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DESCRIPTION
Toxoplasmosis is caused by a protozoan called Toxoplasma gondii (T gondii) infection found in humans and many species of mammals and birds including rodents, sheep, pigs. Domestic and feral cats become infected by an accidental ingestion of infectious oocysts. More than 60 million Americans have been infected with this single-celled parasite, though usually only people with weakened immune system become ill.
There are several types that occur in humans:
- Congenital Toxoplasmosis - is passed from infected mother to her unborn child.
- Ocular Toxoplasmosis - also called retinochoroiditis, which usually results from congenital toxoplasmosis, but symptoms may not occur until ages 20-40.
- Acute Toxoplasmosis - in a basically healthy individual.
- Acute toxoplasmosis - in an immunocompromised individual (person with AIDS, cancer or on immunosuppressant drugs).
Members of the family Felidae (cat family) are the only known definitive hosts for the sexual stages of T gondii and thus are the main reservoirs of infection. Cats become infected with T gondii by eating raw meat (carnivorism). After tissue cysts (oocysts) are ingested by the cat, viable organisms are released and invade epithelial cells of the small intestine where they undergo an asexual followed by a sexual cycle and then form oocysts, which are excreted. They release the oocysts with their excrement. The unsporulated oocyst takes 1 to 5 days after excretion to sporate (become infective). Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed. After a period of days or weeks, depending on environmental factors, the oocysts become infectious agents and may remain so for up to a year. The oocysts can survive in the environment for several months and are remarkably resistant to disinfectants, freezing, and drying, but are killed by heating to 70°C (approximately 160°F) for 10 minutes. If within this time an individual comes in contact with the oocysts when changing cat litter or from gardening, or other contact with infected soil, then they can become infected if contact with the mouth occurs before hands are washed. Infection can also occur from eating unwashed fruits or vegetables that have been contaminated with the oocysts or by consuming undercooked meat or untreated water that has been infected. The parasites form tissue cysts, most commonly in skeletal muscle, myocardium, and brain. These cysts may remain throughout the life of the host.
Geographic Distribution: Serologic prevalence data indicate that toxoplasmosis is one of the most common of humans infections throughout the world. Infection is more common in warm climates and at lower altitudes than in cold climates and mountainous regions. High prevalence of infection in France has been related to a preference for eating raw or undercooked meat, while high prevalence in Central America has been related to the frequency of stray cats in a climate favoring survival of oocysts. The overall seroprevalence in the United States as determined with specimens collected by the third National Health and Nutritional Assessment Survey (NHANES III) between 1988 and 1994 was found to be 22.5%, with seroprevalence among women of childbearing age (15 to 44 years) of 15%.
It is estimated that one-third to one-half of the inhabitants of the world have been infected with Toxoplasma gondii at some point in their lives. The primary evidence of such widespread exposure is the pervasiveness of toxoplasmosis antibodies since demonstrable symptoms of the infection are uncommon. Infection with Toxoplasma gondii may involve the spleen, liver, central nervous system (CNS), and other regions of the body, but symptoms, when they do occur, are usually very mild in otherwise healthy individuals and only entail a fever and some swelling of the glands. Occasionally muscle aches and pain, similar to those experienced with the flu, occur as well, and in very rare instances there may be damage to the eyes.
Ocular injury and other serious effects of toxoplasmosis are much more likely to occur in individuals with weakened immune systems. In AIDS patients, for instance, a form of encephalitis may develop following infection with Toxoplasma gondii. Symptoms of toxoplasmic encephalitis include headache, fever, psychosis, and impaired vision, speech, movement, and thought capacity. Similar grave effects are associated with congenital toxoplasmosis, which is passed on from expectant mothers that are exposed to Toxoplasma gondii to the developing fetus. In some cases, this transmission of the parasite can cause the child to be stillborn or born prematurely. In other severe cases of infection, the disease may affect many of the newborn's organs, including the brain and eyes, and epilepsy, mental retardation, and blindness can ensue.
About half of the toxoplasmosis-related fatalities reported are thought to involve exposure to Toxoplasma gondii through the consumption of contaminated meat, making the disease one of the top causes of foodborne deaths in the United States (only foodborne infection with Salmonella and Listeria are more deadly). Ensuring that all meat consumed is cooked thoroughly can, therefore, significantly lessen one's risk of developing toxoplasmosis, as can freezing meat for several days prior to its use. Other steps that can be taken to decrease the incidence of the disease are washing fruits and vegetables thoroughly or peeling them before eating, wearing gloves when gardening or changing cat litter, washing cutting boards, knives, and other items that come into contact with raw meat or unwashed plant matter with hot water and soap, and keeping domestic cats indoors and only feeding them commercial cat foods or well-cooked human foods.
