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Rubella

Rubella

Rubella

— commonly known as German measles or 3-day measles — is an infection that primarily affects the skin and lymph nodes. It is caused by the rubella virus (not the same virus that causes measles), which is usually transmitted by droplets from the nose or throat that others breathe in. It can also pass through a pregnant woman's bloodstream to infect her unborn child. As this is a generally mild disease in children, the primary medical danger of rubella is the infection of pregnant women, which may cause congenital rubella syndrome in developing babies.

Before a vaccine against rubella became available in 1969, rubella epidemics occurred every 6 to 9 years. Kids ages 5 to 9 were primarily affected, and many cases of congenital rubella occurred as well. Now, due to immunization of children, there are much fewer cases of rubella and congenital rubella.

Most rubella infections today appear in young, non-immunized adults rather than children. In fact, experts estimate that 10% of young adults are currently susceptible to rubella, which could pose a danger to any children they might have someday.
Signs and Symptoms

Rubella infection may begin with 1 or 2 days of mild fever (99–100° Fahrenheit, or 37.2–37.8° Celsius) and swollen, tender lymph nodes, usually in the back of the neck or behind the ears. A rash then appears that begins on the face and spreads downward. As it spreads down the body, it usually clears on the face. This rash is often the first sign of illness that a parent notices.

The rubella rash can look like many other viral rashes. It appears as either pink or light red spots, which may merge to form evenly colored patches. The rash can itch and lasts up to 3 days. As the rash clears, the affected skin occasionally sheds in very fine flakes.

Other symptoms of rubella, which are more common in teens and adults, may include: headache; loss of appetite; mild conjunctivitis (inflammation of the lining of the eyelids and eyeballs); a stuffy or runny nose; swollen lymph nodes in other parts of the body; and pain and swelling in the joints (especially in young women). Many people with rubella have few or no symptoms at all.

When rubella occurs in a pregnant woman, it may cause congenital rubella syndrome, with potentially devastating consequences for the developing fetus. Children who are infected with rubella before birth are at risk for growth retardation; mental retardation; malformations of the heart and eyes; deafness; and liver, spleen, and bone marrow problems.
Contagiousness

The rubella virus passes from person to person through tiny drops of fluid from the nose and throat. People who have rubella are most contagious from 1 week before to 1 week after the rash appears. Someone who is infected but has no symptoms can still spread the virus.

Infants who have congenital rubella syndrome can shed the virus in urine and fluid from the nose and throat for a year or more and may pass the virus to people who have not been immunized.
Prevention

Rubella can be prevented by a rubella vaccine. Widespread immunization against rubella is critical to controlling the spread of the disease, thereby preventing birth defects caused by congenital rubella syndrome.

The vaccine is usually given to children at 12 to 15 months of age as part of the scheduled measles-mumps-rubella (MMR) immunization. A second dose of MMR is generally given at 4 to 6 years of age. As is the case with all immunization schedules, there are important exceptions and special circumstances. Your child's doctor will have the most current information.

The rubella vaccine should not be given to pregnant women or to a woman who may become pregnant within 1 month of receiving the vaccine. If you are thinking about becoming pregnant, make sure that you are immune to rubella through a blood test or proof of immunization. If you're not immune, you should receive the vaccine at least 1 month before you become pregnant.

Pregnant women who are not immune should avoid anyone who has the illness and should be vaccinated after delivery so that they will be immune during any future pregnancies.
Incubation

The incubation period for rubella is 14–23 days, with an average incubation period of 16–18 days. This means that it can take 2–3 weeks for a child to get rubella after they are exposed to someone with the disease.
Duration

The rubella rash typically lasts 3 days. Lymph nodes may remain swollen for a week or more, and joint pain can last for more than 2 weeks. Children who have rubella usually recover within 1 week, but adults may take longer.
Professional Treatment

Rubella cannot be treated with antibiotics because antibiotics do not work against viral infections. Unless there are complications, rubella will resolve on its own.

Any pregnant woman who has been exposed to rubella should contact her obstetrician immediately.
Home Treatment

Rubella is typically a mild illness, especially in kids. Infected children usually can be cared for at home. Monitor your child's temperature, and call the doctor if the fever climbs too high.

To relieve minor discomfort, you can give your child acetaminophen or ibuprofen. Avoid giving aspirin to a child who has a viral illness because its use in such cases has been associated with the development of Reye syndrome, which can lead to liver failure and death.
When to Call the Doctor

Call the doctor if your child develops a fever of 102° Fahrenheit (38.9° Celsius) or above (in a child younger than 6 months, call for a fever above 100.4° Fahrenheit, or 38° Celsius), or if your child appears to be getting sicker than the mild course of symptoms described above

Toxoplasmosis



Kongenital



1. Identifikasi

Merupakan penyakit sistemik Coccidian protozoan, infeksi biasanya tanpa gejala atau muncul dalam bentuk akut dengan gejala limfadenopati atau dengan gejala menyerupai mononucleosis infectiosa disertai dengan demam, linfadenopati dan linfositosis yang berlangsung sampai berhari-hari atau beberapa minggu.



Dengan terbentuknya antibodi, jumlah parasit dalam darah akan menurun namun kista Toxoplasma yang ada dalam jaringan tetap masih hidup. Kista jaringan ini akan reaktif kembali jika terjadi penurunan kekebalan. Infeksi yang terjadi pada orang dengan kekebalan rendah baik infeksi primer maupun infeksi reaktivasi akan menyebabkan terjadinya Cerebritis, Chorioretinitis, pneumonia, terserangnya seluruh jaringan otot, myocarditis, ruam makulopapuler dan atau dengan kematian. Toxoplasmosis yang menyerang otak sering terjadi pada penderita AIDS.



Infeksi primer yang terjadi pada awal kehamilan dapat menyebabkan terjadinya infeksi pada bayi yang dapat menyebabkan kematian bayi atau dapat menyebabkan Chorioretinitis, kerusakan otak disertai dengan kalsifikasi intraserebral, hidrosefalus, mikrosefalus, demam, ikterus, ruam, hepatosplenomegali, Xanthochromic CSF, kejang beberapa saat setelah lahir.



Jika infeksi terjadi pada usia kehamilan yang lebih tua dapat menyebabkan penyakit subklinis yang gejalanya akan timbul kemudian, misalnya berupa Chorioretinitis kronis yang berulang.



