PREFACE

This paper titled the correlation between TORCH Infections on Pregnant Women was created for the purpose of completing the assignment for the Medical English III in Trisakti University, Faculty of Medicine. The reason why this particular tittle was chosen is the issue about the harm of TORCH infection in pregnant women can be lead to congenital disorders. By reading the content of this paper, the reader will know about TORCH infections and the prevention. Many thanks and appreciation to those who have helped in the process of making this paper especially dr. Noviani Prasetyaningsih, Sp.M who have agreed upon this title which makes this paper can be done. Furthermore, my apologies for any errors contained in this paper for it is created during a learning process.

Jakarta, 19 January 2012

Mila Widyastuti

CONTENT

PREFACE CHAPTER I. ABSTRACT

1 3

CHAPTER II. INTRODUCTION

CHAPTER III. DISCUSSION

REFERENCES

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CHAPTER I ABSTRACT

TORCH infections is a medical acronym for a set of perinatal infections (i.e. infections that are passed from a pregnant woman to her fetus). The TORCH infections can lead to severe fetal anomalies or even fetal loss. They are a group of viral, bacterial, and protozoan infections that gain access to the fetal bloodstream transplacentally via the chorionic villi. Hematogenous transmission may occur at any time during gestation or occasionally at the time of delivery via maternal-to-fetal transfusion. The acronym is spelled out as follows: Toxoplasmosis/ Toxoplasma gondii, other infections (Hepatitis B, Coxsackievirus, Syphilis, Varicella-Zoster Virus, HIV, and Parvovirus B19), rubella, cytomegalovirus, herpes simplex virus. The diseases present similarly, involving the heart, skin, eye, and CNS. They all cause chorioretinitis, microcephaly, and focal cerebral calcification. Symptoms of a TORCH infection may include fever and poor feeding. The newborn is often small for gestational age. Hearing impairment, eye problems, mental retardation, autism, and death can be caused by TORCH infections. The mother often has a mild infection with few or no symptoms. Keywords : TORCH Infection, Toxoplasmosis.

CHAPTER II INTRODUCTION

All of the TORCH infections can affect people of any age or sex. However, the term TORCH is only used when it applies to pregnant women and their unborn or newborn children. As a group, the TORCH infections represent a common cause of birth defects. They can also cause stillbirth, the delivery of a dead baby. (1) The infection usually causes few, if any, symptoms in the pregnant woman. On the other hand, babies risk serious birth defects if they catch one of these infections during pregnancy or delivery. Babies are usually most severely affected when the mother gets the infection in the first trimester, or first three months of pregnancy. This is the time of pregnancy when the baby's organs are first starting to form. (1) Each of the TORCH infections has its own causes: Toxoplasmosis may be caused by exposure to raw meat or cats, which sometimes carry the disease. In the US, rubella is mostly a risk to women who have not been vaccinated or whose immunity to rubella has weakened. Cytomegalovirus, or CMV, is easily spread from person to person, either through the saliva, blood transfusions, or sex. Herpes simplex is a sexually transmitted disease.

In general, for the baby to be affected, the woman must get one of these infections for the first time during the pregnancy. The exception is herpes, which the baby can acquire as he or she goes through the birth canal. With TORCH infections, the severity of the mother's illness often has little to do with how severely the baby is affected. (2)

There are some limits established in this paper in order to prevent an over discussion of the subject matter. The limits will only include : cause, sign and symptoms, diagnosis, and treatments of the disease. Although there might be some extra details added. The aim of this paper is to provide the reader with more information in regards to TORCH infections on pregnant women and the effects on their children. By reading this paper, the reader will obtain facts regarding the etiology and treatment of TORCH infections and the sign and symptoms of this disease.

