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    TORCH TORCH Presentation Transcript

    • TORCH INFECTIONS TORCH BYINFECTIONS NKIRU VICTORIA CHUKWUKAEME GROUP 42 6TH COURSE
    • INTRODUCTION TORCH infections Is an acronym for a group of five infectious diseases:• T=Toxoplasmosis• O=Other (Hepatitis B)• R=Rubella (German measles)• C=Cytomegalovirus (CMV)• H=Herpes Simplex Virus (HSV)
    • TORCH INFECTIONS• Each disease may be teratogenic• Each crosses the placenta• Each may adversely affect the developing fetus• The effect of each varies, depending on developmental stage at time of exposure.
    • Toxoplasmosis• Toxoplasmosis is caused by infection with the protozoan Toxoplasma gondii, an obligate Intracellular parasite.Transmission• Ingestion of raw or partially cooked meat, especially pork, lamb or• venison Contact with infected cat feces.• Transplacentally (if new infection occurs during pregnancy)• Through organ transplant or transfusion- very rare• Women with compromised immune systems are at risk for reactivation of a previous infection. ingestion of toxoplasma eggs from the soil.
    • transmission
    • Clinical Manifestations• Most (70-90%) are asymptomatic at birth• Classic triad of symptoms:• Chorioretinitis• Hydrocephalus• Intracranial calcifications• Ocular toxoplasmosis (retinochoroiditis)• Symptoms of retinochoroiditis include the following• Decreased visual acuity - Other deficits depend on the location of the lesion• White focal lesions with inflammation of the vitreous humor (the classic "headlight in the fog" appearance) seen on ophthalmoscopic examination• Recurrent lesions at the border of the retinochoroidal scars
    • Clinical manifestations• Congenital toxoplasmosis• The classic clinical triad of retinochoroiditis, cerebral calcifications, and convulsions defines congenital toxoplasmosis. Other findings include the following:• Hydrocephalus• Microcephaly• Organomegaly• Jaundice• Rash• Fever• Psychomotor retardation
    • Inactive retinochoroidal scar secondary to toxoplasmosis
    • Diagnostic findingsserologic antibody testingELISAMaternal IgG testing indicates past infectionCan be isolated in culture from placenta,umbilical cord, infant serumPCR testing on WBC, CSF, placentaNot standardizedNewborn serologies with IgM/IgA
    • Treatment• for pregnant women- Spiramycin 1 g orally every 8 hours• If the amniotic fluid test result for T gondii is positive: 3 weeks of pyrimethamine (50 mg/day orally) and sulfadiazine (3 g/day orally in 2-3 divided doses) alternating with a 3-week course of spiramycin 1 g 3 times daily for maternal treatment OR• Pyrimethamine (25 mg/day orally) and sulfadiazine (4 g/day orally) divided 2 or 4 times daily until delivery (this agent may be associated with marrow suppression and pancytopenia) AND• Leucovorin 10-25 mg/day orally to prevent bone marrow suppression
    • Treatment• Immunocompetent, nonpregnant patients typically do not require treatment. Treatment of nonpregnant patients is described below.• The 6-week regimen is as follows:• Pyrimethamine (100mg loading dose orally followed by 25-50 mg/day) plus sulfadiazine (2-4 g/day divided 4 times daily) OR• Pyrimethamine (100-mg loading dose orally followed by 25-50 mg/day) plus clindamycin (300 mg orally 4 times daily)• Folinic acid (leucovorin) (10• -25 mg/day) should be given to all patients to prevent hematologic toxicity of pyrimethamine• Trimethoprim (10 mg/kg/day) sulfamethoxazole (50 mg/kg/day) for 4 weeks• Sulfadiazine or clindamycin can be substituted for azithromycin 500 mg daily or atovaquone 750 mg twice daily in immunocompetent patients or in patients with a history of allergy to the former drugs
    • prevention• . Women planning a pregnancy may be tested before pregnancy. If the test• is positive there is no need to worry about passing a new infection to the• baby. Women who test negative can take precautions.• b. Wear gloves and wash hands carefully after handling soil.• c. Cook meat thoroughly (until no longer pink inside and juices run clear)• d. Wash hands and any equipment or surfaces that raw meat contacts• thoroughly with warm water and soap.• e. Keep your cat inside and do not feed raw meat. Avoid handling stray cats• or new kittens that may have eaten raw meat. Have someone else change• the litter box.