Pada wanita hamil dengan kekebalan tubuh yang rendah dengan Toxoplasma seropostif, dapat terjadi reaktivasi dari infeksi laten yang walaupun jarang dapat menyebabkan toxoplasmosis kongenital. Organisme yang “tidur” pada orang dengan infeksi laten dapat terjadi reaktivasi dan menyebabkan toxoplasmosis serebral terutama pada orang yang menderita imunodefisiensi seperti pada penderita AIDS.



Diagnosa ditegakkan selain berdasarkan gejala klinis juga didukung dengan pemeriksaan serologis atau ditemukannya organisme didalam jaringan atau cairan tubuh melalui biopsi atau nekropsi atau isolasi pada binatang atau pada kultur sel. Kenaikan titer antibodi menandakan adanya infeksi aktif. Ditemukannya IgM yang spesifik dan atau terjadinya peningkatan titer IgG pada darah yang diambil secara serial pada bayi baru lahir menunjukkan terjadinya infeksi kongenital. Titer IgG yang tinggi bisa bertahan selama bertahun tahun dan tidak ada hubunganya dengan penyakit aktif.



2. Penyebab Penyakit

Toxoplasma gondii, merupakan suatu coccidian protozoa intraseluler pada kucing, termasuk dalam famili Sarcocystidae yang dikelompokkan kedalam kelas Sporozoa



3. Distribusi Penyakit

Tersebar diseluruh dunia pada mamalia dan burung. Infeksi pada manusia umum terjadi.



4. Reservoir

Hospes definitif dari T. gondii adalah kucing dan hewan sejenis kucing lainnya yang mendapatkan infeksi karena kucing memakan mamalia (terutama rodentia ) atau burung yang terinfeksi dan jarang sekali infeksi terjadi dari kotoran kucing yang terinfeksi.

Hospes perantara dari T. gondii antara lain biri-biri, kambing, binatang pengerat, sapi, babi, ayam, dan burung. Semua binatang tersebut dapat mengandung stadium infektif (cystozoite atau bradizoite) dari T. gondii yang membentuk kista dalam jaringan terutama jaringan otot dan otak. Kista jaringan dapat hidup dalam jangka waktu panjang kemungkinan seumur hidup binatang tersebut.



5. Cara-cara Penularan

Infeksi transplasental pada manusia terjadi pada wanita hamil karena didalam tubuh mereka terdapat trachyzoites yang membelah dengan cepat beredar dalam darah mereka. Biasanya pada infeksi primer. Anak-anak terinfeksi karena menelan oocysts yang mencemari “sandboxes” (kotak berisi pasir tempat bermain), halaman tempat anak-anak bermain dimana ditempat-tempat itu kucing membuang kotoran. Infeksi bisa terjadi karena mengkonsumsi daging mentah atau yang tidak dimasak dengan sempurna (daging babi, daging kambing dan jarang daging sapi) dimana didalam daging tersebut mengandung kista.

Makanan dan air dapat juga tercemar kotoran kucing dan jika Oocysts yang infektif pada makanan dan air yang tercemar tertelan akan terjdi infeksi. Pernah dilaporkan terjadi KLB karena inhalasi Oocysts yang berbentuk spora. Susu dari kambing dan sapi yang terinfeksi mengandng tachyzoites. Pernah dilaporkan terjadi KLB karena minum susu kambing mentah. Infeksi jarang terjadi karena transfusi atau karena transplantasi organ dari donor yang terinfeksi.



6. Masa Inkubasi

Dari 10 sampai 23 hari pada satu KLB “Commonsource” karena makan daging yang tidak dimasak; 5 sampai 10 hari dari satu KLB yang ditularkan oleh kucing.



7. Masa Penularan

Tidak langsung ditularkan dari seseorang kepada orang lain kecuali in utero. Oocysts pada kucing akan membentuk spora dan menjadi infektif dalam 1 sampai 5 hari dan tetap infektif pada air dan tanah basah lebih dari satu tahun. Kista pada daging hewan yang terinfeksi bertahan dan tetap infektif selama daging itu belum dimasak.



8. Kerentanan Dan Kekebalan

Setiap orang rentan terhadap penyakit ini tetapi kekebalan akan terbentuk sesudah infeksi dan hampir semua infeksi bersifat asymptomatic. Lama dan tingkat kekebalan tidak diketahui dengan pasti diduga berlangsung lama dan seumur hidup; antibodi bertahan selama bertahun tahun, mungkin seumur hidup. Pasien yang mendapatkan terapi cytotoxic atau terapi immunosuppressive dan penderita AIDS berisiko tinggi menjadi sakit dan mendapat infeksi ulang.



9. Cara-cara pemberantasan

A. Cara-cara pencegahan

1). Berikan penyuluhan kepada para ibu tentang upaya pencegahan seperti berikut:

a). Daging yang akan dikonsumsi hendaknya daging yang sudah diradiasi atau yang sudah dimasak pada suhu 1500F (660C), daging yang dibekukan mengurangi infektivitas parasit tetapi tidak membunuh parasit.

b). Ibu hamil yang belum diketahui telah mempunyai antibodi terhadap T. gondii, dianjurkan untuk tidak kontak dengan kucing dan tidak membersihkan tempat sampah. Pakailah sarung tangan karet pada waktu berkebun dan cucilah tangan selalu setelah bekerja dan sebelum makan.

2). Kucing diberi makanan kering, makan yang diberikan sebaiknya makanan kaleng atau makanan yang telah dimasak dengan baik. Kucing jangan dibiarkan memburu sendiri makanannya (jaga agar kucing tetap didalam rumah sebagai binatang peliharaan).

3). Buanglah kotoran kucing dan sampah tiap hari (sebelum sporocysts menjadi infektif). Kotoran kucing dapat dibuang kedalam toilet yang saniter, dibakar atau ditanam dalam- dalam. Tempat pembuangan sampah di disinfeksi setiap hari dengan air mendidih. Pakailah sarung tangan atau cuci tangan dengan sabun dan air mengalir setelah menangani barang-barang yang terkontaminasi. Sampah kering dibuang sedemikian rupa tanpa menggoyang goyang agar oocysts tidak tersebar keudara.

4). Cucilah tangan baik-baik sebelum makan dan sesudah menjamah daging mentah atau setelah memegang tanah yang terkontaminasi kotoran kucing.

5). Awasi kucing liar, jangan biarkan kucing tersebut membuang kotoran ditempat bermain anak-anak. Kotak pasir tempat bermain anak ditutup jika tidak dipakai.

6). Penderita AIDS dengan toxoplasmosis simptomatik agar diberikan pengobatan profilaktik seumur hidup dengan pyremethamine, sulfadiazine dan asam folat.


