<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Toxoplasmosis and can you explain it in depth? [/INST] Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii, an apicomplexan. Infections with toxoplasmosis are associated with a variety of neuropsychiatric and behavioral conditions. Occasionally, people may have a few weeks or months of mild, flu-like illness such as muscle aches and tender lymph nodes. In a small number of people, eye problems may develop. In those with a weak immune system, severe symptoms such as seizures and poor coordination may occur. If a person becomes infected during pregnancy, a condition known as congenital toxoplasmosis may affect the child.Toxoplasmosis is usually spread by eating poorly cooked food that contains cysts, exposure to infected cat feces, and from an infected woman to their baby during pregnancy. Rarely, the disease may be spread by blood transfusion. It is not otherwise spread between people. The parasite is known to reproduce sexually only in the cat family. However, it can infect most types of warm-blooded animals, including humans. Diagnosis is typically by testing blood for antibodies or by testing the amniotic fluid in pregnant people for the parasites DNA.Prevention is by properly preparing and cooking food. Pregnant people are also recommended not to clean cat litter boxes or, if they must, to wear gloves and wash their hands afterwards. Treatment of otherwise healthy people is usually not needed. During pregnancy, spiramycin or pyrimethamine/sulfadiazine and folinic acid may be used for treatment.Up to half of the worlds population is infected by toxoplasmosis, but have no symptoms. In the United States, approximately 11% of people have been infected, while in some areas of the world this is more than 60%. Approximately 200,000 cases of congenital toxoplasmosis occur a year. Charles Nicolle and Louis Manceaux first described the organism in 1908. In 1941, transmission during pregnancy from a pregnant parent to their baby was confirmed. There is tentative evidence that infection may affect peoples behavior.

Signs and symptoms
Infection has three stages:

Acute
Acute toxoplasmosis is often asymptomatic in healthy adults. However, symptoms may manifest and are often influenza-like: swollen lymph nodes, headaches, fever, and fatigue, or muscle aches and pains that last for a month or more. It is rare for a human with a fully functioning immune system to develop severe symptoms following infection. People with weakened immune systems are likely to experience headache, confusion, poor coordination, seizures, lung problems that may resemble tuberculosis or Pneumocystis jiroveci pneumonia (a common opportunistic infection that occurs in people with AIDS), or chorioretinitis caused by severe inflammation of the retina (ocular toxoplasmosis). Young children and immunocompromised people, such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an organ transplant, may develop severe toxoplasmosis. This can cause damage to the brain (encephalitis) or the eyes (necrotizing retinochoroiditis). Infants infected via placental transmission may be born with either of these problems, or with nasal malformations, although these complications are rare in newborns. The toxoplasmic trophozoites causing acute toxoplasmosis are referred to as tachyzoites, and are typically found in various tissues and  body fluids, but rarely in blood or cerebrospinal fluid.Swollen lymph nodes are commonly found in the neck or under the chin, followed by the armpits and the groin. Swelling may occur at different times after the initial infection, persist, and recur for various times independently of antiparasitic treatment. It is usually found at single sites in adults, but in children, multiple sites may be more common. Enlarged lymph nodes will resolve within 1–2 months in 60% of cases. However, a quarter of those affected take 2–4 months to return to normal, and 8% take 4–6 months. A substantial number (6%) do not return to normal until much later.

Latent
Due to the absence of obvious symptoms, hosts easily become infected with T. gondii and develop toxoplasmosis without knowing it. Although mild, flu-like symptoms occasionally occur during the first few weeks following exposure, infection with T. gondii produces no readily observable symptoms in healthy human adults. In most immunocompetent people, the infection enters a latent phase, during which only bradyzoites (in tissue cysts) are present; these tissue cysts and even lesions can occur in the retinas, alveolar lining of the lungs (where an acute infection may mimic a Pneumocystis jirovecii infection), heart, skeletal muscle, and the central nervous system (CNS), including the brain. Cysts form in the CNS (brain tissue) upon infection with T. gondii and persist for the lifetime of the host. Most infants who are infected while in the womb have no symptoms at birth, but may develop symptoms later in life.Reviews of serological studies have estimated that 30–50% of the global population has been exposed to and may be chronically infected with latent toxoplasmosis, although infection rates differ significantly from country to country. This latent state of infection has recently been associated with numerous disease burdens, neural alterations, and subtle gender-dependent behavioral changes in immunocompetent humans, as well as an increased risk of motor vehicle collisions.

Skin
While rare, skin lesions may occur in the acquired form of the disease, including roseola and erythema multiforme-like eruptions, prurigo-like nodules, urticaria, and maculopapular lesions. Newborns may have punctate macules, ecchymoses, or "blueberry muffin" lesions.
Diagnosis of cutaneous toxoplasmosis is based on the tachyzoite form of T. gondii being found in the epidermis. It is found in all levels of the epidermis, is about 6 by 2 μm and bow-shaped, with the nucleus being one-third of its size. It can be identified by electron microscopy or by Giemsa staining tissue where the cytoplasm shows blue, the nucleus red.

Cause
Parasitology
In its lifecycle, T. gondii adopts several forms. Tachyzoites are responsible for acute infection; they divide rapidly and spread through the tissues of the body. Tachyzoites are also known as "tachyzoic merozoites", a descriptive term that conveys more precisely the parasitological nature of this stage. After proliferating, tachyzoites convert into bradyzoites, which are inside latent intracellular tissue cysts that form mainly in the muscles and brain. The formation of cysts is in part triggered by the pressure of the host immune system. The bradyzoites (also called "bradyzoic merozoites") are not responsive to antibiotics. Bradyzoites, once formed, can remain in the tissues for the lifespan of the host. In a healthy host, if some bradyzoites convert back into active tachyzoites, the immune system will quickly destroy them. However, in immunocompromised individuals, or in fetuses, which lack a developed immune system, the tachyzoites can run rampant and cause significant neurological damage.The parasites survival is dependent on a balance between host survival and parasite proliferation. T. gondii achieves this balance by manipulating the hosts immune response, reducing the hosts immune response, and enhancing the parasites reproductive advantage. Once it infects a normal host cell, it resists damage caused by the hosts immune system, and changes the hosts immune processes.As it forces its way into the host cell, the parasite forms a parasitophorous vacuole (PV) membrane from the membrane of the host cell. The PV encapsulates the parasite, and is both resistant to the activity of the endolysosomal system, and can take control of the hosts mitochondria and endoplasmic reticulum.When first invading the cell, the parasite releases ROP proteins from the bulb of the rhoptry organelle. These proteins translocate to the nucleus and the surface of the PV membrane where they can activate STAT pathways to modulate the expression of cytokines at the transcriptional level, bind and inactivate PV membrane destroying IRG proteins, among other possible effects. Additionally, certain strains of T. gondii can secrete a protein known as GRA15, activating the NF-κB pathway, which upregulates the pro-inflammatory cytokine IL-12 in the early immune response, possibly leading to the parasites latent phase. The parasites ability to secrete these proteins depends on its genotype and affects its virulence.The parasite also influences an anti-apoptotic mechanism, allowing the infected host cells to persist and replicate. One method of apoptosis resistance is by disrupting pro-apoptosis effector proteins, such as BAX and BAK. To disrupt these proteins, T. gondii causes conformational changes to the proteins, which prevent the proteins from being transported to various cellular compartments where they initiate apoptosis events. T. gondii does not, however, cause downregulation of the pro-apoptosis effector proteins.T. gondii also has the ability to initiate autophagy of the hosts cells. This leads to a decrease in healthy, uninfected cells, and consequently fewer host cells to attack the infected cells. Research by Wang et al finds that infected cells lead to higher levels of autophagosomes in normal and infected cells. Their research reveals that T. gondii causes host cell autophagy using a calcium-dependent pathway. Another study suggests that the parasite can directly affect calcium being released from calcium stores, which are important for the signalling processes of cells.The mechanisms above allow T. gondii to persist in a host. Some limiting factors for the toxoplasma is that its influence on the host cells is stronger in a weak immune system and is quantity-dependent, so a large number of T. gondii per host cell cause a more severe effect. The effect on the host also depends on the strength of the host immune system. Immunocompetent individuals do not normally show severe symptoms or any at all, while fatality or severe complications can result in immunocompromised individuals.Since the parasite can change the hosts immune response, it may also have an effect, positive or negative, on the immune response to other pathogenic threats. This includes, but is not limited to, the responses to infections by Helicobacter felis, Leishmania major, or other parasites, such as Nippostrongylus brasiliensis.

Transmission
Toxoplasmosis is generally transmitted through the mouth when Toxoplasma gondii oocysts or tissue cysts are accidentally eaten. Congenital transmittance from mother to fetus can also occur. Transmission may also occur during the solid organ transplant process or hematogenous stem cell transplants.Oral transmission may occur through:

Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing Toxoplasma cysts: Infection prevalence in countries where undercooked meat is traditionally eaten has been related to this transmission method. Tissue cysts may also be ingested during hand-to-mouth contact after handling undercooked meat, or from using knives, utensils, or cutting boards contaminated by raw meat.
Ingestion of unwashed fruit or vegetables that have been in contact with contaminated soil containing infected cat feces.
Ingestion of cat feces containing oocysts: This can occur through hand-to-mouth contact following gardening, cleaning a cats litter box, contact with childrens sandpits; the parasite can survive in the environment for months.
Ingestion of untreated, unfiltered water through direct consumption or utilization of water for food preparation.
Ingestion of unpasteurized milk and milk products, particularly goats milk.
Ingestion of raw seafood.Cats excrete the pathogen in their feces for a number of weeks after contracting the disease, generally by eating an infected intermediate host that could include mammals (like rodents) or birds. Oocyst shedding usually starts from the third day after ingestion of infected intermediate hosts, and may continue for weeks. The oocysts are not infective when excreted.  After about a day, the oocyst undergoes a process called sporulation and becomes potentially pathogenic. In addition to cats, birds and mammals including human beings are also intermediate hosts of the parasite and are involved in the transmission process. However the pathogenicity varies with the age and species involved in infection and the mode of transmission of T. gondii.Toxoplasmosis may also be transmitted through solid organ transplants. Toxoplasma-seronegative recipients who receive organs from recently infected Toxoplasma-seropositive donors are at risk. Organ recipients who have latent toxoplasmosis are at risk of the disease reactivating in their system due to the immunosuppression occurring during solid organ transplant. Recipients of hematogenous stem cell transplants may experience higher risk of infection due to longer periods of immunosuppression.Heart and lung transplants provide the highest risk for toxoplasmosis infection due to the striated muscle making up the heart, which can contain cysts, and risks for other organs and tissues vary widely. Risk of transmission can be reduced by screening donors and recipients prior to the transplant procedure and providing treatment.