CHAPTER III DISCUSSION

TORCH infections is a medical acronym for a set of perinatal infections (i.e. infections that are passed from a pregnant woman to her fetus). The TORCH infections can lead to severe fetal anomalies or even fetal loss. They are a group of viral, bacterial, and protozoan infections that gain access to the fetal bloodstream transplacentally via the chorionic villi. Hematogenous transmission may occur at any time during gestation or occasionally at the time of delivery via maternal-to-fetal transfusion.(3) The TORCH infections was originally considered to consist of four conditions, with the "TO" referring to "Toxoplasma". The four-term form is still used in many modern references, and the capitalization "ToRCH" is sometimes used in these contexts.(5) Alternatively, the "O" is redefined as "other",and the acronym is spelled out as follows: Toxoplasmosis/ Toxoplasma gondii, other infections (Hepatitis B, Coxsackievirus, Syphilis, Varicella-Zoster Virus, HIV, and Parvovirus B19), rubella, cytomegalovirus, herpes simplex virus.(5,6) The diseases present similarly, involving the heart, skin, eye, and CNS. They all cause chorioretinitis, microcephaly, and focal cerebral calcification. Symptoms of a TORCH infection may include fever and poor feeding. The newborn is often small for gestational age. A petechial rash on the skin may be present, with small reddish or purplish spots due to bleeding from capillaries under the skin. Hearing impairment, eye problems, mental retardation, autism, and death can be caused by TORCH infections. The mother often has a mild infection with few or no symptoms.(7) Toxoplasmosis Toxoplasmosis, one of the most common infectious diseases, is caused by the protozoa Toxoplasma gondii. It usually causes localized infection but may produce significant generalized infection, especially in neonates and
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patients

who

are

immuno-deficient.

Congenital toxoplasmosis, characterized by lesions in the central nervous system, may result in stillbirth or serious birth defects. For this reason, pregnant women are advised to avoid cleaning cat litter boxes because fecal-oral contamination from infected cats transmits toxoplasmosis.(8) T. gondii exists in trophozoite forms in the acute stages of infection and in cystic forms (tissue cysts and oocysts) in the latent stages. In addition to possible fecal-oral transmission from infected cats, ingestion of tissue cysts in raw or uncooked meat (heating, drying, or freezing destroys these cysts) can also transmit toxoplasmosis. Congenital toxoplasmosis follows transplacental transmission from a chronically infected mother or one who acquired toxoplasmosis shortly before or during pregnancy. Toxoplasmosis acquired in the first trimester of pregnancy commonly results in stillbirth. About one-third of infants who survive have congenital toxoplasmosis. The later in pregnancy that maternal infection occurs, the greater the risk of congenital infection in the infant. Obvious signs of congenital toxoplasmosis include retinochoroiditis, hydrocephalus or microcephalus, cerebral calcification, seizures, lymphadenopathy, fever, hepatosplenomegaly, jaundice, and rash. Other defects, which may become apparent months or years later, include strabismus, blindness, epilepsy, and mental retardation.(9) Acquired toxoplasmosis may cause localized (mild lymphatic) or generalized (fulminating, disseminated) infection. Localized infection produces fever and a mononucleosislike syndrome (malaise, myalgia, headache, fatigue, and sore throat) and lymphadenopathy. Generalized infection produces encephalitis, fever, headache, vomiting, delirium, seizures, and a diffuse maculopapular rash (except on the palms, soles, and scalp). Generalized infection may lead to myocarditis, pneumonitis, hepatitis, and polymyositis.(9) A common examination is the Anti-Toxoplasma IgG, IgM and IgA, and Aviditas AntiToxoplasma IgG. Identification of T. gondii in an appropriate tissue specimen confirms the diagnosis of toxoplasmosis. Serologic tests may be useful and, in patients with toxoplasmosis encephalitis, computed tomography scans and magnetic resonance imaging disclose lesions.(10) Treatment of acute disease consists of drug therapy with sulfonamides, pyrimethamine, folinic acid, clindamycin, or co-trimoxazole. In patients who also have acquired