B. Penanganan Penderita, Kontak, Lingkungan Sekitarnya

1). Laporan kepada Dinas Kesehatan setempat: Tidak diperlukan, tetapi di beberapa negara bagian di Amerika dan di beberapa negara penyakit ini wajib dilaporkan untuk pemahaman lebih lanjut terhadap epidemiologi dari penyakit ini.

2). Isolasi: Tidak ada

3). Disinfeksi serentak: Tidak dilakukan

4). Karantina: Tidak dilakukan

5). Imunisasi kontak: Tidak dilakukan

6). Investigasi kontak dan sumber infeksi: Pada infeksi kongenital lakukan pemeriksaan titer antibodi ibu; sedangkan pada infeksi yang didapat, periksalah titer antibodi pada anggota keluarga dan selidiki kemungkinan terjadinya pemajanan terhadap kotoran kucing, tanah, daging mentah tau terpajan dengan binatang yang terinfeksi.

7). Pengobatan spesifik: Untuk orang yang sehat dengan status imunitas yang baik, tidak ada indikasi untuk diberi pengobatan kecuali jika infeksi terjadi pada awal kehamilan atau adanya Chorioretinitis aktif, myocarditis atau ada organ lain yang terkena. Obat yang dipakai adalah Pyrimethamine (Daraprim®) dikombinasi dengan Sulfadiazine dan asam folat (untuk mencegah depresi sumsum tulang). Pengobatan diberikan selama 4 minggu untuk mereka yang menunjukkan gejala klinis berat. Selain obat diatas, untuk toxoplasmosis pada mata ditambahkan Clindamycin. Pada toxoplasmosis okuler, terjadi penurunan visus yang irreversible. Jika yang terserang mata maka yang dapat terkena adalah macula, syaraf mata atau papillomacular bundle, untuk mencegah hal ini diberikan kortikosteroid sistemik.Pengobatan terhadap wanita hamil menjadi masalah. Spiramycin sering digunakan untuk mencegah infeksi plasenta; jika pada pemeriksaan USG ada indikasi telah terjadi infeksi pada bayi maka berikan pengobatan pyrimethamine dan sulfadiazine.

Pyrimethamine tidak diberikan pada 16 minggu pertama kehamilan karena dikawatirkan akan terjadi teratogenik; dalam hal ini sulfadiazine dapat diberikan tersendiri. Bayi yang lahir dari ibu yang menderita infeksi primer atu dari ibu yang HIV positif selama kehamilan diberikan pengobatan pyrimethamine-sulfadiazine-asam folat selama tahun pertama sampai terbukti bahwa bayi tersebut tidak menderita toxoplasmosis kongenital. Hal ini dilakukan untuk mencegah terjadinya Chorioretinitis atau gejala sisa. Belum ada pegangan dan petunjuk yang jelas tentang pengobatan bayi yang lahir dari ibu yang HIV positif disertai toxoplasma seropositif.



C. Penanggulangan wabah: Tidak ada


D. Implikasi bencana: Tidak ada.


E. Tindakan Internasional : Tidak ada.









Toxoplasma



Gondii

Infection is often asymptomatic. Immunocompetent individuals may present with fever, lymphadenopathy, muscle aches, and headache. Congenitally infected children may suffer impaired vision and mental retardation. Immunosuppressed patients may have central nervous system disease (encephalitis).
Structure and Life Cycle

Members of the cat family (Felidae) are the definitive hosts; many mammals and birds serve as intermediate hosts. Infection is contracted by ingesting either oocysts or meat containing live organisms. Organisms enter the intestinal epithelium and can spread to many host tissues. Individual organisms are lunate, about 6 X 2 µm, and multiply within host cells. Tissue cysts containing hundreds of quiescent organisms may form as infection wanes. Toxoplasma reproduces sexually only in cats. Organisms infecting the intestinal epithelium produce oocysts which are shed in the feces. Mature oocysts are approximately 12 µm in diameter and contain eight infective sporozoites.
Classification and Antigenic Types

Toxoplasma gondii, a member of the Apicomplexa, is the sole species.
Multiplication and Life Cycle

A sexual multiplication by cell division can occur in virtually any host cell.
Pathogenesis

Host cells are destroyed by active multiplication of T gondii. Necrotic foci may result. Congenital infection often involves the retina and brain; focal chorioretinitis may result in impaired vision. Brain involvement in immunosuppressed patients may lead to large necrotic abscesses. Disease reactivation in immunosuppressed patients may result from the rupture of a tissue cyst.
Host Defenses

Immunocompetent individuals mount an effective cell mediated immune response that eradicates active infection within weeks or months and results in immunity against reinfection. Tissue cysts are unreactive and may persist for the life of the host.
Epidemiology

Toxoplasmosis shows a nonseasonal worldwide distribution. Most natural infections are acquired by ingesting undercooked meat containing tissue cysts or food contaminated by cat feces.
Diagnosis

Diagnosis is based on serology and on histologic examination of tissues.
Control

Infection may be prevented by thorough cooking of meat and by proper management of cats. Acute cases are treated with sulfadiazine and pyrimethamine.



INTRODUCTION

Toxoplasma gondii is an intestinal coccidium that parasitizes members of the cat family as definitive hosts and has a wide range of intermediate hosts. Infection is common in many warm-blooded animals, including humans. In most cases infection is asymptomatic, but devastating disease can occur.
Clinical Manifestations

Toxoplasma gondii usually parasitizes both definitive and intermediate hosts without producing clinical signs. In humans, severe disease is usually observed only in congenitally infected children and in immunosuppressed individuals, including patients with acquired immune deficiency syndrome (AIDS). Postnatally acquired infections may be local or generalized and are rarely severe in immunocompetent individuals. Lymphadenitis is the most common manifestation in humans. Any node can be infected, but the deep cervical nodes are the most commonly involved. Infected nodes are tender and discrete but not painful; the infection resolves spontaneously in weeks or months. Lymphadenopathy may be accompanied by fever, malaise, fatigue, muscle pains, sore throat, and headache.

Encephalitis is an important and severe manifestation of toxoplasmosis in immunosuppressed patients including patients with AIDS. Symptoms may include headache, disorientation, drowsiness, hemiparesis, reflex changes, and convulsions. Coma and death may ensue.