Pregnancy precautions
Congenital toxoplasmosis is a specific form of toxoplasmosis in which an unborn fetus is infected via the placenta. Congenital toxoplasmosis is associated with fetal death and miscarriage, and in infants, it is associated with hydrocephalus, cerebral calcifications and chorioretinitis, leading to encephalopathy and possibly blindness. A positive antibody titer indicates previous exposure and immunity, and largely ensures the unborn fetus safety. A simple blood draw at the first prenatal doctor visit can determine whether or not a woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to T. gondii while pregnant, the fetus is at particular risk.Not much evidence exists around the effect of education before pregnancy to prevent congenital toxoplasmosis. However educating parents before the baby is born has been suggested to be effective because it may improve food, personal and pet hygiene. More research is needed to find whether antenatal education can reduce congenital toxoplasmosis.For pregnant women with negative antibody titers, indicating no previous exposure to T. gondii, serology testing as frequent as monthly is advisable as treatment during pregnancy for those women exposed to T. gondii for the first time dramatically decreases the risk of passing the parasite to the fetus. Since a babys immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with antiprotozoans, an infection can be very serious in the young.Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries, for reasons of cost-effectiveness and the high number of false positives generated; Portugal, France, Austria, Uruguay, and Italy are notable exceptions, and some regional screening programmes operate in Germany, Switzerland and Belgium. As invasive prenatal testing incurs some risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented), postnatal or neonatal screening is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening can be targeted.Pregnant women should avoid handling raw meat, drinking raw milk (especially goat milk) and be advised to not eat raw or undercooked meat regardless of type. Because of the obvious relationship between Toxoplasma and cats it is also often advised to avoid exposure to cat feces, and refrain from gardening (cat feces are common in garden soil) or at least wear gloves when so engaged. Most cats are not actively shedding oocysts, since they get infected in the first six months of their life, when they shed oocysts for a short period of time (1–2 weeks.) However, these oocysts get buried in the soil, sporulate and remain infectious for periods ranging from several months to more than a year. Numerous studies have shown living in a household with a cat is not a significant risk factor for T. gondii infection, though living with several kittens has some significance.In 2006, a Czech research team discovered women with high levels of toxoplasmosis antibodies were significantly more likely to give birth to baby boys than baby girls. In most populations, the birth rate is around 51% boys, but people infected with T. gondii had up to a 72% chance of a boy.

Diagnosis
Diagnosis of toxoplasmosis in humans is made by biological, serological, histological, or molecular methods, or by some combination of the above. Toxoplasmosis can be difficult to distinguish from primary central nervous system lymphoma. It mimics several other infectious diseases so clinical signs are non-specific and are not sufficiently characteristic for a definite diagnosis. As a result, the possibility of an alternate diagnosis is supported by a failed trial of antimicrobial therapy (pyrimethamine, sulfadiazine, and folinic acid (USAN: leucovorin)), i.e., if the drugs produce no effect clinically and no improvement on repeat imaging.
T. gondii may also be detected in blood, amniotic fluid, or cerebrospinal fluid by using polymerase chain reaction. T. gondii may exist in a host as an inactive cyst that would likely evade detection.Serological testing can detect T. gondii antibodies in blood serum, using methods including the Sabin–Feldman dye test (DT), the indirect hemagglutination assay, the indirect fluorescent antibody assay (IFA), the direct agglutination test, the latex agglutination test (LAT), the enzyme-linked immunosorbent assay (ELISA), and the immunosorbent agglutination assay test (IAAT).The most commonly used tests to measure IgG antibody are the DT, the ELISA, the IFA, and the modified direct agglutination test. IgG antibodies usually appear within a week or two of infection, peak within one to two months, then decline at various rates. Toxoplasma IgG antibodies generally persist for life, and therefore may be present in the bloodstream as a result of either current or previous infection.To some extent, acute toxoplasmosis infections can be differentiated from chronic infections using an IgG avidity test, which is a variation on the ELISA. In the first response to infection, toxoplasma-specific IgG has a low affinity for the toxoplasma antigen; in the following weeks and month, IgG affinity for the antigen increases. Based on the IgG avidity test, if the IgG in the infected individual has a high affinity, it means that the infection began three to five months before testing. This is particularly useful in congenital infection, where pregnancy status and gestational age at time of infection determines treatment.In contrast to IgG, IgM antibodies can be used to detect acute infection but generally not chronic infection. The IgM antibodies appear sooner after infection than the IgG antibodies and disappear faster than IgG antibodies after recovery. In most cases, T. gondii-specific IgM antibodies can first be detected approximately a week after acquiring primary infection and decrease within one to six months; 25% of those infected are negative for T. gondii-specific IgM within seven months. However, IgM may be detectable months or years after infection, during the chronic phase, and false positives for acute infection are possible.  The most commonly used tests for the measurement of IgM antibody are double-sandwich IgM-ELISA, the IFA test, and the immunosorbent agglutination assay (IgM-ISAGA). Commercial test kits often have low specificity, and the reported results are frequently misinterpreted.In 2021, twenty commercial anti-Toxoplasma IgG assays were evaluated in a systematic review, in comparison with an accepted reference method. Most of them were enzyme-immunoassays, followed by agglutination tests, immunochromatographic tests, and a Western-Blot assay. The mean sensitivity of IgG assays ranged from 89.7% to 100% for standard titers and from 13.4% to 99.2% for low IgG titers. A few studies pointed out the ability of some methods, especially WB to detect IgG early after primary infection. The specificity of IgG assays was generally high, ranging from 91.3% to 100%; and higher than 99% for most EIA assays. The positive predictive value (PPV) was not a discriminant indicator among methods, whereas significant disparities (87.5%–100%) were reported among negative predictive values (NPV), a key-parameter assessing the ability to definitively rule out a Toxoplasma infection in patients at-risk for opportunistic infections.

Congenital
Recommendations for the diagnosis of congenital toxoplasmosis include: prenatal diagnosis based on testing of amniotic fluid and ultrasound examinations; neonatal diagnosis based on molecular testing of placenta and cord blood and comparative mother-child serologic tests and a clinical examination at birth; and early childhood diagnosis based on neurologic and ophthalmologic examinations and a serologic survey during the first year of life. During pregnancy, serological testing is recommended at three week intervals.Even though diagnosis of toxoplasmosis heavily relies on serological detection of specific anti-Toxoplasma immunoglobulin, serological testing has limitations. For example, it may fail to detect the active phase of T. gondii infection because the specific anti-Toxoplasma IgG or IgM may not be produced until after several weeks of infection. As a result, a pregnant woman might test negative during the active phase of T. gondii infection leading to undetected and therefore untreated congenital toxoplasmosis. Also, the test may not detect T. gondii infections in immunocompromised patients because the titers of specific anti-Toxoplasma IgG or IgM may not rise in this type of patient.Many PCR-based techniques have been developed to diagnose toxoplasmosis using clinical specimens that include amniotic fluid, blood, cerebrospinal fluid, and tissue biopsy. The most sensitive PCR-based technique is nested PCR, followed by hybridization of PCR products. The major downside to these techniques is that they are time-consuming and do not provide quantitative data.Real-time PCR is useful in pathogen detection, gene expression and regulation, and allelic discrimination. This PCR technique utilizes the 5 nuclease activity of Taq DNA polymerase to cleave a nonextendible, fluorescence-labeled hybridization probe during the extension phase of PCR. A second fluorescent dye, e.g., 6-carboxy-tetramethyl-rhodamine, quenches the fluorescence of the intact probe. The nuclease cleavage of the hybridization probe during the PCR releases the effect of quenching resulting in an increase of fluorescence proportional to the amount of PCR product, which can be monitored by a sequence detector.Toxoplasmosis cannot be detected with immunostaining. Lymph nodes affected by Toxoplasma have characteristic changes, including poorly demarcated reactive germinal centers, clusters of monocytoid B cells, and scattered epithelioid histiocytes.
The classic triad of congenital toxoplasmosis includes: chorioretinitis, hydrocephalus, and intracranial arteriosclerosis. Other consequences include sensorineural deafness, seizures, and intellectual disability.Congenital toxoplasmosis may also impact a childs hearing. Up to 30% of newborns have some degree of sensorineural hearing loss. The childs communication skills may also be affected. A study published in 2010 looked at 106 patients, all of whom received toxoplasmosis treatment prior to 2.5 months. Of this group, 26.4% presented with language disorders.

Treatment
Treatment is recommended for people with serious health problems, such as people with HIV whose CD4 counts are under 200 cells/mm3. Trimethoprim/sulfamethoxazole is the drug of choice to prevent toxoplasmosis, but not for treating active disease.
A 2012 study shows a promising new way to treat the active and latent form of this disease using two endochin-like quinolones.

Acute
The medications prescribed for acute toxoplasmosis are the following:

Pyrimethamine – an antimalarial medication
Sulfadiazine – an antibiotic used in combination with pyrimethamine to treat toxoplasmosis
Combination therapy is usually given with folic acid supplements to reduce incidence of thrombocytopaenia.
Combination therapy is most useful in the setting of HIV.
Clindamycin
Spiramycin – an antibiotic used most often for pregnant women to prevent the infection of their children.(other antibiotics, such as minocycline, have seen some use as a salvage therapy).
If infected during pregnancy, spiramycin is recommended in the first and early second trimesters while pyrimethamine/sulfadiazine and leucovorin is recommended in the late second and third trimesters.

