised are at a much greater hazard for serious inauspicious effects of this status. However. the badness depends upon whether the infection is a latent or primary infection. A latent infection is one that has a long symptomless period. whereas a primary infection refers to the first clip an person is exposed to a pathogen. For illustration. a individual who is HIV positive and who has a reactivated latent Toxoplasma infection can hold symptoms that include fever. confusion. concern. ictuss. sickness. and hapless coordination ( CDC. 2008 ) .

Yet persons who get HIV infection and were non infected antecedently with Toxoplasma are more likely to develop a terrible primary infection. Such an infection includes symptoms like phrenitis. myocardial inflammation and pneumonitis. and decease ( Nguyen. 2006 ) . Diagnosis and Treatment of Toxoplasmosis Both diagnosing and intervention of toxoplasmosis is extremely dependent on the host and their immune province. Diagnosis of toxoplasmosis can be done utilizing a assortment of methods. The trouble finally lies in finding whether an infection is acute or chronic ( Nguyen. 2006 ) .

Acute infections are best verifies by insulating T. gondii or T. gondii Deoxyribonucleic acid from the patient’s blood or by happening tachyzoites in tissue or bodily fluids. The isolation of T. gondii tissue cysts is non sufficient to find whether the infection is still active or has entered the latent stage. To distinguish the two. patients are subjected to several serological tests ( Jones et. Al. 2001 ) . Serology is the scientific survey of blood serum. Antibodies may be created in response to an infection induced by a micro-organism. Detection of these specific antibodies in the blood can assist to diagnosis toxoplasmosis.

Among the serological trials used is the Sabin-Feldman dye trial. which tests for IgG. IgM. and IgA ( specific Ig antibodies ) ( Jones et. Al. 2001 ) . Congenital infections of foetuss can besides be identified by the presence of cysts in the placenta or foetus. every bit good as sensing of T. gondii DNA in amnionic fluid utilizing molecular methods such as polymerase concatenation reaction ( Huynh et. Al. 2003 ) . Polymerase concatenation reaction ( PCR ) is a biochemical engineering utilized to magnify a individual transcript of a piece of DNA across several orders of magnitude.

The terminal consequence of PCR is the coevals of 1000s to 1000000s of transcripts of a peculiar Deoxyribonucleic acid sequence. This procedure allows for the sensing of T. gondii in amnionic fluid even if merely a miniscule sum of its Deoxyribonucleic acid can be harvested. In footings of intervention. most immunocompetent persons recover from this infection without any diagnosing or subsequent medical intercession. Those that do exhibit mild symptoms of the infection may be treated with a combination of drugs such as pyrimethamine and sulfadiazine. which are a folic acid adversary that prevents the consumption of folic acid and an antibiotic. severally ( Sibley & A ; Boothroyd. 1992 ) .

Folinic acid may besides be administered to cut down bone marrow depression caused by the pyrimethamine. In acutely infected pregnant adult females. the recommended intervention includes spiramycin if the foetus has non yet acquired toxoplasmosis. Spiramycin is an antibiotic that localizes to the placenta and has been shown to cut down placental infection by 60 per centum ( CDC. 2008 ) . It does hold some teratogenic effects. which must be weighed against the hazard of inborn infection. If the foetus is infected. the aforesaid drug combination is administered alternatively of spiramycin.

Persons that are immunocompromised demand to recover intervention until they have betterment in their status. The recommended intervention is a combination of pyrimethamine. folinic acid and trisulfapyrimidines ( Nguyen. 2006 ) . This drug combination inhibits the enzyme dihydrofolate reductase in T. gondii. forestalling synthesis of DNA and protein ( Nguyen. 2006 ) . For many septic AIDS patients. continuance of this medicine may be necessary for the remainder of their lives. Clindamycin has been found to be effectual at handling toxoplasma phrenitis in AIDS patients ( Nguyen. 2006 ) .

Keep in head nevertheless. that the T. gondii parasite is non wholly eliminated in any of these instances. The parasites can stay within tissue cells in a less active stage ; their location makes it hard for the medicine to wholly extinguish them. Epidemiology and Prevention The T. gondii parasite has been found worldwide in many species. including mammals and birds. It has besides been discovered in every human population investigated therefore far. In these instances. the unequivocal host was shown to be cats. which have been associated with transmittal of the parasite ( Wang. Wang. & A ; Shu. 2006 ) .