FREQUENT SIGNS & SYMPTOMS
No symptoms usually (80 to 90% of patients)
Fever.
Fatigue.
Swollen lymph glands.
Muscle aches.
Sore throat.
Rash (sometimes).
Retinitis (inflammation of the retina).
CONGENITAL TOXOPLASMOSIS
The consequences of the infection of the fetus can be very different: between subclinical and very serious.The earlier in pregnancy the mother is infected, the lower is the risk of an infection of the fetus, but the the disease is more severe. The later in pregnancy the mother is infected, the higher is the possibility of fetal infection, and the disease is less severe (often subclinical infection).
- Abortion.
- Overt disease. The symptoms vary widely, the classical triad of Congenital Toxoplasmosis is
Subclinical infection: no symptoms at birth
- Hydrozephalus.
- Intracranial calcification.
- Chorioretinitis
- Late onset symptoms (most common in the eyes: Chorioretinitis).
- No symptoms at all.
Some pictures of symptoms of Congenital Toxoplasmosis:
Hydrozephalus
Intracranial calcification
Chorioretinitis
Pictures obtained from www.trojovski.net/toxo/toxosympt.htm
CAUSES
The protozoan, Toxoplasmosis gondii, is usually transmitted by:
- Eating undercooked meats from infected animals.
- Cats who harbor the germ can excrete it in their stools; humans who carelessly handle cat litter (or fail to wash their hands after handling it) may become infected. Small children who eat infected soil (contaminated with dog or cat feces) can become infected.
- Blood transfusion.
- A pregnant woman who gets the infection can transmit it to her unborn child (often with severe effects). A pregnant woman should be extremely careful when changing a cat box containing cat feces. She should make sure she is careful about washing her hands thoroughly after handling the cat box.
BROCHURES - CDC INFORMATION
Toxoplasmosis: An Important Message for Women (PDF format)
You Can Prevent Toxo: A Guide for People with HIV Infection
An Important Message for Cat Owners (PDF format)
RISK INCREASES WITH
Immunosuppression due to illness or drugs.
Contact with cats.
PREVENTIVE MEASURES
Washing hands frequently, particularly after using the bathroom, after outdoor activities such as gardening, after preparing food, and before eating. Wash hands thoroughly after changing a cat box.
Wash foods grown in a garden or purchased from a store or farm stand thoroughly before eating.
Avoid eating raw or undercooked meats or uncooked eggs or drinking unpasterized milk. Use proper techniques for preparation and storage of meat products. Wash hands carefully after handling raw meats. Wearing gloves when cooking or if ill, having someone who is healthy and not pregnant handle raw meat. Cook all meat thoroughly until the juices run clear and it is no longer pink inside. Wash all utensils and cutting boards that have come into contact with raw meat in hot water and soap.
A pregnant woman should have a laboratory blood test early in pregnancy to determine if she has antibodies to toxoplasmosis (about 55% of the U.S. population have them, which means they were infected at some time). She should also be tested again at 16-18 weeks of pregnancy to determine if she has acquired an infection, and if so, may consider a therapeutic abortion.
Immunocompromised persons and pregnant women should avoid contact with cat feces. Cat boxes should be changed by someone who is healthy and not pregnant.
Protect children's play area, including sand boxes, from cat and dog feces.
Change cat litter boxes daily: feed indoor cats only canned, dry or cooked meats because cats can pick up the parasite from eating raw meat. Keeping cats inside will help to prevent them from becoming infected. Do not touch strange or stray cats or let any cat into the home that might have lived outside and eaten raw meat.
EXPECTED OUTCOME
The majority of infected persons have no symptoms, and those with mild symptoms recover spontaneously with no after effects.
POSSIBLE COMPLICATIONS
For pregnant female - when infection occurs early in pregnancy: miscarriage, stillbirth, various chronic disorders (seizures) and birth defects (blindness, deafness) in the newborn (some may not be apparent for years). An infection later in pregnancy usually has no ill effects.
For immunocompromised persons - lung and heart damage, brain inflammation, recurrence.
For non-immunocompromised persons (basically healthy) - rarely, may develop lung or brain inflammation. Younger children (under 5 years) may develop eye inflammation.
Approximately 750 deaths are attributed to toxoplasmosis annually. Many of these deaths could be avoided by following relatively simple preventative recommendations.