Latent
In people with latent toxoplasmosis, the cysts are immune to these treatments, as the antibiotics do not reach the bradyzoites in sufficient concentration.
The medications prescribed for latent toxoplasmosis are:

Atovaquone – an antibiotic that has been used to kill Toxoplasma cysts inside AIDS patients
Clindamycin – an antibiotic that, in combination with atovaquone, seemed to optimally kill cysts in mice

Congenital
When a pregnant woman is diagnosed with acute toxoplasmosis, amniocentesis can be used to determine whether the fetus has been infected or not. When a pregnant woman develops acute toxoplasmosis, the tachyzoites have approximately a 30% chance of entering the placental tissue, and from there entering and infecting the fetus. As gestational age at the time of infection increases, the chance of fetal infection also increases.If the parasite has not yet reached the fetus, spiramycin can help to prevent placental transmission. If the fetus has been infected, the pregnant woman can be treated with pyrimethamine and sulfadiazine, with folinic acid, after the first trimester. They are treated after the first trimester because pyrimethamine has an antifolate effect, and lack of folic acid can interfere with fetal brain formation and cause thrombocytopaenia. Infection in earlier gestational stages correlates with poorer fetal and neonatal outcomes, particularly when the infection is untreated.Newborns who undergo 12 months of postnatal anti-toxoplasmosis treatment have a low chance of sensorineural hearing loss. Information regarding treatment milestones for children with congenital toxoplasmosis have been created for this group.

Epidemiology
T. gondii infections occur throughout the world, although infection rates differ significantly by country. For women of childbearing age, a survey of 99 studies within 44 countries found the areas of highest prevalence are within Latin America (about 50–80%), parts of Eastern and Central Europe (about 20–60%), the Middle East (about 30–50%), parts of Southeast Asia (about 20–60%), and parts of Africa (about 20–55%).In the United States, data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2004 found 9.0% of US-born persons 12–49 years of age were seropositive for IgG antibodies against T. gondii, down from 14.1% as measured in the NHANES 1988–1994. In the 1999–2004 survey, 7.7% of US-born and 28.1% of foreign-born women 15–44 years of age were T. gondii seropositive. A trend of decreasing seroprevalence has been observed by numerous studies in the United States and many European countries. Toxoplasma gondii is considered the second leading cause of foodborne-related deaths and the fourth leading cause of foodborne-related hospitalizations in the United States.The protist responsible for toxoplasmosis is T. gondii. There are three major types of T. gondii responsible for the patterns of toxoplasmosis throughout the world. There are types I, II, and III. These three types of T. gondii have differing effects on certain hosts, mainly mice and humans due to their variation in genotypes.
Type I: virulent in mice and humans, seen in people with AIDS.
Type II: non-virulent in mice, virulent in humans (mostly Europe and North America), seen in people with AIDS.
Type III: non-virulent in mice, virulent mainly in animals but seen to a lesser degree in humans as well.Current serotyping techniques can only separate type I or III from type II parasites.Because the parasite poses a particular threat to fetuses when it is contracted during pregnancy, much of the global epidemiological data regarding T. gondii comes from seropositivity tests in women of childbearing age. Seropositivity tests look for the presence of antibodies against T. gondii in blood, so while seropositivity guarantees one has been exposed to the parasite, it does not necessarily guarantee one is chronically infected.

History
Toxoplasma gondii was first described in 1908 by Nicolle and Manceaux in Tunisia, and independently by Splendore in Brazil. Splendore reported the protozoan in a rabbit, while Nicolle and Manceaux identified it in a North African rodent, the gundi (Ctenodactylus gundi). In 1909 Nicolle and Manceaux differentiated the protozoan from Leishmania. Nicolle and Manceaux then named it Toxoplasma gondii after the curved shape of its infectious stage (Greek root toxon= bow).The first recorded case of congenital toxoplasmosis was in 1923, but it was not identified as caused by T. gondii. Janků (1923) described in detail the autopsy results of an 11-month-old boy who had presented to hospital with hydrocephalus. The boy had classic marks of toxoplasmosis including chorioretinitis (inflammation of the choroid and retina of the eye). Histology revealed a number of "sporocytes", though Janků did not identify these as T. gondii.It was not until 1937 that the first detailed scientific analysis of T. gondii took place using techniques previously developed for analyzing viruses. In 1937 Sabin and Olitsky analyzed T. gondii in laboratory monkeys and mice. Sabin and Olitsky showed that T. gondii was an obligate intracellular parasite and that mice fed T. gondii-contaminated tissue also contracted the infection. Thus Sabin and Olitsky demonstrated T. gondii as a pathogen transmissible between animals.
T. gondii was first described as a human pathogen in 1939 at Babies Hospital in New York City. Wolf, Cowen and Paige identified T. gondii infection in an infant girl delivered full-term by Caesarean section. The infant developed seizures and had chorioretinitis in both eyes at three days. The infant then developed encephalomyelitis and died at one month of age. Wolf, Cowen and Paige isolated T. gondii from brain tissue lesions. Intracranial injection of brain and spinal cord samples into mice, rabbits and rats produced encephalitis in the animals. Wolf, Cowen and Page reviewed additional cases and concluded that T. gondii produced recognizable symptoms and could be transmitted from mother to child.The first adult case of toxoplasmosis was reported in 1940 with no neurological signs. Pinkerton and Weinman reported the presence of Toxoplasma in a 22-year-old man from Peru who died from a subsequent bacterial infection and fever.In 1948, a serological dye test was created by Sabin and Feldman based on the ability of the patients antibodies to alter staining of Toxoplasma. The Sabin Feldman Dye Test is now the gold standard for identifying Toxoplasma infection.Transmission of Toxoplasma by eating raw or undercooked meat was demonstrated by Desmonts et al. in 1965 Paris. Desmonts observed that the therapeutic consumption of raw beef or horse meat in a tuberculosis hospital was associated with a 50% per year increase in Toxoplasma antibodies. This means that more T. gondii was being transmitted through the raw meat.
In 1974, Desmonts and Couvreur showed that infection during the first two trimesters produces most harm to the fetus, that transmission depended on when mothers were infected during pregnancy, that mothers with antibodies before pregnancy did not transmit the infection to the fetus, and that spiramycin lowered the transmission to the fetus.Toxoplasma gained more attention in the 1970s with the rise of immune-suppressant treatment given after organ or bone marrow transplants and the AIDS epidemic of the 1980s. Patients with lowered immune system function are much more susceptible to disease.

Society and culture
"Crazy cat-lady"
"Crazy cat-lady syndrome" is a term coined by news organizations to describe scientific findings that link the parasite Toxoplasma gondii to several mental disorders and behavioral problems. The suspected correlation between cat ownership in childhood and later development of schizophrenia suggested that further studies were needed to determine a risk factor for children; however, later studies showed that T. gondii was not a causative factor in later psychoses. Researchers also found that cat ownership does not strongly increase the risk of a T. gondii infection in pregnant women.The term crazy cat-lady syndrome draws on both stereotype and popular cultural reference. It was originated as instances of the aforementioned afflictions were noted amongst the populace. A cat lady is a cultural stereotype of a woman who compulsively hoards and dotes upon cats. The biologist Jaroslav Flegr is a proponent of the theory that toxoplasmosis affects human behaviour.

Notable cases
Tennis player Arthur Ashe developed neurological problems from toxoplasmosis (and was later found to be HIV-positive).
Actor Merritt Butrick was HIV-positive and died from toxoplasmosis as a result of his already-weakened immune system.
Pedro Zamora, reality television personality and HIV/AIDS activist, was diagnosed with toxoplasmosis as a result of his immune system being weakened by HIV.
Prince François, Count of Clermont, pretender to the throne of France had congenital toxoplasmosis; his disability caused him to be overlooked in the line of succession.
Actress Leslie Ash contracted toxoplasmosis in the second month of pregnancy.
British middle-distance runner Sebastian Coe contracted toxoplasmosis in 1983, which was probably transmitted by a cat while he trained in Italy.
Tennis player Martina Navratilova experienced toxoplasmosis during the 1982 US Open.

Other animals
Although T. gondii has the capability of infecting virtually all warm-blooded animals, susceptibility and rates of infection vary widely between different genera and species. Rates of infection in populations of the same species can also vary widely due to differences in location, diet, and other factors.
Although infection with T. gondii has been noted in several species of Asian primates, seroprevalence of T. gondii antibodies were found for the first time in toque macaques (Macaca sinica) that are endemic to the island of Sri Lanka.Australian marsupials are particularly susceptible to toxoplasmosis. Wallabies, koalas, wombats, pademelons and small dasyurids can be killed by it, with eastern barred bandicoots typically dying within about 3 weeks of infection.It is estimated that 23% of wild swine worldwide are seropositive for T. gondii.  Seroprevalence varies across the globe with the highest seroprevalence in North America (32%) and Europe (26%) and the lowest in Asia (13%) and South America (5%). Geographical regions located at higher latitudes and regions that experience warmer, humid climates are associated with increased seroprevalence of T. gondii among wild boar.  Wild boar infected with T. gondii pose a potential health risk for humans who consume their meat.

Livestock
Among livestock, pigs, sheep and goats have the highest rates of chronic T. gondii infection. The prevalence of T. gondii in meat-producing animals varies widely both within and among countries, and rates of infection have been shown to be dramatically influenced by varying farming and management practices. For instance, animals kept outdoors or in free-ranging environments are more at risk of infection than animals raised indoors or in commercial confinement operations.