Prenatally acquired T gondii often infects the brain and retina and can cause a wide spectrum of clinical disease. Mild disease may consist of slightly diminished vision, whereas severely diseased children may exhibit a classic tetrad of signs: retinochoroiditis, hydrocephalus, convulsions, and intracerebral calcifications. Hydrocephalus is the least common but most dramatic lesion of congenital toxoplasmosis (Fig. 1). Ocular disease is the most common sequela.



FIGURE 84-1 Girl with hydrocephalus due to congenital toxoplasmosis. (From Dubey JP, and Beattie CP. Toxoplasmosis of animals and Man. CRC Press, Baca Raton, Florida, 52, 1988.)

Toxoplasma gondii is capable of causing severe disease in animals other than humans. It is one of the major causes of abortion in sheep and goats in many countries, including Australia and the United States. It is important to diagnose toxoplasmic abortion to distinguish it from other causes of abortion, because congenital transmission of T gondii occurs only during the initial infection of the mother and the animal is safe for breeding thereafter. Cats, dogs, and many other pets can die of pneumonia, hepatitis, and encephalitis due to toxoplasmosis. In dogs, clinical toxoplasmosis is often associated with concurrent distemper virus infection. Certain species of marsupials and New World monkeys are highly susceptible to toxoplasmosis.
Structure, Multiplication, and Life Cycle

The life cycle of T gondii was described only in 1970, when it was discovered that the definitive hosts are members of the family Felidae, including domestic cats. Various warm-blooded animals serve as intermediate hosts. Toxoplasma gondii is transmitted by three known modes: congenitally, through the consumption of uncooked infected meat, and via fecal matter. Figure 2 shows the life cycle of T gondii.



Figure 84-2 Life cycle of Toxoplasma gondii. Cats, the definitive hosts of T gondii, can become infected by ingesting sporulated oocysts or (most often) infected animals. The oocysts are infectious to most mammals and birds. Toxoplasma can be transmitted to intermediate hosts through oocysts, by carnivorism, or transplacentally. Transplacental transmission is most important in humans and sheep. (From Dubey JP, Toxoplasmosis. J Am Vet Med Assoc 189:166, 1986.)

Cats acquire Toxoplasma by ingesting any of three infectious stages of the organism: the rapidly multiplying forms called tachyzoites (Fig. 3), the quiescent bradyzoites that occupy cysts in infected tissue (Fig. 4), and the oocysts shed in feces (Fig. 5). Successful infection of the cat is revealed by the shedding of oocysts in the feces. The chance of infection and the prepatent period (the time between infection and the shedding of oocysts) varies with the stage of T gondii ingested. Fewer than 50 percent of cats shed oocysts after ingesting tachyzoites or oocysts, whereas nearly all cats shed oocysts after ingesting tissue cysts. Only the cyst-induced cycle has been studied in detail.



FIGURE 84-3 Tachyzoites of T gondii.

A. Extracellular (arrow) released from host cells. Compare their size with red blood cells and a lymphocyte. Impression smear, Giemsa stain. Bar = 20 µm.

B. Intracellular in cell culture. Note a group arranged in a rosette (arrow) and vacuole (arrowhead) around a tachyzoite. Immunohistochemical stain with a tachyzoite-specific monoclonal antibody. Bar = 20 µm.

C. Transmission electron micrograph of an intracellular tachyzoite. Note a parasitophorous vacuole (PV) around the tachyzoite. Parasite organelles visible in this picture include a conoid (c), micronemes (m), dense granules (dg) nucleus (n) and rhoptries (r). Bar=0.8 µm. (Courtesy of Dr. D.S. Lindsay, Auburn University, AL.)



FIGURE 84-4 Tissue cysts of T gondii.

A. Tissue cyst freed from mouse brain. Note a thin (arrow) cyst wall enclosing hundreds of bradyzoites. Unstrained. Bar = 20 µm.

B. Two tissue cysts (arrows) in section of brain. Hematoxylin and eosin stain. Bar = 20 µm.

C. Transmission electron micrograph of a small tissue cyst in cell culture. Note thin cyst wall (arrow) enclosing 6 bradyzoites (arrowheads). Bar = 1.0 µm. (Courtesy of Dr. D.S. Lindsay, Auburn University, Auburn, AL.)

When a cat ingests meat containing tissue cysts, the cyst wall is dissolved by the proteolytic enzymes in the stomach and small intestine, releasing the bradyzoites. The bradyzoites, which are a slow multiplying stage, penetrate the epithelial cells of the small intestine and initiate the formation of numerous asexual generations before the sexual cycle (gametogony, the production of gametes) begins (Fig. 5A). After the male gamete (Fig. 5B) fertilizes the female gamete, two walls are laid down around the fertilized zygote to form the oocyst, which is excreted in the feces in an unsporulated stage (Fig. 5C).



FIGURE 84-5 Sexual states of T gondii

A. Schizonts (double arrowheads), female gamonts (arrows), and male gamonts (arrowheads) in section of superficial epithelial cells of the small intestine of a cats. Hematoxylin and eosin stain. Bar = 15 µm.

B. Three male gametes each with 2 flagella (arrowheads) compared with a merozoite (arrow). Impression of intestinal epithelium of a cat. Giemsa stain. Bar = 10 µm.

C. Unsporulated oocytes (arrowheads) in feces of a cat. Note 2 oocysts of another feline coccidium, Isospora felis (arrowheads). Isospora felis sporulates faster than T gondii. The oocysts on top of the picture already contains 2 sporocysts while all T gondii oocysts are unsporulated. Unstained. Bar - 65 µm.

D. Transmission electron micrograph of a sporulated oocyst. Note thin oocyst wall (arrow), 2 sporocysts (arrowheads) and 4 sporozoites (double arrowheads) in sporocysts. Bar - 2.25 µm. (Courtesy of Dr. D.S. Lindsay, Auburn University, Auburn, AL.)

Oocysts measure approximately 10 by 12 µm. Sporulation occurs outside the body, and the oocyst becomes infectious 1 to 5 days after excretion. Each sporulated oocyst contains two sporocysts and each sporocyst contains four sporozoites (Fig. 5D). Sporulated oocysts are remarkably resistant and can survive in soil for several months.