Harmonizing to the Center for Disease Control and Prevention. toxoplasmosis is the taking cause of decease attributed to foodborne unwellness in the United States. Most infections occur through consumption of contaminated meat. particularly porc and lamb ( CDC. 2008 ) . Numerous surveies have been conducted to find the seroprevalence of this parasite in assorted populations. Seroprevalence refers to the sensing of specific antibodies found in blood serum in response to T. gondii infection. One study of hogs in the United States found a seroprevalence of 42 % in breeder hogs and 23 % in market hogs ( CDC. 2008 ) .

The prevalence or estimated population of people infected with toxoplasmosis in the United States is about 1 in 4 people. which equates to more than 60 million people ( CDC. 2008 ) . However. as mentioned antecedently. really few of these persons exhibit symptoms because of equal immune map. Extra attending is given to at-risk persons such as pregnant adult females and immunocompromised persons. Due to the possibility of conveying inborn infection from female parents to their unborn kids. prevalence in adult females of childbearing age is closely tracked.

The seroprevalence in the group of 15 to 44 twelvemonth old adult females has been reported to be about 15 per centum ( Jones. Kruszon-Moran & A ; McAuley. 2001 ) . The same is true for AIDS patients. In AIDS patients. toxoplasma phrenitis is particularly frequent. happening in 10-50 % of seropositive patients with CD4 T-cell ( the type of white blood cell specifically targeted by HIV ) counts less than 100/ ? L ( Jones et. Al. 2001 ) . In other parts of the universe. the prevalence of toxoplasmosis may be every bit high as 95 % of the population ( CDC. 2008 ) .

Infection rates are frequently highest in countries of the universe that have hot. humid climes. and are found at lower heights ( CDC. 2008 ) . Despite the fact that T. gondii is considered the taking cause of decease related to foodborne unwellness. it is still one of five “Neglected Parasitic Infections. ” that the CDC has targeted for public wellness action ( CDC. 2008 ) . Presently. the best manner to forestall toxoplasmosis appears to be through wellness instruction. The CDC has released several recommendations that address ways to extenuate the opportunities of undertaking the T. gondii parasite.

Recommendations include cooking meat to an internal temperature of at least 150 grades Fahrenheit before ingestion and turning away of managing natural meat without baseball mitts on. Cat proprietors are besides warned to avoid direct contact with litter trays. which may be contaminated with cat fecal matters. this is particularly true for pregnant adult females ( CDC. 2008 ) . Public wellness enterprises have besides been initiated to convey that bar of inborn transmittal is possible through early diagnosing of acute infection in female parents and disposal of a contraceptive regimen of spiramycin ( Dubey & A ; Speer. 1998 ) .

By doing the populace more cognizant of these issues. it may be possible to interrupt the concatenation of infection and diminish the prevalence of toxoplasmosis in the United States. Presently. there are no vaccinums available for T. gondii. Much of the trouble in developing an effectual vaccinum lies in the fact that T. gondii is a eucaryotic protozoon with similar cell biological science to that of its human hosts. Conversely. bacteriums are prokaryotes with blunt cellular differences that are easier to pull strings and aim with antibiotics.

With parasites such as T. gondii. nevertheless. scientists seem to be doing some headroom and several possible vaccinums are presently in the early phases of development. Preliminary surveies have shown that DNA vaccinums may convey partial protection against this parasite ( Nguyen. 2006 ) . The current literature suggests that a individual DNA vaccinum incorporating ROP1 ( a particular treating site on the rhoptry proteins antecedently discussed ) and an adjuvant ( a substance that enhances immune response to an antigen ) may be effectual against T. ondii infection in mice ( Bradley & A ; Boothroyd. 2001 ) . Following intramuscular immunisation. cytokine and antibody degrees were assessed. every bit good as mortality rate. The consequences showed that mice immunized with the vaccinum produced a higher immune response than those that did non have the vaccinum. However. this vaccinum merely somewhat prolonged the survival clip of the immunised mice ( Bradley & A ; Boothroyd. 2001 ) .

With rapid progresss in medical biotechnology emerging every twelvemonth. it is non hard to conceive of that a feasible vaccinum will one twenty-four hours go widely available to the populace. Upon reexamining the parasitology. pathology. and epidemiology of Toxoplasma gondii. it becomes clear that it is both a wonder and a threat. It is amazing to believe that such a little being could hold such serious and widespread deductions for the medical field. However. it is besides clear that this parasite is armed and dangerous—an model arm created by evolutionary inventiveness.