Pigs
Worldwide, the percentage of pigs harboring viable parasites has been measured to be 3–71.43% and in the United States (via bioassay in mice or cats) to be as high as 92.7% and as low as 0%, depending on the farm or herd. Surveys of seroprevalence (T. gondii antibodies in blood) are more common, and such measurements are indicative of the high relative seroprevalence in pigs across the world. Neonatal piglets have been found to experience the entire range of severity, including progression to stillbirth.: 95  This was especially demonstrated in the foundational Thiptara et al. 2006, reporting a litter birth of three stillborns and six live in Thailand. This observation has been relevant not only to that country but to toxoplasmosis control in porciculture around the world.: 95

Sheep
Along with pigs, sheep and goats are among the most commonly infected livestock of epidemiological significance for human infection. Prevalence of viable T. gondii in sheep tissue has been measured (via bioassay) to be as high as 78% in the United States, and a 2011 survey of goats intended for consumption in the United States found a seroprevalence of 53.4%.

Chickens
Due to a lack of exposure to the outdoors, chickens raised in large-scale indoor confinement operations are not commonly infected with T. gondii. Free-ranging or backyard-raised chickens are much more commonly infected. A survey of free-ranging chickens in the United States found its prevalence to be 17–100%, depending on the farm. Because chicken meat is generally cooked thoroughly before consumption, poultry is not generally considered to be a significant risk factor for human T. gondii infection.

Cattle
Although cattle and buffalo can be infected with T. gondii, the parasite is generally eliminated or reduced to undetectable levels within a few weeks following exposure. Tissue cysts are rarely present in buffalo meat or beef, and meat from these animals is considered to be low-risk for harboring viable parasites.

Horses
Horses are considered resistant to chronic T. gondii infection. However, viable cells have been isolated from US horses slaughtered for export, and severe human toxoplasmosis in France has been epidemiologically linked to the consumption of horse meat.

Domestic cats
In 1942, the first case of feline toxoplasmosis was diagnosed and reported in a domestic cat in Middletown, New York. The investigators isolated oocysts from feline feces and found that the oocysts could be infectious for up to 12 months in the environment.The seroprevalence of T. gondii in domestic cats, worldwide has been estimated to be around 30–40% and exhibits significant geographical variation. In the United States, no official national estimate has been made, but local surveys have shown levels varying between 16% and 80%. A 2012 survey of 445 purebred pet cats and 45 shelter cats in Finland found an overall seroprevalence of 48.4%, while a 2010 survey of feral cats from Giza, Egypt found a seroprevalence rate of 97.4%. Another survey from Colombia recorded seroprevalence of 89.3%, whereas a Chinese (Guangdong) study found just a 2.1% prevalence.T. gondii infection rates in domestic cats vary widely depending on the cats diets and lifestyles. Feral cats that hunt for their food are more likely to be infected than domestic cats, and naturally also depends on the prevalence of T. gondii-infected prey such as birds and small mammals.Most infected cats will shed oocysts only once in their lifetimes, for a period of about one to two weeks. This shedding can release millions of oocysts, each capable of spreading and surviving for months. An estimated 1% of cats at any given time are actively shedding oocysts.It is difficult to control the cat population with the infected oocysts due to lack of an effective vaccine. This remains a challenge in most cases and the programs that are readily available are questionable in efficacy.

Rodents
Infection with T. gondii has been shown to alter the behavior of mice and rats in ways thought to increase the rodents chances of being preyed upon by cats. Infected rodents show a reduction in their innate aversion to cat odors; while uninfected mice and rats will generally avoid areas marked with cat urine or with cat body odor, this avoidance is reduced or eliminated in infected animals. Moreover, some evidence suggests this loss of aversion may be specific to feline odors: when given a choice between two predator odors (cat or mink), infected rodents show a significantly stronger preference to cat odors than do uninfected controls.In rodents, T. gondii–induced behavioral changes occur through epigenetic remodeling in neurons associated with observed behaviors; for example, it modifies epigenetic methylation to induce hypomethylation of arginine vasopressin-related genes in the medial amygdala to greatly decrease predator aversion. Similar epigenetically induced behavioral changes have also been observed in mouse models of addiction, where changes in the expression of histone-modifying enzymes via gene knockout or enzyme inhibition in specific neurons produced alterations in drug-related behaviors. Widespread histone–lysine acetylation in cortical astrocytes appears to be another epigenetic mechanism employed by T. gondii.T. gondii-infected rodents show a number of behavioral changes beyond altered responses to cat odors. Rats infected with the parasite show increased levels of activity and decreased neophobic behavior. Similarly, infected mice show alterations in patterns of locomotion and exploratory behavior during experimental tests. These patterns include traveling greater distances, moving at higher speeds, accelerating for longer periods of time, and showing a decreased pause-time when placed in new arenas. Infected rodents have also been shown to have lower anxiety, using traditional models such as elevated plus mazes, open field arenas, and social interaction tests.

Marine mammals
A University of California, Davis study of dead sea otters collected from 1998 to 2004 found toxoplasmosis was the cause of death for 13% of the animals. Proximity to freshwater outflows into the ocean was a major risk factor. Ingestion of oocysts from cat feces is considered to be the most likely ultimate source. Surface runoff containing wild cat feces and litter from domestic cats flushed down toilets are possible sources of oocysts. These same sources may have also introduced the toxoplasmosis infection to the endangered Hawaiian monk seal. Infection with the parasite has contributed to the death of at least four Hawaiian monk seals. A Hawaiian monk seals infection with T. gondii was first noted in 2004. The parasites spread threatens the recovery of this highly endangered pinniped. The parasites have been found in dolphins and whales. Researchers Black and Massie believe anchovies, which travel from estuaries into the open ocean, may be helping to spread the disease.

Giant panda
Toxoplasma gondii has been reported as the cause of death of a giant panda kept in a zoo in China, who died in 2014 of acute gastroenteritis and respiratory disease. Although seemingly anecdotal, this report emphasizes that all warm-blooded species are likely to be infected by T. gondii, including endangered species such as the giant panda.

Research
Chronic infection with T. gondii has traditionally been considered asymptomatic in people with normal immune function. Some evidence suggests latent infection may subtly influence a range of human behaviors and tendencies, and infection may alter the susceptibility to or intensity of a number of psychiatric or neurological disorders.In most of the current studies where positive correlations have been found between T. gondii antibody titers and certain behavioral traits or neurological disorders, T. gondii seropositivity tests are conducted after the onset of the examined disease or behavioral trait; that is, it is often unclear whether infection with the parasite increases the chances of having a certain trait or disorder, or if having a certain trait or disorder increases the chances of becoming infected with the parasite. Groups of individuals with certain behavioral traits or neurological disorders may share certain behavioral tendencies that increase the likelihood of exposure to and infection with T. gondii; as a result, it is difficult to confirm causal relationships between T. gondii infections and associated neurological disorders or behavioral traits.

Mental health
Some evidence links T. gondii to schizophrenia. Two 2012 meta-analyses found that the rates of antibodies to T. gondii in people with schizophrenia were 2.7 times higher than in controls. T. gondii antibody positivity was therefore considered an intermediate risk factor in relation to other known risk factors. Cautions noted include that the antibody tests do not detect toxoplasmosis directly, most people with schizophrenia do not have antibodies for toxoplasmosis, and publication bias might exist. While the majority of these studies tested people already diagnosed with schizophrenia for T. gondii antibodies, associations between T. gondii and schizophrenia have been found prior to the onset of schizophrenia symptoms. Sex differences in the age of schizophrenia onset may be explained in part by a second peak of T. gondii infection incidence during ages 25–30 in females only. Although a mechanism supporting the association between schizophrenia and T. gondii infection is unclear, studies have investigated a molecular basis of this correlation. Antipsychotic drugs used in schizophrenia appear to inhibit the replication of T. gondii tachyzoites in cell culture. Supposing a causal link exists between T. gondii and schizophrenia, studies have yet to determine why only some individuals with latent toxoplasmosis develop schizophrenia; some plausible explanations include differing genetic susceptibility, parasite strain differences, and differences in the route of the acquired T. gondii infection.Correlations have also been found between antibody titers to T. gondii and OCD, as well as suicide among people with mood disorders including bipolar disorder. Positive antibody titers to T. gondii appear to be uncorrelated with major depression or dysthymia. Although there is a correlation between T. gondii and many psychological disorders, the underlying mechanism is unclear. A 2016 study of 236 persons with high levels of toxoplasmosis antibodies found that "there was little evidence that T. gondii was related to increased risk of psychiatric disorder, poor impulse control, personality aberrations or neurocognitive impairment".

Neurological disorders
Latent infection has been linked to Parkinsons disease and Alzheimers disease.Individuals with multiple sclerosis show infection rates around 15% lower than the general public.

Traffic accidents
Latent T. gondii infection in humans has been associated with a higher risk of automobile accidents, potentially due to impaired psychomotor performance or enhanced risk-taking personality profiles.

Climate change
Climate change has been reported to affect the occurrence, survival, distribution and transmission of T. gondii.  T. gondii has been identified in the Canadian arctic, a location that was once too cold for its survival. Higher temperatures increase the survival time of T. gondii.  More snowmelt and precipitation can increase the amount of T. gondii oocysts that are transported via river flow.  Shifts in bird, rodent, and insect populations and migration patterns can impact the distribution of T. gondii due to their role as reservoir and vector.  Urbanization and natural environmental degradation are also suggested to affect T. gondii transmission and increase risk of infection.