At the same time that some bradyzoites enter the surface epithelial cells of the feline intestine and multiply there to produce oocysts, other bradyzoites penetrate the lamina propria and begin to multiply as tachyzoites. Tachyzoites are about 6 X 2 µm in size and generally lunate (Fig. 3A). Within a few hours of infection, tachyzoites may disseminate to extraintestinal tissues through the lymph and blood. Tachyzoites can enter almost any type of host cell (Fig. 3C) and multiply until the host cell is filled with parasites and dies (Fig. 3B). The released tachyzoites enter new host cells and multiply. This cycle may result in microfoci of tissue necrosis. The host usually overcomes this phase of infection, and the parasite then enters the "resting" stage in which bradyzoites are isolated in tissue cysts. Tissue cysts are formed most commonly in the brain, liver, and muscles. Cysts in neural tissues are up to 60 µm in diameter and contain hundreds of bradyzoites in a thin membrane (Fig. 4). Tissue cysts usually cause no host reaction and may remain for the life of the host.

In nonfeline intermediate hosts, such as humans or mice, the extraintestinal cycle of T gondii is similar to the cycle in cats. However, sexual stages are produced only in the feline definitive hosts.
Pathogenesis

Most cases of toxoplasmosis in humans are probably acquired by the ingestion of either tissue cysts in infected meat or oocysts in food contaminated with cat feces. Bradyzoites from the tissue cysts or sporozoites released from oocysts penetrate the intestinal epithelial cells and multiply in the intestine. Toxoplasma gondii may spread both locally to mesenteric lymph nodes and to distant organs by invading the lymphatics and blood. Necrosis in intestinal and mesenteric lymph nodes may occur before other organs become severely damaged. Focal areas of necrosis may develop in many organs. The clinical picture is determined by the extent of injury to these organs, especially to vital and vulnerable organs such as the eye, heart, and adrenals. Toxoplasma gondii does not produce a toxin; necrosis is caused by intracellular multiplication of tachyzoites.

Opportunistic toxoplasmosis in AIDS patients usually represents reactivation of chronic infection. The predominant lesion of toxoplasmosis - encephalitis in these patients is necrosis, which often results in multiple abscesses, some as large as a tennis ball (Fig. 6).



Host Defenses

The host may die from toxoplasmosis but much more often recovers and acquires immunity. Inflammation usually follows necrosis. By about the third week after infection, Toxoplasma gondii tachyzoites begin to disappear from visceral tissues and may localize as tissue cysts in neural and muscular tissues. Toxoplasma tachyzoites may persist longer in the spinal cord and brain because immune responses are less effective in these organs. Chronic infections may be reactivated locally (for example, in the eye). Reactivation possibly results from the rupture of a tissue cyst. Probably tissue cysts rupture periodically during the life of the host, and the bradyzoites released are normally destroyed by the host's immune responses. This reaction may cause local necrosis accompanied by inflammation. Hypersensitivity is said to play a major role in such reactions; however, in immunocompetent hosts the infection usually subsides, with no local renewed multiplication of Toxoplasma. In immunosuppressed patients, rupture of a tissue cyst may result in renewed multiplication of bradyzoites into tachyzoites, and the host may die from toxoplasmosis. The cause of cyst rupture is not known. Chronic latent T gondii infection can be experimentally reactivated by excessive doses of corticosteroids, antilymphocyte serum and other immunosuppressive therapies.
Epidemiology

Toxoplasma gondii infection in humans is widespread throughout the world. Approximately half a billion humans have antibodies to T gondii. The incidence of infection in humans and animals may vary in different parts of a country. The cause for these variations is not yet known: environmental conditions, cultural habits, and animal species are among factors that may determine the degree of natural spread of Toxoplasma gondii. Only a small proportion (less than 0.1 percent) of people acquire infection congenitally. Immunocompetent mothers of congenitally infected children do not give birth to infected children in subsequent pregnancies. However, repeated congenital infection can occur in mice, rats, guinea pigs, and hamsters without reinfection from outside sources.

The relative frequency with which postnatal toxoplasmosis is acquired by eating raw meat and by ingesting food contaminated by oocysts from cat feces is unknown and difficult to investigate. Both modes of infection are reported to cause clinical toxoplasmosis. Toxoplasma gondii infection occurs commonly in many animals used for food (for example, sheep, goats, pigs, and rabbits). Infection is less prevalent in cattle than in sheep or pigs.

Oocysts are shed by cats - not only the domestic cat - but also other felids such as ocelots, margays, jaguarundi, bobcats, Pallas cats, and Bengal tigers. However, oocyst formation is greatest in the domestic cat. Widespread natural infection is possible because a cat may excrete millions of oocysts after ingesting few tissue cysts. Oocysts are resistant to most ordinary environmental conditions and can survive in moist conditions for months and even years. Invertebrates such as flies, cockroaches, and earthworms can spread oocysts mechanically.

Only a few cats may be involved at any one time in spreading T gondii in an area: at any given time as little as 1 percent of the domestic cat population in the United States is shedding oocysts. It is not known whether cats shed oocysts only once or several times in nature. Under experimental conditions, cats usually do not shed oocysts after reinoculation with T gondii tissue cysts, but this immunity to T gondii in cats does wane with time.
Diagnosis

Diagnosis of toxoplasmosis can be aided by serologic or histocytologic examination. Clinical signs of toxoplasmosis are nonspecific and cannot be depended on for a definite diagnosis; toxoplasmosis clinically mimics several other infectious diseases.

Many serologic tests have been used to detect antibodies to T gondii. The most reliable of these is the Sabin-Feldman dye test. Live virulent tachyzoites of T gondii are used as antigen and are exposed to dilutions of the test serum and to a complement accessory factor resembling complement that is obtained from Toxoplasma-antibody free-human serum. This test is sensitive and so far is the most specific test for toxoplasmosis. Its main disadvantages are its high cost and the human hazard of using live organisms.

The indirect fluorescent antibody test (IFAT) overcomes some of the disadvantages of the dye test. In IFAT, killed tachyzoites of Toxoplasma, which are available commercially, are used as antigen. Titers obtained by IFAT are similar to those from the dye test. Disadvantages of the IFAT are that a microscope with UV light is needed, fluorescent anti-species globulin is required for each species to be tested, and false-positive titers may occur in hosts with anti-nuclear antibodies. The suitability of IFAT in animal diagnostic work is therefore limited, but it has proved useful in diagnosing acquired human toxoplasmosis. Other serologic tests including the indirect hemagglutination test, the latex agglutination test, modified agglutination test, and the enzyme-linked immunoabsorbent assay (ELISA), offer some advantages. For example, agglutination tests are easy to perform.

Soluble antigens used for indirect hemagglutination tests are now commercially available in several countries, including the United States. Although this test is easy to perform, it usually does not detect antibodies during the acute phase of toxoplasmosis. In the modified agglutination test, whole killed tachyzoites are used as antigen, and the test serum is treated with 2-mercaptoethanol to eliminate nonspecific agglutinins. The ELISA test using soluble antigens appears to be specific and may become the standard test in the future.