TREATMENT
GENERAL MEASURES
DIAGNOSIS
Diagnosis involves a medical history, physical exam and laboratory studies of blood to detect the infection. If a health care provider suspects toxoplasmosis, he or she will draw a blood sample and test it for evidence of the parasite. An eye care provider may use a special lamp called a slit lamp to check the eyes for abnormalities of the retinas. People with weakened immune systems who are more likely to develop a severe infection might have magnetic resonance imaging (MRI), a computerized tomography (CT) scan of the head, or rarely, a brain biopsy (removing a small sample of brain tissue to examine) to look for signs of damage caused by the parasite. Infants with congenital toxoplasmosis also will need a CT scan of the head and thorough examination of other areas of the body possibly affected by the parasite.
TREATMENT
Treatment is usually unnecessary for a healthy, non-pregnant individual who has no symptoms. For a child under the age of 5, medications will be prescribed to prevent eye complications.
Pregnant female - your midwife or health care provider will discuss the treatment available, the risks involved and the expected outcomes.
Newborns with infection - are treated with medications (with or without symptoms as the germs can multiply after birth).
Immunocompromised persons - treatment is with medication.
By www.hivandhepatitis.com
Toxoplasmosis, caused by the protozoan Toxoplasma gondii (T gondii), is a potentially life-threatening AIDS-defining opportunistic infection that affects people with severely weakened immune systems, even in the era of HAART. The AIDS Education and Training Centers (AETC) National Resource Center provides on its web site a central repository for training materials for healthcare providers treating people with HIV/AIDS. Following is the Center's manual on management of toxoplasmosis.
Toxoplasma gondii (T gondii) is a common intracellular protozoan that preferentially infects the central nervous system (CNS) of immunodeficient patients, causing severe neurologic disease. T gondii also can cause local disease such as chorioretinitis or pneumonia. Toxoplasma has an infectious reservoir in almost all animals; humans acquire infection either through ingestion of tissue cysts contained in undercooked meat (usually pork or lamb) or oocysts on contaminated vegetables or through exposure to cat feces containing oocysts. There is no transmission by person-to-person contact.
Clinical disease usually occurs through reactivation of latent infection in patients who have CD4 counts of <100 cells/無. Seroprevalence varies widely, from 15% in the United States to 75% in some European countries, and even higher in certain resource-limited countries. In the absence of prophylaxis, toxoplasmic encephalitis occurs in more than 30% of patients with advanced HIV disease who are seropositive for T gondii.
CNS toxoplasmosis is an AIDS-defining condition that can be progressive and fatal. However, antimicrobial therapy, especially if given in conjunction with antiretroviral therapy (ART) that results in immune reconstitution, can be successful in treating toxoplasmosis. Specific prophylaxis and effective ART also may be used to prevent toxoplasmosis in patients with advanced AIDS who have latent T gondii infection (as demonstrated by the presence of anti-Toxoplasma immunoglobulin G (IgG) antibodies; see chapter Preventing Exposure to Opportunistic and Other Infections).
Subjective: The patient may complain of subacute onset of dull, constant headache, fever, visual changes or other focal neurologic symptoms, confusion, or disorientation. Seizures may occur. Caregivers may report subtle alterations in mental status or mood. Take a careful history from the patient and caregivers about the symptoms listed above and their duration, progression, and severity. Inquire about other related symptoms. Ask whether the patient is taking Toxoplasma prophylaxis or ART.
Objective:
- Measure vital signs (temperature, heart rate, blood pressure, respiratory rate).
- Perform a full physical examination including a thorough neurologic examination, looking for focal or nonfocal neurologic deficits, particularly weakness, cranial nerve abnormalities, visual field defects, gait disturbances, and abnormalities in speech, cognitive, or affective functions.
- Review previous laboratory values, particularly:
- CD4 count (which usually is <50-100 cells/無 in patients with toxoplasmosis).
- Toxoplasma IgG (>95% of patients with toxoplasmosis have positive IgG).
Assessment: Rule out other infectious or neoplastic causes of headache, fever, and neurologic changes. A partial differential diagnosis includes:
- CNS lymphoma.
- Cryptococcal meningitis.
- Progressive multifocal leukoencephalopathy (PML).
- Tuberculous meningitis.
- Brain abscesses of bacterial, fungal, or mycobacterial etiologies.
- Herpes simplex virus or cytomegalovirus (CMV) encephalitis.
- Primary HIV encephalopathy.
- AIDS dementia complex.
- Cerebrovascular accident secondary to hemorrhage, hypoxia, or emboli from vegetative endocarditis.
- Neurosyphilis.
- Other causes of chorioretinitis such as CMV, HIV, and cryptosporidiosis.