See also
Toxoplasmic chorioretinitis
TORCH infection
Pyrimethamine

References
Parts of this article are taken from the public domain CDC factsheet: Toxoplasmosis

Bibliography
Weiss, L. M.; Kim, K. (28 April 2011). Toxoplasma gondii: The Model Apicomplexan. Perspectives and Methods. Academic Press. ISBN 978-0-08-047501-1. Retrieved 12 March 2013.
Dubey, J. P. (2016). Toxoplasmosis of Animals and Humans (2nd ed.). Boca Raton: CRC Press. pp. xvii+313. ISBN 978-1-4200-9237-0. OCLC 423572366. ISBN 1-4200-9236-7 ISBN 9781420092363
Dubey JP, Lindsay DS, Speer CA (April 1998). "Structures of Toxoplasma gondii tachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts". Clinical Microbiology Reviews </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Trachoma and can you explain it in depth? [/INST] Trachoma is an infectious disease caused by bacterium Chlamydia trachomatis. The infection causes a roughening of the inner surface of the eyelids. This roughening can lead to pain in the eyes, breakdown of the outer surface or cornea of the eyes, and eventual blindness. Untreated, repeated trachoma infections can result in a form of permanent blindness when the eyelids turn inward.The bacteria that cause the disease can be spread by both direct and indirect contact with an affected persons eyes or nose. Indirect contact includes through clothing or flies that have come into contact with an affected persons eyes or nose. Children spread the disease more often than adults. Poor sanitation, crowded living conditions, and not enough clean water and toilets also increase spread.Efforts to prevent the disease include improving access to clean water and treatment with antibiotics to decrease the number of people infected with the bacterium. This may include treating, all at once, whole groups of people in whom the disease is known to be common. Washing, by itself, is not enough to prevent disease, but may be useful with other measures. Treatment options include oral azithromycin and topical tetracycline. Azithromycin is preferred because it can be used as a single oral dose. After scarring of the eyelid has occurred, surgery may be required to correct the position of the eyelashes and prevent blindness.Globally, about 80 million people have an active infection. In some areas, infections may be present in as many as 60–90% of children. Among adults, it more commonly affects women than men – likely due to their closer contact with children. The disease is the cause of decreased vision in 2.2 million people, of whom 1.2 million are completely blind. Trachoma is a public health problem in 44 countries across Africa, Asia, and Central and South America, with 136.9 million people at risk. It results in US$8 billion of economic losses a year. It belongs to a group of diseases known as neglected tropical diseases.

Signs and symptoms
The bacterium has an incubation period of 6 to 12 days, after which the affected individual experiences symptoms of conjunctivitis, or irritation similar to "pink eye". Blinding endemic trachoma results from multiple episodes of reinfection that maintains the intense inflammation in the conjunctiva. Without reinfection, the inflammation gradually subsides.The conjunctival inflammation is called "active trachoma" and usually is seen in children, especially preschool children. It is characterized by white lumps in the undersurface of the upper eyelid (conjunctival follicles or lymphoid germinal centres) and by nonspecific inflammation and thickening often associated with papillae. Follicles may also appear at the junction of the cornea and the sclera (limbal follicles). Active trachoma often can be irritating and have a watery discharge. Bacterial secondary infection may occur and cause a purulent discharge.The later structural changes of trachoma are referred to as "cicatricial trachoma". These include scarring in the eyelid (tarsal conjunctiva) that leads to distortion of the eyelid with buckling of the lid (tarsus) so the lashes rub on the eye (trichiasis). These lashes can lead to corneal opacities and scarring and then to blindness. Linear scars present in the sulcus subtarsalis are called Arlts lines (named after Carl Ferdinand von Arlt). In addition, blood vessels and scar tissue can invade the upper cornea (pannus). Resolved limbal follicles may leave small gaps in the pannus (Herberts pits).Most commonly, children with active trachoma do not present with any symptoms, as the low-grade irritation and ocular discharge is just accepted as normal, but further symptoms may include:

Eye discharge
Swollen eyelids
Trichiasis (misdirected eyelashes)
Swelling of lymph nodes in front of the ears
Sensitivity to bright lights
Increased heart rate
Further ear, nose, and throat complications.The major complication or the most important one is corneal ulcer occurring due to rubbing by concentrations, or trichiasis with superimposed bacterial infection.

Cause
Trachoma is caused by Chlamydia trachomatis, serotypes (serovars) A, B, and C. It is spread by direct contact with eye, nose, and throat secretions from affected individuals, or contact with fomites (inanimate objects that carry infectious agents), such as towels and/or washcloths, that have had similar contact with these secretions. Flies can also be a route of mechanical transmission. Untreated, repeated trachoma infections result in entropion (the inward turning of the eyelids), which may result in blindness due to damage to the cornea. Children are the most susceptible to infection due to their tendency to get dirty easily, but the blinding effects or more severe symptoms are often not felt until adulthood.Blinding endemic trachoma occurs in areas with poor personal and family hygiene. Many factors are indirectly linked to the presence of trachoma including lack of water, absence of latrines or toilets, poverty in general, flies, close proximity to cattle, and crowding. The final common pathway, though, seems to be the presence of dirty faces in children, facilitating the frequent exchange of infected ocular discharge from one childs face to another.  Most transmission of trachoma occurs within the family.

Diagnosis
McCallans classification
McCallan in 1908 divided the clinical course of trachoma into four stages:

WHO classification
The World Health Organization recommends a simplified grading system for trachoma. The Simplified WHO Grading System is summarized below:
Trachomatous inflammation, follicular (TF)—Five or more follicles of >0.5 mm on the upper tarsal conjunctiva
Trachomatous inflammation, intense (TI)—Papillary hypertrophy and inflammatory thickening of the upper tarsal conjunctiva obscuring more than half the deep tarsal vessels
Trachomatous scarring (TS)—Presence of scarring in tarsal conjunctiva.
Trachomatous trichiasis (TT)—At least one ingrown eyelash touching the globe, or evidence of epilation (eyelash removal)
Corneal opacity (CO)—Corneal opacity blurring part of the pupil margin

Prevention
Although trachoma was eliminated from much of the developed world in the 20th century (Australia being a notable exception), this disease persists in many parts of the developing world, particularly in communities without adequate access to water and sanitation.

Environmental measures
Environmental improvement: Modifications in water use, fly control, latrine use, health education, and proximity to domesticated animals have all been proposed to reduce transmission of C. trachomatis. These changes pose numerous challenges for implementation. These environmental changes are likely to ultimately affect the transmission of ocular infection by means of lack of facial cleanliness. Particular attention is required for environmental factors that limit clean faces.
A systematic review examining the effectiveness of environmental sanitary measures on the prevalence of active trachoma in endemic areas showed that use of insecticide spray resulted in significant reductions of trachoma and fly density in some studies. Health education also resulted in reductions of active trachoma when implemented.  Improved water supply did not result in a reduction of trachoma incidence.

Antibiotics
WHO Guidelines recommend that a region should receive community-based, mass antibiotic treatment when the prevalence of active trachoma among one- to nine-year-old children is greater than 10%. Subsequent annual treatment should be administered for three years, at which time the prevalence should be reassessed. Annual treatment should continue until the prevalence drops below 5%. At lower prevalences, antibiotic treatment should be family-based.

Management
Antibiotics
Azithromycin (single oral dose of 20 mg/kg) or topical tetracycline (1% eye ointment twice a day for six weeks). Azithromycin is preferred because it is used as a single oral dose. Although it is expensive, it is generally used as part of the international donation program organized by Pfizer. Azithromycin can be used in children from the age of six months and in pregnancy. As a community-based antibiotic treatment, some evidence suggests that oral azithromycin was more effective than topical tetracycline, but no consistent evidence supported either oral or topical antibiotics as being more effective. Antibiotic treatment reduces the risk of active trachoma in individuals infected with chlamydial trachomatis.

Surgery
For individuals with trichiasis, a bilamellar tarsal rotation procedure is warranted to direct the lashes away from the globe. Evidence suggests that use of a lid clamp and absorbable sutures would result in reduced lid contour abnormalities and granuloma formulation after surgery. Early intervention is beneficial as the rate of recurrence is higher in more advanced disease.

Lifestyle measures
The WHO-recommended SAFE strategy includes:

Surgery to correct advanced stages of the disease
Antibiotics to treat active infection, using azithromycin
Facial cleanliness to reduce disease transmission
Environmental change to increase access to clean water and improved sanitationChildren with visible nasal discharge, discharge from the eyes, or flies on their faces are at least twice as likely to have active trachoma as children with clean faces. Intensive community-based health education programs to promote face-washing can reduce the rates of active trachoma, especially intense trachoma. If an individual is already infected, washing ones face is encouraged, especially a child,  to prevent reinfection. Some evidence shows that washing the face combined with topical tetracycline might be more effective in reducing severe trachoma compared to topical tetracycline alone. The same trial found no statistical benefit of eye washing alone or in combination with tetracycline eye drops in reducing follicular trachoma amongst children.

Prognosis
If not treated properly with oral antibiotics, the symptoms may escalate and cause blindness, which is the result of ulceration and consequent scarring of the cornea.  Surgery may also be necessary to fix eyelid deformities.
Without intervention, trachoma keeps families in a cycle of poverty, as the disease and its long-term effects are passed from one generation to the next.

Epidemiology
As of 2011, about 21 million people are actively affected by trachoma, with around 2.2 million people being permanently blind or have severe visual impairment from trachoma. An additional 7.3 million people are reported to have trichiasis. 51 countries are currently classified as endemic for blinding trachoma. Of these, Africa is considered the worst affected area, with over 85% of all known active cases of trachoma.  Within the continent, South Sudan and Ethiopia have the highest prevalence. In many of these communities, women are three times more likely than men to be blinded by the disease, due to their roles as caregivers in the family. Approximately 158 million people are living in areas were trachoma is common. An additional 229 million live where trachoma could potentially occur. Australia is the only developed country that has trachoma. In 2008, trachoma was found in half of Australias very remote communities.

Elimination
In 1996, the WHO launched its Alliance for the Global Elimination of Trachoma by 2020, and in 2006, the WHO officially set 2020 as the target to eliminate trachoma as a public-health problem. The International Coalition for Trachoma Control  has produced maps and a strategic plan called 2020 INSight that lays out actions and milestones to achieve global elimination of blinding trachoma by  2020. The program recommends the SAFE protocol for blindness prevention: Surgery for trichiasis, Antibiotics to clear infection, Facial cleanliness, and Environmental improvement to reduce transmission. This includes sanitation infrastructure to reduce the open presence of human feces that can breed flies.As of 2018, Cambodia, Ghana, Iran, Laos, Mexico, Nepal, Morocco, and Oman have been certified as having eliminated trachoma as a public-health problem; China, Gambia, Iran, Iraq, and Myanmar make that claim, but have not sought certification. Eradication of the bacterium that causes the disease is seen as impractical; the WHO definition of "eliminated as a public-health problem" means less than 5% of children have any symptoms, and less than 0.1% of adults have vision loss. Having already donated more doses (about 700 million since 2002) of the drug than it has sold during the same time period, the drug company Pfizer has agreed to donate azithromycin until 2025, if necessary, for elimination of the disease. The campaign unexpectedly found distribution of azithromycin to very poor children reduced their early death rate by up to 25%.