    • Hepatitis B (HBV)• Description – Hepatitis B (HBV) is a serious viral disease responsible for• 4000 to 5000 deaths each year in the U.S. due to cirrhosis and liver cancer.• Acute infection occurs in 1 to 2 pregnancies per 1000. Estimated that 300• million people worldwide are chronically infected with HBV
    • Transmission• Incubation usually 50-180 days• Mode of transmission• - Sexual contact• - Perinatal• - Transplacental• - Contact with blood, stool and saliva• - Shared razors, toothbrushes, towels, and other personal items.• At risk populations• Southeast Asians, Eskimos, Africans, Chinese, Flipinos and Indonesians• Homosexuals• IV drug users• Hemophiliacs• Transfusion or organ recipients• Hemodialysis patients
    • Clinical manifestations Physical Findings – Low-grade fever, nausea,anorexia, jaundice,• hepatomegaly, and malaise. Potential Maternal and Neonatal Effects• a. Maternal – Premature labor and delivery, cirrhosis and liver cancer• b. Neonatal – Stillbirth. Infants infected at birth have a 90% chance of• becoming chronically infected.
    • Treatment and prevention Treatment Maternal – Pregnant women who are exposed to HBV should receive• vaccine and HBIG. Pregnant women who are already infected should eat• well, get sufficient rest, avoid stress and avoid alcohol. Alpha interferon• and lamivudine are not recommended during pregnancy.• Neonatal - Infants of infected women should receive HBV vaccine and HGIB. prevention• Hepatitis B vaccination is the best prevention.• The proper and consistent use of latex condoms may prevent sexual• transmission.• Do not use IV drugs. Never share needles, syringes, water or “works”.• Do not share personal items that may have blood on them – razors,• toothbrushes.• Consider the risks before getting a tattoo or piercing.• Health care workers should use BSP and safe handling of sharps
    • RUBELLA• The name rubella is derived from a Latin term meaning "little red." Rubella is generally a benign communicable exanthematous disease. It is caused by rubella virus, which is a member of the Rubivirus genus of the family Togaviridae. Nearly one half of individuals infected with this virus are asymptomatic.• The major complication of rubella is its teratogenic effects when pregnant women contract the disease, especially in the early weeks of gestation. The virus can be transmitted to the fetus through the placenta and is capable of causing serious congenital defects, abortions, and stillbirths.
    • TRANSMISSION AND CLINICAL FEATURES• Incubation – 2 to 3 weeks .• Highly contagious .• Spread through nasopharyngeal secretions . • Transplacental transmission . Clinical features• Conjunctivitis• Sore throat• Headache• General body aches• Low-grade fever• Chills• Anorexia• Nausea• Tender lymphadenopathy
    • Postnatal Rubella• Rash in adults may be quite pruritic.• The synonym "3-day measles" derives from the typical course of rubella exanthem that starts initially on the face and neck and spreads centrifugally to the trunk and extremities within 24 hours. It then begins to fade on the face on the second day and disappears throughout the body by the end of the third day.• Temperature• Fever is usually not higher than 38.5°C (101.5°F).• Lymph nodes• Enlarged posterior auricular and suboccipital lymph nodes are usually found on physical examination.• Mouth• The Forchheimer sign may still be present on the soft palate.
    • Postnatal Rubella
    • Congenital Rubella Syndrome• Sensorineural hearing loss is the most common manifestation of congenital rubella syndrome. It occurs in approximately 58% of patients. Studies have demonstrated that approximately 40% of patients with congenital rubella syndrome may present with deafness as the only abnormality without other manifestations. Hearing impairment may be bilateral or unilateral and may not be apparent until the second year of life.• Ocular abnormalities including cataract, infantile glaucoma, and pigmentary retinopathy occur in approximately 43% of children with congenital rubella syndrome. Both eyes are affected in 80% of patients, and the most frequent findings are cataract and rubella retinopathy. Rubella retinopathy consists of a salt- and-pepper pigmentary change or a mottled, blotchy, irregular pigmentation, usually with the greatest density in the macula. The retinopathy is benign and nonprogressive and does not interfere with vision (in contrast to the cataract) unless choroid neovascularization develops in the macula.• Congenital heart disease including patent ductus arteriosus (PDA) and pulmonary artery stenosis is present in 50% of infants infected in the first 2 months gestation. Cardiac defects and deafness occur in all infants infected during the first 10 weeks of pregnancy and deafness alone is noted in one third of those infected at 13-16 weeks of gestation.
    • Congenital Rubella Syndrome• Skin manifestations, including blueberry muffin spots that represent dermal erythropoiesis and dermatoglyphic abnormalities
    • Diagnostic findings→ ELISA→Isolation of virus from urine or endocervicalsecretions.→Fluorescent antibody (FA)→complement fixation (CF) test
    • Management and prevention.• Maternal – Mild analgesics, rest and support.• Neonatal - No specific treatment for congenital rubella treatment. Eye or• cardiac defects may be corrected or improved with surgery. Careful• screening for problems and special education are indicated.• Health Education• Vaccination of non-immune women before pregnancy is the best• prevention. The rubella and MMR (measles, mumps, rubella) vaccines are not• recommended during pregnancy. A woman should wait 28 days after• vaccination to attempt conception (although the risk to an inadvertent• pregnancy during this time is very small). Breastfeeding women may be• vaccinated.• Pregnant women who are non-immune for rubella should avoid anyone• with rubella or the symptoms of rubella.