immunodeficiency syndrome, treatment continues indefinitely. No safe, effective treatment exists for chronic toxoplasmosis or toxoplasmosis occurring in the first trimester of pregnancy.(10) Rubella Rubella, commonly called German measles, is an acute, mildly contagious viral disease that produces a distinctive 3-day rash and lymphadenopathy. It usually occurs among children ages 5 to 9, adolescents, and young adults. Rubella flourishes worldwide during the spring (particularly in big cities), and epidemics occur sporadically. This disease is self-limiting, with an excellent prognosis.(11) The rubella virus is transmitted through contact with the blood, urine, stools, or nasopharyngeal secretions of infected people and, possibly, by contact with contaminated articles of clothing. Transplacental transmission, especially in the first trimes-ter of pregnancy, can cause serious birth defects, such as microcephaly, mental retardation, patent ductus arteriosus, glaucoma, and bone defects. Humans are the only known hosts for the rubella virus. The disease is contagious from about 10 days before the rash appears until 5 days after it has appeared.(12) In children, after an incubation period of from 14 to 21 days, an exanthematous, maculopapular rash erupts abruptly. In adolescents and adults, prodromal signs and symptoms headache, malaise, anorexia, low-grade fever, coryza, lymphadenopathy and, sometimes, conjunctivitis are the first to appear. Suboccipital, postauricular, and postcervical lymph node enlargement is a hallmark of this disease and precedes the rash. Typically, the rubella rash begins on the face and spreads rapidly, in many cases covering the trunk and extremities within hours. Small, red, petechial macules on the soft palate (Forschheimer spots) may precede or accompany the rash but are not diagnostic of rubella. By the end of the second day, the facial rash begins to fade, but the rash on the trunk may become confluent and be mistaken for scarlet fever. The rash continues to fade in the downward order in which it appeared. It generally disappears on the third day, but it may persist for 4 or 5 days sometimes accompanied by mild coryza and conjunctivitis. The rapid appearance and disappearance of the rubella rash distinguishes it from rubeola. In rare cases, rubella can occur without a rash. Low-grade fever may accompany the rash (99 to 101 F [37.2 to 38.3 C]), but
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it usually doesnt persist after the first day of the rash; rarely, temperature may reach 104 F (40 C). (13) Complications seldom occur in children with rubella, but when they do, they commonly appear as hemorrhagic problems such as thrombocytopenia. Many young women, however, experience transient joint pain or arthritis, usually just as the rash is fading. Fever may then recur. These complications usually subside spontaneously within 5 to 30 days. (13) The rubella rash, lymphadenopathy, other characteristic signs, and a history of exposure to infected people usually permit clinical diagnosis without laboratory tests. The rubella rash has been confused with scarlet fever, measles (rubeola), infectious mononucleosis, roseola, erythema infectiosum, and other viral exanthems. Therefore, without exposure history, laboratory confirmation is beneficial. Cell cultures of the throat, blood, urine, and cerebrospinal fluid can confirm the virus presence. Convalescent serum that shows a fourfold rise in antibody titers corroborates the diagnosis. (13,14) Because the rubella rash is self-limiting and only mildly pruritic, it doesnt require topical or systemic medication. Treatment consists of aspirin for fever and joint pain. Bed rest isnt necessary, but the patient should be isolated until the rash disappears. Immunization with live virus vaccine RA27/3, the only rubella vaccine available in the United States, is necessary for prevention and appears to be more immunogenic than previous vaccines. The rubella vaccine should be given with measles and mumps vaccines at age 15 months to decrease the cost and number of injections. (14) Cytomegalovirus Cytomegalovirus (CMV) infection is caused by the cytomegalovirus, a deoxyribonucleic acid, ether-sensitive virus belonging to the herpes family. Also known as generalized salivary gland disease or cytomegalic inclusion disease, CMV infection occurs worldwide and is transmitted by human contact. CMV has been found in the saliva, urine, semen, breast milk, feces, blood, and vaginal and cervical secretions of infected people. The virus is usually transmitted through contact with these infected secretions, which can harbor the virus for months or even years. It may be transmitted by sexual contact and can travel across the placenta, causing
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a congenital infection. Immunosuppressed patients, especially those who have received transplanted organs, run a 90% chance of contracting CMV infection. Recipients of blood transfusions from donors with positive CMV antibodies are at some risk. CMV infection during pregnancy can be hazardous to the fetus, possibly leading to stillbirth, brain damage, and other birth defects or to severe neonatal illness. About 1% of all neonates have CMV. (15) CMV probably spreads through the body in lymphocytes or mononuclear cells to the lungs, liver, GI tract, eyes, and central nervous system, where it commonly produces inflammatory reactions. Most patients with CMV infection have mild, nonspecific complaints or none at all, even though antibody titers indicate infection. In these patients, the disease usually runs a self-limiting course. However, immunodeficient patients and those receiving immunosuppressants may develop pneumonia or other secondary infections. In patients with acquired immunodeficiency syndrome, disseminated CMV infection may cause chorioretinitis (resulting in blindness), colitis, encephalitis, abdominal pain, diarrhea, or weight loss. Infected infants ages 3 to 6 months usually appear asymptomatic but may develop hepatic dysfunction, hepatosplenomegaly, spider angiomas, pneumonitis, and lymphadenopathy. (16) Congenital CMV infection is seldom apparent at birth, although the neonates urine contains the virus. CMV can cause brain damage that may not show up for months after birth. It also can produce a rapidly fatal neonatal illness characterized by jaundice, petechial rash, hepatosplenomegaly, fatal. (16) Laboratoty tests supporting the diagnosis include complement fixation studies, hemagglutination inhibition antibody tests and, for congenital infections, indirect immunofluorescent tests for CMV immunoglobulin M antibody.(17) thrombocytopenia, hemolytic anemia, microcephaly, psychomotor retardation, mental deficiency, and hearing loss. Occasionally, this form is rapidly