History
The disease is one of the earliest known eye afflictions, having been identified in Egypt as early as 15 BC.Its presence was also recorded in ancient China and Mesopotamia. Trachoma became a problem as people moved into crowded settlements or towns where hygiene was poor. It became a particular problem in Europe in the 19th century. After the Egyptian Campaign (1798–1802) and the Napoleonic Wars (1798–1815), trachoma was rampant in the army barracks of Europe and spread to those living in towns as troops returned home. Stringent control measures were introduced, and by the early 20th century, trachoma was essentially controlled in Europe, although cases were reported until the 1950s. Today, most victims of trachoma live in underdeveloped and poverty-stricken countries in Africa, the Middle East, and Asia.In the United States, the Centers for Disease Control says, "No national or international surveillance [for trachoma] exists. Blindness due to trachoma has been eliminated from the United States. The last cases were found among Native American populations and in Appalachia, and those in the boxing, wrestling, and sawmill industries (prolonged exposure to combinations of sweat and sawdust often led to the disease). In the late 19th and early 20th centuries, trachoma was the main reason for an immigrant coming through Ellis Island to be deported."In 1913, President Woodrow Wilson signed an act designating funds for the eradication of the disease. Immigrants who attempted to enter the U.S </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Travelers diarrhea and can you explain it in depth? [/INST] Travelers diarrhea (TD) is a stomach and intestinal infection. TD is defined as the passage of unformed stool (one or more by some definitions, three or more by others) while traveling. It may be accompanied by abdominal cramps, nausea, fever, headache and bloating. Occasionally bloody diarrhea may occur. Most travelers recover within three to four days with little or no treatment. About 10% of people may have symptoms for a week.Bacteria are responsible for more than half of cases, typically via foodborne illness and waterborne diseases. The bacteria enterotoxigenic Escherichia coli (ETEC) are typically the most common except in Southeast Asia, where Campylobacter is more prominent. About 10 to 20 percent of cases are due to norovirus. Protozoa such as Giardia may cause longer term disease. The risk is greatest in the first two weeks of travel and among young adults. People affected are more often from the developed world.Recommendations for prevention include eating only properly cleaned and cooked food, drinking bottled water, and frequent hand washing. The oral cholera vaccine, while effective for cholera, is of questionable use for travelers diarrhea. Preventive antibiotics are generally discouraged. Primary treatment includes rehydration and replacing lost salts (oral rehydration therapy). Antibiotics are recommended for significant or persistent symptoms, and can be taken with loperamide to decrease diarrhea. Hospitalization is required in less than 3 percent of cases.Estimates of the percentage of people affected range from 20 to 50 percent among travelers to the developing world. TD is particularly common among people traveling to Asia (except for Japan and Singapore), the Middle East, Africa, Mexico, and Central and South America. The risk is moderate in Southern Europe, Russia, and China. TD has been linked to later irritable bowel syndrome and Guillain–Barré syndrome. It has colloquially been known by a number of names, including "Montezumas revenge," the "Nile runs" and "Delhi belly".

Signs and symptoms
The onset of TD usually occurs within the first week of travel, but may occur at any time while traveling, and even after returning home, depending on the incubation period of the infectious agent. Bacterial TD typically begins abruptly, but Cryptosporidium may incubate for seven days, and Giardia for 14 days or more, before symptoms develop.  Typically, a traveler experiences four to five loose or watery bowel movements each day. Other commonly associated symptoms are abdominal cramping, bloating, fever, and malaise.  Appetite may decrease significantly.  Though unpleasant, most cases of TD are mild, and resolve in a few days without medical intervention.Blood or mucus in the diarrhea, significant abdominal pain, or high fever suggests a more serious cause, such as cholera, characterized by a rapid onset of weakness and torrents of watery diarrhea with flecks of mucus (described as "rice water" stools).  Medical care should be sought in such cases; dehydration is a serious consequence of cholera, and may trigger serious sequelae—including, in rare instances, death—as rapidly as 24 hours after onset if not addressed promptly.

Causes
Infectious agents are the primary cause of travelers diarrhea. Bacterial enteropathogens cause about 80% of cases.  Viruses and protozoans account for most of the rest.The most common causative agent isolated in countries surveyed has been enterotoxigenic Escherichia coli (ETEC). Enteroaggregative E. coli is increasingly recognized. Shigella spp. and Salmonella spp. are other common bacterial pathogens.  Campylobacter, Yersinia, Aeromonas, and Plesiomonas spp. are less frequently found.  Mechanisms of action vary: some bacteria release toxins which bind to the intestinal wall and cause diarrhea; others damage the intestines themselves by their direct presence.Brachyspira pilosicoli pathogen also appears to be responsible for many chronic intermittent watery diarrhea and is only diagnosed through colonic biopsies and microscopic discovery of a false brush border  on H&E or Warthin silver stain: its brush-border is stronger and longer that Brachyspira aalborgis brush-border. It is unfortunately often not diagnosed as coproculture does not allow growth and 16S PCR panel primers do not match Brachyspira sequences.While viruses are associated with less than 20% of adult cases of travelers diarrhea, they may be responsible for nearly 70% of cases in infants and children. Diarrhea due to viral agents is unaffected by antibiotic therapy, but is usually self-limited.  Protozoans such as Giardia lamblia, Cryptosporidium and Cyclospora cayetanensis can also cause diarrhea. Pathogens commonly implicated in travelers diarrhea appear in the table in this section.A subtype of travelers diarrhea afflicting hikers and campers, sometimes known as wilderness diarrhea, may have a somewhat different frequency of distribution of pathogens.

Risk factors
The primary source of infection is ingestion of fecally contaminated food or water. Attack rates are similar for men and women.The most important determinant of risk is the travelers destination. High-risk destinations include developing countries in Latin America, Africa, the Middle East, and Asia. Among backpackers, additional risk factors include drinking untreated surface water and failure to maintain personal hygiene practices and clean cookware. Campsites often have very primitive (if any) sanitation facilities, making them potentially as dangerous as any developing country.Although travelers diarrhea usually resolves within three to five days (mean duration: 3.6 days), in about 20% of cases, the illness is severe enough to require bedrest, and in 10%, the illness duration exceeds one week.  For those prone to serious infections, such as  bacillary dysentery, amoebic dysentery, and cholera, TD can occasionally be life-threatening.  Others at higher-than-average risk include young adults, immunosuppressed persons, persons with inflammatory bowel disease or diabetes, and those taking H2 blockers or antacids.

Immunity
Travelers often get diarrhea from eating and drinking foods and beverages that have no adverse effects on local residents. This is due to immunity that develops with constant, repeated exposure to pathogenic organisms. The extent and duration of exposure necessary to acquire immunity has not been determined; it may vary with each individual organism. A study among expatriates in Nepal suggests that immunity may take up to seven years to develop—presumably in adults who avoid deliberate pathogen exposure.
Conversely, immunity acquired by American students while living in Mexico disappeared, in one study, as quickly as eight weeks after cessation of exposure.

Prevention
Sanitation
Recommendations include avoidance of questionable foods and drinks, on the assumption that TD is fundamentally a sanitation failure, leading to bacterial contamination of drinking water and food. While the effectiveness of this strategy has been questioned, given that travelers have little or no control over sanitation in hotels and restaurants, and little evidence supports the contention that food vigilance reduces the risk of contracting TD, guidelines continue to recommend basic, common-sense precautions when making food and beverage choices:
Maintain good hygiene and use only safe water for drinking and brushing teeth.
Safe beverages include bottled water, bottled carbonated beverages, and water boiled or appropriately treated by the traveler (as described below). Caution should be exercised with tea, coffee, and other hot beverages that may be only heated, not boiled.
In restaurants, insist that bottled water be unsealed in your presence; reports of locals filling empty bottles with untreated tap water and reselling them as purified water have surfaced. When in doubt, a bottled carbonated beverage is the safest choice, since it is difficult to simulate carbonation when refilling a used bottle.
Avoid ice, which may not have been made with safe water.
Avoid green salads, because the lettuce and other uncooked ingredients are unlikely to have been washed with safe water.
Avoid eating raw fruits and vegetables unless cleaned and peeled personally.If handled properly, thoroughly cooked fresh and packaged foods are usually safe. Raw or undercooked meat and seafood should be avoided. Unpasteurized milk, dairy products, mayonnaise, and pastry icing are associated with increased risk for TD, as are foods and beverages purchased from street vendors and other establishments where unhygienic conditions may be present.

Water
Although safe bottled water is now widely available in most remote destinations, travelers can treat their own water if necessary, or as an extra precaution.
Techniques include boiling, filtering, chemical treatment, and ultraviolet light; boiling is by far the most effective of these methods. Boiling rapidly kills all active bacteria, viruses, and protozoa. Prolonged boiling is usually unnecessary; most microorganisms are killed within seconds at water temperature above 55–70 °C (130–160 °F). The second-most effective method is to combine filtration and chemical disinfection.  Filters eliminate most bacteria and protozoa, but not viruses. Chemical treatment with halogens—chlorine bleach, tincture of iodine, or commercial tablets—have low-to-moderate effectiveness against protozoa such as Giardia, but work well against bacteria and viruses.
UV light is effective against both viruses and cellular organisms, but only works in clear water, and it is ineffective unless manufacturers instructions are carefully followed for maximum water depth/distance from UV source, and for dose/exposure time. Other claimed advantages include short treatment time, elimination of the need for boiling, no taste alteration, and decreased long-term cost compared with bottled water.  The effectiveness of UV devices is reduced when water is muddy or turbid; as UV is a type of light, any suspended particles create shadows that hide microorganisms from UV exposure.