A single positive serum sample proves only that the host has been infected at some time in the past. Serologic evidence for an acute acquired infection is obtained when antibody titers rise by a factor of 4 to 16 in serum taken 2 to 4 weeks after the initial serum collection, or when specific IgM antibody is detected. The finding of antibody in even undiluted serum is useful in the diagnosis of ocular toxoplasmosis because patients with this disorder usually have low T gondii antibody titers.

Diagnosis can be made by finding T gondii in host tissue removed by biopsy or at necropsy. This procedure is particularly useful in immunosuppressed patients or patients with AIDS, in whom antibody synthesis may be delayed and low. Toxoplasma gondii infection can be rapidly diagnosed by making impression smears of lesions on glass slides. After drying for 10 to 30 minutes, the smears are fixed in methyl alcohol and stained with Giemsa stain. Well-preserved T gondii organisms are crescent-shaped and stain well with any of the Romanowsky stains (Fig. 3A); however, degenerating organisms common in lesions usually appear oval and have cytoplasm that stains poorly compared to the nucleus. A diagnosis of toxoplasmosis should not be made unless organisms with the typical structure are seen, as degenerating host cells may resemble degenerating T gondii parasites. In thin sections the tachyzoites are oval to round and usually do not stain differently from host cells. Tissue cysts are occasionally encountered in areas with lesions (Fig. 4B). Tissue cysts are usually spherical and have silver-positive walls; the bradyzoites stain strongly with periodic acidSchiff stain. Immunohistochemical staining and polymerase chain reaction (PCR) can be used to identify T gondii tissue cysts or tachyzoites in tissues, even those fixed in formalin. Electron-micrographic examination can aid in diagnosis (Fig. 3C). Computed tomography techniques are also useful in the diagnosis of human cerebral toxoplasmosis. Inoculation of biopsy materials into laboratory mice and/or cell cultures can help diagnosis.
Control

Sulfonamides and pyrimethamine (Daraprim) are two drugs widely used to treat toxoplasmosis in humans. They act synergistically by blocking the metabolic pathway involving p-aminobenzoic acid and the folic-folinic acid cycle, respectively. These two drugs usually are well tolerated by the patient, but sometimes thrombocytopenia, leukopenia, or both may develop. These effects can be overcome without interrupting treatment by administering folinic acid and yeast because the vertebrate host can utilize presynthesized folinic acid, whereas T gondii cannot. The commonly used sulfonamides, sulfadiazine, sulfamethazine, and sulfamerazine, are all effective against toxoplasmosis. Generally, any sulfonamide that diffuses across the host cell membrane is useful in antitoxoplasmid therapy. Although these drugs are helpful when given in the acute stage of the disease, usually they will not eradicate infection when active multiplication of the parasite occurs. Because sulfa compounds are excreted within a few hours of administration, they must be administered in daily divided doses. Spiramycin, a drug used in France to treat pregnant women to minimize the effects of congenital toxoplasmosis, is not approved for toxoplasmosis in the United States. As yet, there are no effective drugs to kill tissue cysts.

No killed vaccine is currently available to reduce or prevent congenital infections in humans and animals, but research to develop such an agent is under way. A live vaccine using a nonpersistent T gondii strain is available in Europe and New Zealand to reduce abortion in sheep.

To prevent T gondii infection, several precautions should be taken. Meat should be cooked to 66°C throughout before eating. Hands should be washed with soap and water after handling meat. Raw meat should never be fed to cats; only dry or canned food or cooked meat should be fed. Cats should be kept indoors and litter boxes changed daily. Cat feces should be flushed down the toilet or burned. Litter pans should be cleaned by immersing them in boiling water. Gloves should be used while working in the garden. Children's sandboxes should be covered when not in use.


REFERENCES

Dubey JP, Beattie CP: Toxoplasmosis of Animals and Man. CRC Press, Boca Raton, FL, 1988

Gazzinelli RT, Denkers EY, Sher A.: Host resistance to Toxoplasma gondii: model for studying the selective induction of cell-mediated immunity by intracellular parasites. Infect Agent Dis 2:139, 1993

Georgie VA: Management of toxoplasmosis. Drugs, 48:179, 1994

Guerina NG, Hsu HW, Meissner HC, Meissner HC, et al. Neonatal serologic screening and early treatment for congenital Toxoplasma gondii infection. N Eng J Med, 330:1858, 1994

Remington, JS, McLeond R, Desmonts G.: Toxoplasmosis. In: Remington JS, Klein JO, (eds.): Infectious Diseases of the Fetus and Newborn Infant. Philadelphia: W.B. Saunders Company, 1995

Saturday, October 07, 2006

Tentang RUBELLA

1. Identifikasi

Rubella adalah penyakit yang disebabkan oleh virus dan menimbulkan demam ringan dengan ruam pungtata dan ruam makulopapuler yang menyebar dan kadang-kadang mirip dengan campak atau demam scarlet. Anak-anak biasanya memberikan gejala konstitusional yang minimal, tetapi orang dewasa akan mengalami gejala prodromal selama 1-5 hari berupa demam ringan, sakit kepala, malaise, coryza ringan dan konjungtivitis. Limfadenopati post aurikuler, oksipital dan servikal posterior muncul dan merupakan ciri khas dari infeksi virus ini yang biasanya muncul 5-10 hari sebelum timbulnya ruam. Hampir separuh dari infeksi ini tanpa ruam. Lekopeni umum terjadi dan trombositopeni juga bisa terjadi, tetapi manifestasi perdarahan jarang. Arthalgia dan, yang lebih jarang terjadi, arthritis sebagai komplikasi infeksi ini terutama pada wanita dewasa. Ensefalitis dan trombositopeni jarang terjadi pada anak-anak; ensefalitis terjadi lebih sering pada orang dewasa.

Rubella menjadi penting karena penyakit ini dapat menimbulkan kecacatan pada janin. Sindroma rubella congenital (Congenital Rubella Syndrome, CRS) terjadi pada 90% bayi yang dilahirkan oleh wanita yang terinfeksi rubella selama trimester pertama kehamilan; risiko kecacatan congenital ini menurun hingga kira-kira 10-20% pada minggu ke-16 dan lebih jarang terjadi bila ibu terkena infeksi pada usia kehamilan 20 minggu.