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Figure 1. Micrograph of cytomegalovirus (CMV) infection of the placenta The characteristic large nucleus of a CMV infected cell is seen off-centre at the bottomright of the image. H&E stain. Treatment aims to relieve symptoms and prevent complications. In the

immunosuppressed patient, CMV may be treated with acyclovir, ganciclovir, valganciclovir, cidofovir and, possibly, foscarnet. Most important, parents of children with severe congenital CMV infection need support and counseling to help them cope with the possibility of brain damage or death. Herpes Simplex Herpes simplex, a recurrent viral infection, is caused by Herpesvirus hominis (HVH), a widespread infectious agent. Herpes type I, which is transmitted by oral and respiratory secretions, affects the skin and mucous membranes, commonly producing cold sores and fever blisters. Herpes type II primarily affects the genital area and is transmitted by sexual contact.(18) Primary HVH is the leading cause of childhood gingivostomatitis in children ages 1 to 3. It causes the most common form of nonepidemic encephalitis and is the second most common viral infection in pregnant women. It can pass to the fetus transplacentally and, in early pregnancy, may cause spontaneous abortion or premature birth.(19) In neonates, HVH symptoms usually appear 1 to 2 weeks after birth. They range from localized skin lesions to a disseminated infection of organs, such as the liver, lungs, or brain. Common complications include seizures, mental retardation, blindness, chorioretinitis, deafness,
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microcephaly, diabetes insipidus, and spasticity. Up to 90% of infants with disseminated disease die.(19) Primary infection in childhood may be localized or generalized and occurs after an incubation period of 2 to 12 days. After brief prodromal tingling and itching, localized infection causes typical primary lesions. These erupt as vesicles on an erythematous base, eventually rupture and leave a painful ulcer, followed by a yellowish crust. Vesicles may form on any part of the oral mucosa, especially the tongue, gingiva, and cheeks. Healing begins 7 to 10 days after onset and is complete in 3 weeks. Generalized infection begins with fever, pharyngitis, erythema, and edema. Vesicles occur with submaxillary lymphadenopathy, increased salivation, halitosis, anorexia, and a fever of up to 105 F (40.6 C). Herpetic stomatitis may lead to severe dehydration in children. A generalized infection usually runs its course in 4 to 10 days. In this form, virus reactivation causes cold sores a single or group of vesicles in and around the mouth. Usually, herpetic keratoconjunctivitis is unilateral and causes only local signs and symptoms: conjunctivitis, regional adenopathy, blepharitis, and vesicles on the lid. Other ocular effects may include excessive lacrimation, edema, chemosis, photophobia, and purulent exudate. Both types of HVH can cause acute sporadic encephalitis with altered level of consciousness, personality changes, and seizures. Other effects may include smell and taste hallucinations and neurologic abnormalities such as aphasia.(19,20) Typical lesions may suggest HVH infection. However, confirmation requires isolation of the virus from local lesions and histologic biopsy. A rise in antibodies and moderate leukocytosis may support the diagnosis.

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Figure 2. Micrograph of a pap test showing changes associated with herpes simplex virus No cure for herpes exists; however, recurrences tend to be milder and of shorter duration than the primary infection. Symptomatic and supportive therapy is essential. Generalized primary infection usually requires an analgesic-antipyretic to reduce fever and relieve pain. Drying agents, such as calamine lotion, ease the pain of labial or skin lesions. Avoid petroleumbased ointments, which promote viral spread and slow healing. Refer patients with eye infections to an ophthalmologist. Topical corticosteroids are contraindicated in active infection, but idoxuridine, trifluridine, and vidarabine are effective. Oral acyclovir may bring relief to patients with genital herpes. Frequent prophylactic use of acyclovir in immunosuppressed transplant patients prevents disseminated disease.Foscarnet can be used to treat HVH thats resistant to acyclovir. Anti-viral agents similar to acyclovir are valacyclovir and famciclovir. These agents are more active than acyclovir.(20)