    • Cytomegalovirus• Cytomegalovirus (CMV) is a double-stranded DNA virus and is a member of the Herpesviridae family. Risk factors individuals who attend or work at daycare centers, patients who undergo blood transfusions, persons who have multiple sex partners, and recipients of CMV mismatched organ or bone marrow transplants.
    • transmission• Incubation – unknown. CMV is in the herpes family and like herpes can reactivate.• CMV is very common in young children (perhaps 70% of children• between 1 and 3 years of age in childcare will be excreting (CMV). Transmission can occur through contact with saliva, urine, feces, blood, and mucous. It can also be transmitted sexually and through transfusion and organ donation.• Transplacental transmission tends to be most serious.• Infants who are infected during birth or from breastfeeding rarely have serious problems from the infection.
    • transmission
    • Clinical manifestations• Physical Findings – Sore throat, fever, body aches, fatigue and hepatomegaly. . Maternal – Most infections are asymptomatic• Neonatal – Infection is most likely to occur with primary maternal• infection. Approximate congenital infection rate of 1%. Of these, 10 %• will be symptomatic, of which 25 % will have fatal disease and 90% of the• survivors will have serious sequelae- IUGR, microcephaly, CNS• abnormalities, hydrocephaly, periventricular calcification, deafness,• blindness, and mental retardation. A small percentage of newborns• asymptomatic at birth will also develop late sequelae.
    • diagnosis• Maternal - ELISA, fluorescent antibody (FA), complement fixation (CF),• seroconversion to +IgM, and isolation of the virus by culture.• Prenatal• - Affected infant’s may demonstrate the following ultrasound findings:• microcephaly, hydrocephalus, necrotic cystic or calcified lesions in the• brain, liver or placenta, IUGR, oligohydramnios, ascites, pleural or• pericardial effusion, hypoechogenic bowel and hydrops.• -Amniocentisis with culture or DNA identification.• -Cordocentesis can be used to document presence and severity of disease.• Newborn – virus isolation is the optimal method of documenting CMV• infection. Specimens can be taken from urine, nasopharnyx, conjunctiva• and spinal fluid.
    • Treatment and prevention• Maternal – treat symptoms Ganciclovir , Valganciclovir• Neonatal - no satisfactory treatment available. Infant is contagious andshould be isolated.. Women can reduce their risk of CMV by practicing universal precautionsand careful hand washing, especially after any contact with saliva, urine,feces, blood and mucous. Avoid sharing glasses or eating utensils. Medical or day care workers may consider being tested prior to pregnancyto determine if they have had CMV, as they would then have little causefor concern.
    • Herpes Simplex Virus (HSV)• Herpes is caused by the herpes simplex viruses, which are similar to the viruses that cause chickenpox and shingles. After the initial infection, the herpes simplex viruses can hide within nerve cells and later launch new attacks. There are 2 main kinds of herpes simplex virus (HSV):• type I→ which is usually associated with cold sores around the mouth;• type 2→ which is usually associated with genital sores. However, either type can infect either the mouth or genitals and both can be passed on to the newborn.
    • Clinical features• Acute herpetic gingivostomatitis• This is a manifestation of primary HSV-1 infection that occurs in children aged 6 months to 5 years. Adults may also develop acute gingivostomatitis, but it is less severe and is associated more often with a posterior pharyngitis.• Infected saliva from an adult or another child is the mode of infection. The incubation period is 3-6 days.• Clinical features include the following:• Abrupt onset• High temperature (102-104°F)• Anorexia and listlessness• Gingivitis (This is the most striking feature, with markedly swollen, erythematous, friable gums.)• Vesicular lesions (These develop on the oral mucosa, tongue, and lips and later rupture and coalesce, leaving ulcerated plaques.)• Tender regional lymphadenopathy• Perioral skin involvement due to contamination with infected saliva• Course: Acute herpetic gingivostomatitis lasts 5-7 days, and the symptoms subside in 2 weeks. Viral shedding from the saliva may continue for 3 weeks or more.