Infeksi janin pada usia lebih muda mempunyai risiko kematian di dalam rahim, abortus spontan dan kecacatan congenital dari sistem organ tubuh utama. Cacat yang terjadi bisa satu atau kombinasi dari jenis kecacatan berikut seperti tuli, katarak, mikroftalmia, glaucoma congenital, mikrosefali, meningoensefalitis, keterbelakangan mental, patent ductus arteriosus, defek septum atrium atau ventrikel jantung, purpura, hepatosplenomegali, icterus dan penyakit tulang radiolusen. Penyakit CRS yang sedang dan berat biasanya sudah dapat diketahui ketika bayi baru lahir; sedangkan kasus ringan yang mengganggu organ jantung atau tuli sebagian, bisa saja tidak terdeteksi beberapa bulan bahkan hingga beberapa tahun setelah bayi baru lahir. Diabetes mellitus dengan ketergantungan insulin diketahui sebagai manifestasi lambat dari CRS. Malformasi congenital dan bahkan kematian janin bisa terjadi pada ibu yang menderita rubella tanpa gejala.

Membedakan rubella dengan campak (q.v.), demam scarlet (lihat infeksi Streptokokus) dan penyakit ruam lainnya (misalnya infeksi eritema dan eksantema subitum) perlu dilakukan karena gejalanya sangat mirip. Ruam makuler dan makulopapuler juga terjadi pada sekitar 1-5% penderita dengan infeksi mononucleosis (terutama jika diberikan ampisilin), juga pada infeksi dengan enterovirus tertentu dan sesudah mendapat obat tertentu.

Diangosa klinis rubella kadang tidak akurat. Konfirmasi laboratorium hanya bisa dipercaya untuk infeksi akut. Infeksi rubella dapat dipastikan dengan adanya peningkatan signifikan titer antibodi fase akut dan konvalesens dengan tes ELISA, HAI, pasif HA atau tes LA, atau dengan adanya IgM spesifik rubella yang mengindikasikan infeksi rubella sedang terjadi.

Sera sebaiknya dikumpulkan secepat mungkin (dalam kurun waktu 7-10 hari) sesudah onset penyakit dan pengambilan berikutnya setidaknya 7-14 hari (lebih baik 2-3 minggu) kemudian. Virus bisa diisolasi dari faring 1 minggu sebelum dan hingga 2 minggu sesudah timbul ruam. Virus bisa ditemukan dari contoh darah, urin dan tinja. Namun isolasi virus adalah prosedur panjang yang membutuhkan waktu sekitar 10-14 hari. Diagnosa dari CRS pada bayi baru lahir dipastikan dengan ditemukan adanya antibodi IgM spesifik pada spesimen tunggal, dengan titer antibodi spesifik terhadap rubella diluar waktu yang diperkirakan titer antibodi maternal IgG masih ada, atau melalui isolasi virus yang mungkin berkembang biak pada tenggorokan dan urin paling tidak selama 1 tahun. Virus juga bisa dideteksi dari katarak kongenital hingga bayi berumur 3 tahun.



2. Penyebab penyakit: Virus rubella (famili Togaviridae; genus Rubivirus).



3. Distribusi penyakit

Tersebar di seluruh dunia, umumnya endemis, kecuali pada masyarakat yang terisolasi, terutama masyarakat kepulauan tertentu yang mengalami KLB setiap 10-15 tahun. Penyakit ini banyak muncul pada musim dingin dan musim semi. Wabah yang sangat luas terjadi di AS pada tahun 1935, 1943 dan 1964 dan di Australia pada tahun 1940. Sebelum vaksin rubella diijinkan beredar pada tahun 1969, puncak insidensi rubella terjadi di AS setiap 6-9 tahun sekali. Selama tahun 1990-an insidensi rubella di AS menurun dengan drastic. Namun persentasi kasus diantara orang asing yang lahir disana meningkat tajam pada saat yang sama. Selama tahun 1990-an, KLB rubella di AS terjadi di tempat kerja, pada institusi, di masyarakat umum dan lingkungan lain dimana anak-anak muda dan mereka yang berangkat dewasa berkumpul. Virus rubella bertahan pada orang yang tidak diimunisasi.






4. Reservoir: - Manusia.

5. Cara Penularan

Kontak dengan sekret nasofaring dari orang terinfeksi. Infeksi terjadi melalui droplet atau kontak langsung dengan penderita. Pada lingkungan tertutup seperti di asrama calon prajurit, semua orang yang rentan dan terpajan bisa terinfeksi. Bayi dengan CRS mengandung virus pada sekret nasofaring dan urin mereka dalam jumlah besar, sehingga menjadi sumber infeksi.



6. Masa inkubasi: dari 14-17 hari kisaran antara 14-21 hari.

7. Masa penularan

Sekitar 1 minggu sebelum dan paling sedikit 4 hari sesudah onset ruam; penyakit ini sangat menular. Bayi dengan CRS kemungkinan tetap mengandung virus selama berbulan-bulan sesudah lahir.

8. Kerentanan dan Kekebalan

Semua orang rentan terhadap infeksi virus rubella setelah kekebalan pasif yang didapat melalui plasenta dari ibu hilang. Imunitas aktif didapat melalui infeksi alami atau setelah mendapat imunisasi; kekebalan yang didapat biasanya permanent sesudah infeksi alami dan sesudah imunisasi diperkirakan kekebalan juga akan berlangsung lama, bisa seumur hidup, namun hal ini tergantung juga pada tingkat endemisitas. Di AS, sekitar 10% dari penduduk tetap rentan. Bayi yang lahir dari ibu yang imun biasanya terlindungi selama 6-9 bulan,tergantung dari kadar antibodi ibu yang didapat secara pasif melalui plasenta.



9. Cara-cara Pemberantasan

A. Tindakan pencegahan

1) Lakukan penyuluhan kepada masyarakat umum mengenai cara penularan dan pentingnya imunisasi rubella. Penyuluhan oleh petugas kesehatan sebaiknya menganjurkan pemberian imunisasi rubella untuk semua orang yang rentan. Upaya diarahkan untuk meningkatkan cakupan imunisasi rubella pada orang dewasa dan dewasa muda yang rentan; perlu dikaji tingkat kekebalan orang-orang yang lahir di luar AS, hal ini perlu diberikan Perhatian khusus.

2) Berikan dosis tunggal vaksin hidup, yaitu vaksin virus rubella yang dilemahkan (Rubella virus vaccine, Live), dosis tunggal ini memberikan respons antibodi yang signifikan, yaitu kira-kira 98-99% dari orang yang rentan.