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CHAPTER IV CONCLUSION Pregnancy is the period of time when a fetus develops inside a womans uterus and ends with the birth of the infant. Pregnancies typically involve a variety of clinical laboratory tests. The tests provide useful information from the time pregnancy is first considered through the initial days of the newborn's life. Now, the diagnosis for infectious diseases has been developed among others in the direction of immunological tests. The principle of this examination is the detection of anti(antibody) specific to the bacteria causing the infection as the bodys response to the presence of a foreign body (the worst kuman. Antibodies can be immunoglobulin M (IgM) and immunoglobulin G (IgG). A treatment called immune globulin can be given to the mother or child in certain settings. This is a protein mixture that helps protect the mother or child after an exposure to the infection. Some affected infants can be given antibiotics, such as those with syphilis, herpes, or toxoplasma infections. Prevention is related to the specific infection. Avoiding cats and raw meat can help prevent most cases of toxoplasmosis. rubella can be prevented by making sure the mother is immune (by testing her blood). Cytomegalovirus can rarely be prevented, but safer sex practices can help prevent some cases. Cases due to Syphilis, herpes, and hepatitis B can also often be prevented by safer sex. Women who have active herpes lesions at the time of delivery are often advised to have a caesarean section. This is thought to lower the risk of passing the infection on to the baby during delivery.

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1. Torch Infections. Available at :

http://www.medicineonline.com/articles/t/2/TORCH-Infections.html 2. Boyer KM. Toxoplasmosis: Current status of diagnosis, treatment and prevention. Semin Pediatr Infect Dis 2000;11:165-171. 3. Robbins and Cotran Pathological Basis of Disease, pg 480
4. Li D, Yang H, Zhang WH, et al. (2006). "A simple parallel analytical method of

prenatal screening". Gynecol. Obstet. Invest. 62 (4): 2205

5. Springhouse, (2005). Professional Guide to Diseases (Eighth Edition)

6. Torch infections on pregnancy. Available at : http://momandkids.us/torch-infection-in-pregnancy.htm 7. Klein J, Remington J. Current concepts in infections of the fetus and newborn. In Infectious Diseases of the Fetus and Newborn Infant, eds Remington J and Klein J. Saunders, Philadelphia, PA 2001, 1-24. 8. Boyer KM. Toxoplasmosis: Current status of diagnosis, treatment and prevention. Semin Pediatr Infect Dis 2000;11 9. Update on TORCH Infections in the Newborn Infant. Available at : http://www.medscape.com/viewarticle/472409 10. Guerina NG, Hsu HW, Meissner HC, et al. Neonatal serologic screening and early treatment for congenital Toxoplasma gondii infection. N Engl J Med 1994;330:1858-1863. 11. Reef SE, Frey TK, Theall K, et al. The changing epidemiology of rubella in the 1990s: On the verge of elimination and new challenges for control and prevention. JAMA 2002;287:464-472.

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12. Best JM, O'Shea S. Rubella virus. In Diagnostic Procedures for Viral, Rickettsial and Chamydial Infections, eds Lennette EH and Schmidt NJ. American Public Health Association, Washington DC 1989, 731-795.
13. Centers for Disease Control and Prevention. Rubella and congenital rubella

syndromeUnited States 19911997. MMWR 1997;46:350-354. 14. Maldonado Y. Rubella. In Nelson Textbook of Pediatrics, eds Behrman R, Kliegman R and Jenson H. 2004, 1032-1034. Philadelphia, PA.
15. Fowler KB, Stagno S, Pass RF. Maternal age and congenital cytomegalovirus

infection: Screening of two diverse newborn populations: 19801990. J Infect Dis 1993;168:552. 16. Pass R. Cytomegalovirus. In Principles and Practice of Pediatric Infectious Diseases, eds Long S, Pickering L and Prober C. Churchill-Livingston, New York, NY 2003, 1050-1059. 17. Hicks T, Fowler K, Richardson M, et al. Congenital cytomegalovirus infection and neonatal auditory screening. J Pediatr 1993;123:779. 18. Arvin A, Whitley R. Herpes simplex virus infections. In Infectious Diseases of the Fetus and Newborn Infant, eds Remington J and Klein J. Saunders, Philadelphia, PA 2001, 425-446. 19. Prober CG, Yasukawa L, Aud S, et al. Low risk of herpes simplex virus infection in neonates exposed to virus at the time of vaginal delivery with recurrent herpes virus infection. N Engl J Med 1987;316:240-245. 20. Kohl S. Herpes simplex virus. In Nelson Textbook of Pediatrics, eds Behrman R, Kliegman R and Jenson H. Saunders, Philadelphia PA 2004, 1051-1057.

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