    • Clinical features• Acute herpetic pharyngotonsillitis• In adults, oropharyngeal HSV-1 infection causes pharyngitis and tonsillitis more often than gingivostomatitis.• Fever, malaise, headache, and sore throat are presenting features.• The vesicles rupture to form ulcerative lesions with grayish exudates on the tonsils and the posterior pharynx.• Associated oral and labial lesions occur in fewer than 10% of patients.• HSV-2 infection can cause similar symptoms and can be associated with orogenital contact or can occur concurrently with genital herpes.• Herpes labialis• This is the most common manifestation of recurrent HSV-1 infection. A prodrome of pain, burning, and tingling often occurs at the site, followed by the development of erythematous papules that rapidly develop into tiny, thin-walled, intraepidermal vesicles that become pustular and ulcerate. In most patients, fewer than two recurrences manifest each year, but some individuals experience monthly recurrences.• Maximum viral shedding is in the first 24 hours of the acute illness but may last 5 days.
    • Primary genital herpes• Primary genital herpes can be caused by both HSV-1 and HSV-2 and can be asymptomatic. The clinical features and course of primary genital herpes caused by both HSV-1 and HSV-2 are indistinguishable, but recurrences are more common with HSV-2.• Primary genital herpes is characterized by severe and prolonged systemic and local symptoms. The symptoms of persons with a first episode of secondary HSV-2 infection are less severe and of shorter duration.• Preexisting antibodies to HSV-1 have an ameliorating effect on disease severity caused by HSV-2.• Prior orolabial HSV-1 infection protects against genital HSV-1 but not HSV-2.• Symptoms of primary genital herpes are more severe in women, as are complications.• Clinical features: The incubation of primary genital herpes period is 3-7 days (range, 1 d to 3 wk). Constitutional symptoms include fever, headache, malaise, and myalgia (prominent in the first 3-4 d). Local symptoms include pain, itching, dysuria, vaginal and urethral discharge, and tender lymphadenopathy.• Clinical features in women: Herpetic vesicles appear on the external genitalia, labia majora, labia minora, vaginal vestibule, and introitus. In moist areas, the vesicles rupture, leaving exquisitely tender ulcers. The vaginal mucosa is inflamed and edematous. The cervix is involved in 70%-90% of cases and is characterized by ulcerative or necrotic cervical mucosa. Cervicitis is the sole manifestation in some patients. Dysuria may be very severe and may cause urinary retention. Dysuria is associated with urethritis, and HSV can be isolated in the urine. HSV-1 infection causes urethritis more often than does HSV-2 infection.• Clinical features in men: Herpetic vesicles appear in the glans penis, the prepuce, the shaft of the penis, and sometimes on the scrotum, thighs, and buttocks. In dry areas, the lesions progress to pustules and then encrust. Herpetic urethritis occurs in 30%-40% of affected men and is characterized by severe dysuria and mucoid discharge. The perianal area and rectum may be involved in persons who engage in anal intercourse, resulting in herpetic proctitis.
    • Recurrent mucocutaneous HSV infections• Following the establishment of latency in the corresponding sensory nerve ganglion cells, HSV can cause recurrent infection that can be subclinical (manifesting as viral excretion without lesions) or overt (manifesting as mucosal or cutaneous lesions with viral excretion).• Oral recurrences are often triggered by recognizable stimuli such as pyrexia (fever blisters and cold sores), stress, or sunburn. Genital recurrences are more likely to be linked to stress rather than to pyrexia. Females may relate a relationship to the menstrual cycle.• Localized burning or paraesthesias may precede recurrent lesions. Unlike primary infection, constitutional symptoms are minimal in most cases.• Recurrences last 3-7 days and can occur numerous times per year or once or twice in a lifetime. Overall, the number of yearly recurrences tends to decrease over time.• Because recurrences can be clinically unrecognizable, transmission to susceptible individuals can occur in the absence of overt lesions. In genital HSV infections, barrier protection should be used regardless of existing lesions, even in the absence of a history of genital HSV infection.
    • diagnostics• a. Tissue culture-swab specimen from vesicles• b. Pap smear of lesion• c. Visualization of a blister or ulcer-like, painful lesion by experienced• clinician.
    • Treatment and prevention• Anti-viral drugs can shorten the duration of a herpes attack, alleviate• symptoms and reduce the number of attacks. Oral acyclovir is sometimes• used in late pregnancy to decrease the need for cesarean birth.• Acyclovir and vidarabine are used to treat neonatal HSV – more• successful with localized infection than one that has spread to brain and• other internal organs.• prevention• Encourage women with a history of genital herpes to avoid “triggers”• (heat, friction, intercourse, peanuts, chocolate, fever or stress), especially• during the later part of pregnancy.• Recommend condoms or abstinence in pregnant women without HSV who• have partners with HSV.• Encourage careful hand washing to prevent spread of HSV to others or to• other parts of the body• People with active cold sore lesions should avoid kissing others, especially• newborns.• Educate women of the importance of reporting prodromal symptoms or• lesions to their care providers with suspected labor or ruptured
    • Herpes simplex