Diagnostic Evaluation Plan: Definitive diagnosis requires identification of T gondii in tissue biopsy or body fluid samples. Brain biopsy usually is not performed if toxoplasmosis is strongly suspected; instead, presumptive diagnosis is made on the basis of clinical presentation, laboratory and imaging tests, and response to therapy. Brain biopsy should be considered in patients who do not respond to therapy or in whom the diagnosis is unclear.
- Serum Toxoplasma IgG antibody test results are positive in nearly all patients with toxoplasmic encephalitis. A negative IgG test result makes the diagnosis very unlikely but does not rule it out. (Antibody titer changes are uncommon in reactivation disease and are not useful in making a diagnosis.)
- CNS imaging with computed tomography (CT) typically shows multiple contrast-enhancing mass lesions, but may show a single lesion or no lesions. Magnetic resonance imaging (MRI) is more sensitive than CT for CNS toxoplasmosis. Other imaging studies, such as single photon emission CT (SPECT), may be useful in distinguishing toxoplasmic lesions from CNS lymphoma.
- Polymerase chain reaction (PCR) tests for T gondii in the cerebrospinal fluid have poor sensitivity.
- Other diagnostic tests should be performed as indicated to rule out other potential causes of the patient's symptoms.
- Patients with toxoplasmic encephalitis typically respond quickly to treatment. If clinical improvement is not seen after 10-14 days of appropriate treatment, or if clinical worsening is seen in the first week, consider brain biopsy for alternative diagnoses.
Treatment consists of 2 phases: acute and chronic maintenance. Note: Presumptive treatment often is begun on the basis of clinical presentation, positive Toxoplasma IgG, and results of brain imaging studies. If patients do not respond quickly to treatment, other diagnoses should be considered. The following recommendations are based on treatment guidelines published by the Centers for Disease Control and Prevention, National Institutes of Health, and HIV Medicine Association/Infectious Diseases Society of America (see references below).
Acute Therapy:
Preferred - Pyrimethamine 200 mg orally as a single loading dose, then 50 mg (<60 kg body weight) to 75 mg (>60 kg body weight) daily + sulfadiazine 1,000 mg (<60 kg body weight) to 1,500 mg orally every 6 hours (>60 kg body weight) + folinic acid (leucovorin) 10-20 mg daily. Dosage adjustments to the lower end of therapeutic range of pyrimethamine and sulfadiazine may be considered for patients with significant bone marrow suppression despite folinic acid supplementation. Monitor patients carefully for cytopenias, especially if they are on other agents that cause bone marrow suppression, such as zidovudine, valganciclovir, and ganciclovir. Note: Patients at risk for G6PD deficiency should be checked for G6PD deficiency before starting pyrimethamine.
Alternatives
Pyrimethamine + folinic acid (administered as described above) + 1 of the following:
- Clindamycin 600 mg every 6 hours; recommended for patients with significant allergic reactions to sulfa medications.
- Atovaquone 750 mg every 6-12 hours.
- Azithromycin 900-1,200 mg daily.
Trimethoprim/sulfamethoxazole (TMP/SMX) 5 mg/kg TMP and 25 mg/kg SMX orally or intravenously. This can be considered when the availability of other regimens is limited or when patients need intravenous therapy.
Atovaquone 1,500 mg orally twice daily + sulfadiazine 1,000-1,500 mg orally every 6 hours.
Note: The regimens that contain sulfadiazine, TMP/SMX, or atovaquone also are effective in preventing Pneumocystis jiroveci pneumonia (PCP), so patients on these regimens do not need additional PCP prophylaxis.
Adjunctive corticosteroids (eg, dexamethasone 4 mg orally or intravenously every 6 hours) may be indicated for patients with significant edema or mass effect. Use is based on clinical judgment and should be discontinued as soon as clinically feasible.
Anticonvulsant therapy should be given to patients with seizures.
Ventilatory support may be necessary if severe CNS symptomatology is present.
Chronic Maintenance Therapy: After at least 6 weeks of initial therapy, and significant clinical and radiologic improvement, chronic maintenance therapy can be considered.
Preferred - Pyrimethamine 25-50 mg orally once daily + sulfadiazine 500-1,000 mg orally every 6 hours + folinic acid 10 mg orally once daily (also effective as PCP prophylaxis).
Alternatives
Pyrimethamine 25-50 mg PO daily + clindamycin 300-450 mg orally every 6-8 hours + folinic acid 10 mg orally once daily.
Pyrimethamine 25-50 mg orally once daily + atovaquone 1,500 mg + folinic acid 10 mg orally once daily (also effective as PCP prophylaxis).