Medications
Bismuth subsalicylate four times daily reduces rates of travelers diarrhea. Though many travelers find a four-times-per-day regimen inconvenient, lower doses have not been shown to be effective. Potential side effects include black tongue, black stools, nausea, constipation, and ringing in the ears. Bismuth subsalicylate should not be taken by those with aspirin allergy, kidney disease, or gout, nor concurrently with certain antibiotics such as the quinolones, and should not be taken continuously for more than three weeks.  Some countries do not recommend it due to the risk of rare but serious side effects.A hyperimmune bovine colostrum to be taken by mouth is marketed in Australia for prevention of ETEC-induced TD. As yet, no studies show efficacy under actual travel conditions.Though effective, antibiotics are not recommended for prevention of TD in most situations because of the risk of allergy or adverse reactions to the antibiotics, and because intake of preventive antibiotics may decrease effectiveness of such drugs should a serious infection develop subsequently. Antibiotics can also cause vaginal yeast infections, or overgrowth of the bacterium Clostridium difficile, leading to pseudomembranous colitis and its associated severe, unrelenting diarrhea.Antibiotics may be warranted in special situations where benefits outweigh the above risks, such as immunocompromised travelers, chronic intestinal disorders, prior history of repeated disabling bouts of TD, or scenarios in which the onset of diarrhea might prove particularly troublesome. Options for prophylactic treatment include the quinolone antibiotics (such as ciprofloxacin), azithromycin, and trimethoprim/sulfamethoxazole, though the latter has proved less effective in recent years.  Rifaximin may also be useful.  Quinolone antibiotics may bind to metallic cations such as bismuth, and should not be taken concurrently with bismuth subsalicylate. Trimethoprim/sulfamethoxazole should not be taken by anyone with a history of sulfa allergy.

Vaccination
The oral cholera vaccine, while effective for prevention of cholera, is of questionable use for prevention of TD. A 2008 review found tentative evidence of benefit. A 2015 review stated it may be reasonable for those at high risk of complications from TD. Several vaccine candidates targeting ETEC or Shigella are in various stages of development.

Probiotics
One 2007 review found that probiotics may be safe and effective for prevention of TD, while another review found no benefit. A 2009 review confirmed that more study is needed, as the evidence to date is mixed.

Treatment
Most cases of TD are mild and resolve in a few days without treatment, but severe or protracted cases may result in significant fluid loss and dangerous electrolytic imbalance. Dehydration due to diarrhea can also alter the effectiveness of medicinal and contraceptive drugs. Adequate fluid intake (oral rehydration therapy) is therefore a high priority. Commercial rehydration drinks are widely available; alternatively, purified water or other clear liquids are recommended, along with salty crackers or oral rehydration salts (available in stores and pharmacies in most countries) to replenish lost electrolytes. Carbonated water or soda, left open to allow dissipation of the carbonation, is useful when nothing else is available.  In severe or protracted cases, the oversight of a medical professional is advised.

Antibiotics
If diarrhea becomes severe (typically defined as three or more loose stools in an eight-hour period), especially if associated with nausea, vomiting, abdominal cramps, fever, or blood in stools, medical treatment should be sought. Such patients may benefit from antimicrobial therapy.  A 2000 literature review found that antibiotic treatment shortens the duration and severity of TD; most reported side effects were minor, or resolved on stopping the antibiotic.The antibiotic recommended varies based upon the destination of travel. Trimethoprim–sulfamethoxazole and doxycycline are no longer recommended because of high levels of resistance to these agents. Antibiotics are typically given for three to five days, but single doses of azithromycin or levofloxacin have been used.  Rifaximin and rifamycin are approved in the U.S. for treatment of TD caused by ETEC. If diarrhea persists despite therapy, travelers should be evaluated for bacterial strains resistant to the prescribed antibiotic, possible viral or parasitic infections, bacterial or amoebic dysentery, Giardia, helminths, or cholera.

Antimotility agents
Antimotility drugs such as loperamide and diphenoxylate reduce the symptoms of diarrhea by slowing transit time in the gut </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Trichinosis and can you explain it in depth? [/INST] Trichinosis, also known as trichinellosis, is a parasitic disease caused by roundworms of the Trichinella type. During the initial infection, invasion of the intestines can result in diarrhea, abdominal pain, and vomiting. Migration of larvae to muscle, which occurs about a week after being infected, can cause swelling of the face, inflammation of the whites of the eyes, fever, muscle pains, and a rash. Minor infection may be without symptoms. Complications may include inflammation of heart muscle, central nervous system involvement, and inflammation of the lungs.Trichinosis is mainly spread when undercooked meat containing Trichinella cysts is eaten. In North America this is most often bear, but infection can also occur from pork, boar, and dog meat. Several species of Trichinella can cause disease, with T. spiralis being the most common. After being eaten, the larvae are released from their cysts in the stomach. They then invade the wall of the small intestine, where they develop into adult worms. After one week, the females release new larvae that migrate to voluntarily controlled muscles, where they form cysts. The diagnosis is usually based on symptoms and confirmed by finding specific antibodies in the blood, or larvae on tissue biopsy.The best way to prevent trichinosis is to fully cook meat. A food thermometer can verify that the temperature inside the meat is high enough. Infection is typically treated with antiparasitic medication such as albendazole or mebendazole. Rapid treatment may kill adult worms and thereby stop further worsening of symptoms. Both medications are considered safe, but have been associated with side effects such as bone marrow suppression. Their use during pregnancy or in children under the age of 2 years is poorly studied, but appears to be safe. Treatment with steroids is sometimes also required in severe cases. Without treatment, symptoms typically resolve within three months.Worldwide, about 10,000 infections occur a year. At least 55 countries including the United States, China, Argentina, and Russia have had recently documented cases. While the disease occurs in the tropics, it is less common there. Rates of trichinosis in the United States have decreased from about 400 cases per year in the 1940s to 20 or fewer per year in the 2000s. The risk of death from infection is low.

Signs and symptoms
The great majority of trichinosis infections have either minor or no symptoms and no complications. The two main phases for the infection are enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species of Trichinella, quantity of encysted larvae ingested, age, sex, and host immunity.

Enteral phase
A large burden of adult worms in the intestines promotes symptoms such as nausea, heartburn, dyspepsia, and diarrhea from two to seven days after infection, while small worm burdens generally are asymptomatic. Eosinophilia presents early and increases rapidly.

Parenteral phase
The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced. As the larvae migrate through tissue and vessels, the bodys inflammatory response results in edema, muscle pain, fever, and weakness. A classic sign of trichinosis is periorbital edema, swelling around the eyes, which may be caused by vasculitis. Splinter hemorrhage in the nails is also a common symptom.They may very rarely cause enough damage to produce serious neurological deficits (such as ataxia or respiratory paralysis) from worms entering the central nervous system (CNS), which is compromised by trichinosis in 10–24% of reported cases of cerebral venous sinus thrombosis, a very rare form of stroke (three or four cases per million annual incidence in adults). Trichinosis can be fatal depending on the severity of the infection; death can occur 4–6 weeks after the infection, and is usually caused by myocarditis, encephalitis, or pneumonia.

Cause
The classical agent is T. spiralis (found worldwide in many carnivorous and omnivorous animals, both domestic and sylvatic (wild), but seven primarily sylvatic species of Trichinella also are now recognized:

Species and characteristics
T. spiralis is most adapted to swine, most pathogenic in humans, and is cosmopolitan in distribution.
T. britovi is the second-most common species to infect humans; it is distributed throughout Europe, Asia, and northern and western Africa, usually in wild carnivores, crocodiles, birds, wild boar, and domesticated pigs.
T. murrelli also infects humans, especially from black bear meat; it is distributed among wild carnivores in North America.
T. nativa, which has a high resistance to freezing, is found in the Arctic and subarctic regions; reservoir hosts include polar bears, Arctic foxes, walruses, and other wild game.
T. nelsoni, found in East African predators and scavengers, has been documented to cause a few human cases.
T. papuae infects both mammals and reptiles, including crocodiles, humans, and wild and domestic pigs; this species, found in Papua New Guinea and Thailand, is also nonencapsulated.
T. pseudospiralis infects birds and mammals, and has demonstrated infection in humans; it is a nonencapsulated species.
T. zimbabwensis can infect mammals, and possibly humans; this nonencapsulated species was detected in crocodiles in Africa.

Taxonomy
Kingdom: Animalia
Phylum: Nematoda
Class: Adenophorea
Order: Trichurida
Family: Trichinellidae
Genus: Trichinella

Lifecycle
The typical lifecycle for T. spiralis involves humans, pigs, and rodents. A pig becomes infected when it eats infectious cysts in raw meat, often porcine carrion or a rat (sylvatic cycle). A human becomes infected by consuming raw or undercooked infected pork (domestic cycle). In the stomach, the cysts from infected undercooked meat are acted on by pepsin and hydrochloric acid, which help release the larvae from the cysts into the stomach. The larvae then migrate to the small intestine, and burrow into the intestinal mucosa, where they molt four times before becoming adults.Thirty to 34 hours after the cysts were originally ingested, the adults mate, and within five days produce larvae. Adult worms can only reproduce for a limited time, because the immune system eventually expels them from the small intestine. The larvae then use their piercing mouthpart, called the "stylet", to pass through the intestinal mucosa and enter the lymphatic vessels, and then enter the bloodstream.The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst. The larval host cell becomes a nurse cell, in which the larva will be encapsulated, potentially for the life of the host, waiting for the host to be eaten. The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the parasite does not lay eggs, nor can it survive long outside a host.

Diagnosis
Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing.

Exposure history
An epidemiological investigation can be done to determine a patients exposure to raw infected meat. Often, an infection arises from home-preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory-confirmed infected animal, or sharing of a common exposure with a laboratory-confirmed infected human.

Clinical diagnosis
Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness, splinter hemorrhage, nonspecific gastroenteritis, and muscle pain. The case definition for trichinosis at the European Center for Disease Control states, "at least three of the following six: fever, muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and subconjunctival, subungual, and retinal hemorrhages."