Chronic maintenance therapy generally should be continued for life. For patients who complete acute therapy successfully, have resolution of signs and symptoms of toxoplasmosis, and have immune reconstitution (with CD4 counts >200 cells/無) for more than 6 months on ART, it is reasonable to consider discontinuing maintenance therapy. Some specialists would require resolution of CNS lesions on radiologic studies before discontinuation of therapy. Patients must be observed for recurrence of symptoms, and treatment should be restarted if the CD4 count decreases to <200 cells/無.
Considerations in Pregnancy: All pregnant women should be tested for T gondii. If the result is positive, evaluate the mother for toxoplasmosis and the neonate for evidence of congenital infection. Perinatal transmission usually occurs only with acute maternal infection, but in advanced HIV, it may occur with reactivation of chronic infection. If T gondii infection occurs during pregnancy, consult with a maternal-fetal specialist. Treatment for pregnant women is the same as for non pregnant adults (see above). Note that sulfadiazine taken at the time of delivery may increase the risk of neonatal hyperbilirubinemia and kernicterus.
Patient Education:
Advise patients that antimycobacterial therapy alone will not eradicate toxoplasmosis, but should decrease symptoms and improve quality of life. If medications are discontinued, the disease is likely to recur, unless the CD4 count increases to >100-200 cells/無 in response to ART.
Inform patients that suppressive therapy must be continued to prevent recurrence. This therapy may be lifelong.
It is essential for patients to take all medicines exactly as prescribed. If doses are missed, or if the medications are stopped and restarted, Toxoplasma can develop resistance to the medications. If patients are having trouble taking the medication on schedule, they should contact their health care providers immediately.
Educate patients about the benefits of ART in strengthening the immune system and preventing opportunistic infections such as toxoplasmosis.
Advise patients to return to clinic promptly if symptoms worsen or new symptoms develop.
Toxoplasmosis is a late-stage HIV opportunistic infection and indicates profound immune suppression. Some patients may not respond to treatment or to ART. As with any patient who is at risk for a life-threatening HIV-related disease, clinicians should discuss advance directives and durable power of attorney with patients. Referral to a social worker, mental health clinician, or chaplain experienced in such issues may facilitate this discussion.
References:
Bartlett JG, Gallant JE. 2005-2006 Medical Management of HIV Infection. Baltimore: Johns Hopkins University Division of Infectious Diseases; 2005. Available online at www.hopkins-aids.edu/mmhiv/order.html.
Centers for Disease Control and Prevention, National Institutes of Health, HIV Medicine Association/Infectious Diseases Society of America. Treating Opportunistic Infections Among HIV-Infected Adults and Adolescents. MMWR Recomm Rep. 2004 Dec 17; 53(RR15);1-112.
Kirton C, ed. ANAC's Core Curriculum for HIV/AIDS Nursing; 2nd ed. Thousand Oaks, CA: Sage; 2003:87-89.
Liesenfeld O, Wang SY, Remington JS. Toxoplasmosis in the Setting of AIDS. In: Merigan TC, Bartlett JG, Bolognesi D, eds. Textbook of AIDS Medicine, 2nd Edition. Baltimore: Williams and Wilkins; 1999:225-259.
Murray HW. Toxoplasmosis. In: Dolin R, Masur H, Saag M,S, eds. AIDS Therapy 1999. Philadelphia: Churchill Livingstone; 1999:307-327.
Subauste CS. Toxoplasmosis and HIV. In: Peiperl L, Coffey S, Volberding PA, eds. HIV InSite Knowledge Base [textbook online]. San Francisco: UCSF Center for HIV Information; 2006. Accessed June 1, 2006.
Source: AIDS Education and Training Centers (AETC) National Resource Center. Clinical Manual for Management of the HIV-infected Adult. Section 6: Toxoplasmosis. 2006 edition.
MEDICATION
Pyrimethamine, sulfadiazine or trisulfapyrimidines for 3 to 4 weeks and folinic acid to reduce the side effects of pyrimethamine are often prescribed.
Corticosteroids, if necessary, for inflammation.
Other medications are currently being evaluated.
If drugs are prescribed for you, your midwife or health care provider will do frequent blood tests to monitor side effects.
ACTIVITY
Level of activity will be determined by severity of symptoms.
DIET
No special diet. However it is important that a person maintains a healthy nutritious dietary plan to build and maintain a healthy immune system.
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NOTIFY YOUR MIDWIFE OR HEALTH CARE PROVIDER IF...
You, a child or a family member has symptoms of toxoplasmosis or if you are pregnant and/or you have had contact with cats or infected material.
Symptoms worsen or do not improve after diagnosis and treatment.
New, unexplained symptoms develop. Drugs used in treatment may produce side effects.
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