Laboratory testing
Blood tests and microscopy can be used to aid in the diagnosis of trichinosis. Blood tests include a complete blood count for eosinophilia, creatine phosphokinase activity, and various immunoassays such as ELISA for larval antigens.

Prevention
Legislation
Laws and rules for food producers may improve food safety for consumers, such as the rules established by the European Commission for inspections, rodent control, and improved hygiene. A similar protocol exists in the United States, in the USDA guidelines for farms and slaughterhouse responsibilities in inspecting pork.

Education and training
Public education about the dangers of consuming raw and undercooked meat, especially pork, may reduce infection rates. Hunters are also an at-risk population due to their contact and consumption of wild game, including bear. As such, many states, such as New York, require the completion of a course in such matters before a hunting license can be obtained.

Meat testing
Testing methods are available for both individual carcasses and monitoring of the herds. Artificial digestion method is usually used for the testing of individual carcasses, while the testing for specific antibodies is usually used for herd monitoring.

Food preparation
Larvae may be killed by the heating or irradiation of raw meat. Freezing is normally only effective for T. spiralis, since other species, such as T. nativa, are freeze-resistant and can survive long-term freezing.
All meat (including pork) can be safely prepared by cooking to an internal temperature of 165 °F (74 °C) or higher for 15 seconds or more.
Wild game: Wild game meat must be cooked thoroughly (see meat preparation above) Freezing wild game does not kill all trichinosis larval worms, because the worm species that typically infests wild game can resist freezing.
Pork: Freezing cuts of pork less than 6 inches thick for 20 days at 5 °F (−15 °C) or three days at −4 °F (−20 °C) kills T. spiralis larval worms; but this will not kill other trichinosis larval worm species, such as T. nativa, if they have infested the pork food supply (which is unlikely, due to geography).Pork can be safely cooked to a slightly lower temperature, provided that the internal meat temperature is at least as hot for at least as long as listed in the USDA table below. Nonetheless, allowing a margin of error for variation in internal temperature within a particular cut of pork, which may have bones that affect temperature uniformity, is prudent. In addition, kitchen thermometers have measurement error that must be considered. Pork may be cooked for significantly longer and at a higher uniform internal temperature than listed below to be safe.
Unsafe and unreliable methods of cooking meat include the use of microwave ovens, curing, drying, and smoking, as these methods are difficult to standardize and control.

Pig farming
Incidence of infection can be reduced by:
Keeping pigs in clean pens, with floors that can be washed (such as concrete)
Not allowing hogs to eat carcasses of other animals, including rats, which may be infected with Trichinella
Cleaning meat grinders thoroughly when preparing ground meats
Control and destruction of meat containing trichinae, e.g., removal and proper disposal of porcine diaphragms prior to public sale of meatThe US Centers for Disease Control and Prevention  make the following recommendation: "Curing (salting), drying, smoking, or microwaving meat does not consistently kill infective worms."
However, under controlled commercial food processing conditions, some of these methods are considered effective by the USDA.The USDA Animal and Plant Health Inspection Service (APHIS) is responsible for the regulations concerning the importation of swine from foreign countries. The Foreign Origin Meat and Meat Products, Swine section covers swine meat (cooked, cured and dried, and fresh). APHIS developed the National Trichinae Certification Program; this is a voluntary "preharvest" program for U.S. swine producers "that will provide documentation of swine management practices" to reduce the incidence of Trichinella in swine. The CDC reports 0.013% of U.S. swine are infected with Trichinella.

Treatment
As with most diseases, early treatment is better and decreases the risk of developing disease. If larvae do encyst in skeletal muscle cells, they can remain infectious for months to years.

Primary treatment
Early administration of anthelmintics, such as mebendazole or albendazole, decreases the likelihood of larval encystation, particularly if given within three days of infection. However, most cases are diagnosed after this time.  In humans, mebendazole (200–400 mg three times a day for three days) or albendazole (400 mg twice a day for 8–14 days) is given to treat trichinosis. These drugs prevent newly hatched larvae from developing, but should not be given to pregnant women or children under two years of age.Medical references from the 1940s described no specific treatment for trichinosis at the time, but intravenous injection of calcium salts was found to be useful in managing symptoms related to severe toxemia from the infection..

Secondary treatment
After infection, steroids, such as prednisone, may be used to relieve muscle pain associated with larval migration.

Vaccine research
Researchers trying to develop a vaccine for Trichinella have tried using either "larval extracts, excretory–secretory antigen, DNA, or recombinant antigen protein." Currently, no marketable vaccine is available for trichinosis, but experimental mouse studies have suggested possibilities.

In one study, microwaved Trichinella larvae were used to immunize mice (orally or intraperitoneally), which were subsequently infected. Depending on the dosage and frequency of immunization, results ranged from a decreased larval count to complete protection from trichinosis.
Another study used extracts and excretory–secretory products from first-stage larvae to produce an oral vaccine. To prevent gastric acids from dissolving the antigens before reaching the small intestine, scientists encapsulated the antigens in microcapsules. This vaccine significantly increased CD4+ cell levels, and increased antigen-specific serum IgGq and IgA, resulting in a statistically significant reduction in the average number of adult worms in the small intestines of mice. The significance of this approach is that, if the white blood cells in the small intestine have been exposed to Trichinella antigens (through vaccination), when an individual does get infected, the immune system will respond to expel the worms from the small intestine fast enough to prevent the female worms from releasing their larvae.
A DNA vaccine tested on mice "induced a muscle larva burden reduction in BALB/c mice by 29% in response to T. spiralis infection".

Epidemiology
About 11 million humans are infected with Trichinella; T. spiralis is the species responsible for most of these infections. Infection was once very common, but this disease is now rare in the developed world, but two known outbreaks occurred in 2015. In the first outbreak, around 40 people were infected in Liguria, Italy, during a New Years Eve celebration. The second outbreak in France was associated with pork sausages from Corsica, which were eaten raw, affecting 14 people in total.
The incidence of trichinosis in the U.S. has decreased dramatically in the past century from an average of 400 cases per year mid-20th century down to an annual average of 20 cases per year (2008–10). The number of cases has decreased because of legislation prohibiting the feeding of raw meat garbage to hogs, increased commercial and home freezing of pork, and the public awareness of the danger of eating raw or undercooked pork products.China reports around 10,000 cases every year, so is the country with the highest number of cases. In China, between 1964 and 1998, over 20,000 people became infected with trichinosis, and more than 200 people died.Trichinosis is common in developing countries where meat fed to pigs is raw or undercooked, but infections also arise in developed countries in Europe where raw or undercooked pork, wild boar and horse meat may be consumed as delicacies.In the developing world, most infections are associated with undercooked pork. For example, in Thailand, between 200 and 600 cases are reported annually around the Thai New Year. This is mostly attributable to a particular delicacy, larb, which calls for undercooked pork as part of the recipe.In parts of Eastern Europe, the World Health Organization reports, some swine herds have trichinosis infection rates above 50%, with correspondingly large numbers of human infections.

United States
Historically, pork products were thought to have the most risk of infecting humans with T. spiralis. However, a trichinosis surveillance conducted between 1997 and 2001 showed a higher percentage of cases caused by consumption of wild game (the sylvatic transmission cycle). This is thought to be due to the Federal Swine Health Protection Act (Public Law 96-468) that was passed by Congress in 1980. Prior to this act, swine were fed garbage that could potentially be infected by T. spiralis. This act was put in place to prevent trichinella-contaminated food from being given to swine. Additionally, other requirements were put in place, such as rodent control, limiting commercial swine contact with wildlife, maintaining good hygiene, and removing dead pigs from pens immediately.Between 2002 and 2007, 11 trichinosis cases were reported to the CDC each year on average in the United States, and 2008–10 averaged 20 cases per year; these were mostly the result of consuming undercooked game (sylvatic transmission) or home-reared pigs (domestic transmission).

Religious groups
The kashrut and halal dietary laws of Judaism and Islam prohibit eating pork. In the 19th century, when the association between trichinosis and undercooked pork was first established, this association was suggested to be the reason for the prohibition, reminiscent of the earlier opinion of  medieval Jewish philosopher Maimonides that food forbidden by Jewish law was "unwholesome". This theory was controversial, and eventually fell out of favor.

Reemergence
The disappearance of the pathogen from domestic pigs has led to a relaxation of legislation and control efforts by veterinary public health systems. Trichinosis has lately been thought of as a re-emerging zoonosis, supplemented by the increased distribution of meat products, political changes, a changing climate, and increasing sylvatic transmission.Major sociopolitical changes can produce conditions that favor the resurgence of Trichinella infections in swine and, consequently, in humans. For instance, "the overthrow of the social and political structures in the 1990s" in Romania led to an increase in the incidence rate of trichinosis.

History
As early as 1835, trichinosis was known to have been caused by a parasite, but the mechanism of infection was unclear at the time. A decade later, American scientist Joseph Leidy pinpointed undercooked meat as the primary vector for the parasite, and two decades afterwards, this hypothesis was fully accepted by the scientific community.

Parasite
The circumstances surrounding the first observation and identification of T. spiralis are controversial, due to a lack of records. In 1835, James Paget, a first-year medical student, first observed the larval form of T. spiralis, while witnessing an autopsy at St. Bartholomew’s Hospital in London. Paget took special interest in the presentation of muscle with white flecks, described as a "sandy diaphragm".  Although Paget is most likely the first person to have noticed and recorded these findings, the parasite was named and published in a report by his professor, Richard Owen, who is now credited for the discovery of the T. spiralis larval form.

Lifecycle
A series of experiments conducted between 1850 and 1870 by the German researchers Rudolf Virchow, Rudolf Leuckart, and Friedrich Albert von Zenker, which involved feeding infected meat to a dog and performing the subsequent necropsy, led to the discovery of the lifecycle of Trichinella. Through these experiments, Virchow was able to describe the development and infectivity of T </s>