3) Vaksin ini dikemas dalam bentuk kering dan sesudah dilarutkan harus disimpan dalam suhu 2-80C (35,60- 46,40F) atau pada suhu yang lebih dingin dan dilindungi dari sinar matahari agar tetap poten. Vaksin virus bisa ditemukan pada nasofaring dari orang-orang yang telah diimunisasi pada minggu ke-2 hingga ke-4 sesudah imunisasi, umumnya hanya bertahan selama beberapa hari, namun virus ini tidak menular. Di AS, imunisasi kepada semua anak-anak direkomendasikan diberikan pada usia 12-15 bulan sebagai bagian dari vaksin kombinasi campak dan vaksin gondongan (Measles Mumps and Rubella=MMR) dan dosis kedua MMR diberikan pada usia anak masuk sekolah atau dewasa muda. Ditemukannya penyakit rubella terus-menerus diantara orang-orang yang lahir di luar AS, mengindikasikan bahwa pemberian imunisasi rubella harus dilakukan pada komunitas ini. Vaksin rubella dapat diberikan kepada semua wanita yang tidak hamil tanpa kontraindikasi. Dewasa muda yang rentan dan mempunyai riwayat kontak dengan anak-anak atau berkumpul bersama di kampus atau institusi lain seperti tinggal di asrama sebaiknya diimunisasi. Semua petugas kesehatan sebaiknya sudah kebal terhadap rubella terutama orang-orang yang kontak dan merawat penderita di bagian prenatal. Bukti adanya kekebalan diindikasikan dengan adanya antibodi spesifik terhadap rubella dan pemeriksaan laboratorium atau bukti tertulis bahwa seseorang telah diimunisasi rubella pada saat atau sesudah ulang tahunnya yang pertama.

Vaksin rubella sebaiknya tidak diberikan kepada orang yang tidak mempunyai sistem kekebalan atau mendapat terapi imunosupresif; namun MMR direkomendasikan untuk diberikan kepada orang-orang dengan infeksi HIV yang asimtomatik. Pemberian vaksin MMR sebaiknya dipertimbangkan bagi penderita HIV dengan gejala. Secara teoritis, wanita yang diketahui hamil atau merencanakan hamil, 3 bulan mendatang sebaiknya tidak diimunisasi. Namun dari hasil catatan di CDC Atlanta menunjukkan bahwa dari 321 wanita yang diimunisasi rubella pada waktu hamil, semuanya melahirkan aterm dengan bayi yang sehat.

Hal-hal yang perlu diperhatikan pada program imunisasi rubella adalah selalu menanyakan kepada wanita pasca pubertas apakah mereka hamil, dan mereka yang menyatakan ya tidak diberikan imunisasi dan kepada yang lain yang tidak hamil diberi penjelasan pentingnya mencegah kehamilan selama 3 bulan mendatang serta diberi penjelasan risiko teoritis yang akan terjadi jika hal ini dilanggar. Status imunisasi seseorang hanya dapat dapat dipercaya bila dilakukan tes serologis, namun hal ini tidak terlalu penting untuk diketahui sebelum pemberian imunisasi karena vaksin ini sangat aman diberikan kepada orang yang sudah kebal. Di beberapa negara, imunisasi rutin diberikan kepada gadis remaja usia 11 hingga 13 tahun dengan atau tanpa tes antibodi sebelumnya. Di banyak negara yaitu AS, Australia dan Skandinavia, dosis kedua vaksin MMR direkomendasikan untuk diberikan kepada remaja pria maupun wanita. Untuk lebih jelasnya, lihat penjelasan mengenai Campak, 9A1.

4) Jika diketahui adanya infeksi alamiah pada awal kehamilan, tindakan aborsi sebaiknya dipertimbangkan karena risiko terjadinya cacat pada janin sangat tinggi. Pada beberapa penelitian yang dilakukan pada wanita hamil yang tidak sengaja diimunisasi, kecacatan kongenital pada bayi yang lahir hidup tidak ditemukan; dengan demikian imunisasi yang terlanjur diberikan pada wanita yang kemudian ternyata hamil tidak perlu dilakukan aborsi, tetapi risiko mungkin terjadi sebaiknya dijelaskan. Keputusan akhir apabila akan dilakukan aborsi diserahkan kepada wanita tersebut dan dokter yang merawatnya.

5) IG yang diberikan sesudah pajanan pada awal masa kehamilan mungkin tidak melindungi terhadap terjadinya infeksi atau viremia, tetapi mungkin bisa mengurangi gejala klinis yang timbul. IG kadang-kadang diberikan dalam dosis yang besar (20 ml) kepada wanita hamil yang rentan yang terpajan penyakit ini yang tidak menginginkan dilakukan aborsi karena alasan tertentu, tetapi manfaatnya belum terbukti.



B. Pengawasan penderita, kontak dan lingkungan sekitar

1) Laporan kepada petugas kesehatan setempat: Semua kasus rubella dan CRS harus dilaporkan. Di AS, laporan wajib dilakukan, Kelas 3 B (lihat tentang pelaporan penyakit menular).

2) Isolasi: Di rumah sakit dan institusi lain, terhadap penderita yang dicurigai menderita rubella sebaiknya dirawat dengan tindakan pencegahan isolasi kontak dan ditempatkan di ruang terpisah; upaya harus dilakukan untuk mencegah pajanan kepada wanita hamil yang tidak diimunisasi . Anak-anak yang sakit dilarang ke sekolah dan begitu juga orang dewasa yang sakit dilarang bekerja selama 7 hari sesudah munculnya ruam. Bayi dengan CRS mungkin mengandung virus dalam tubuhnya untuk jangka waktu yang lama. Semua orang yang kontak dengan bayi dengan CRS harus sudah kebal terhadap rubella dan bayi-bayi ini sebaiknya dipisahkan di ruang isolasi. Terhadap bayi yang menderita CRS ini tindakan tindakan kewaspadaan isolasi sebaiknya diberlakukan setiap saat bayi ini dirawat di rumah sakit sebelum bayi berusia 1 tahun, kecuali hasil kultur faring dan urin negatif tidak ditemukan virus sesudah bayi berumur lebih dari 3 bulan.

3) Disinfeksi serentak: Tidak dilakukan.

4) Karantina: Tidak dilakukan.

5) Imunisasi kontak: Pemberian imunisasi selama tidak ada kontraindikasi (kecuali selama kehamilan) tidak mencegah infeksi atau kesakitan. Imunisasi pasif dengan IG tidak dianjurkan (kecuali seperti yang dijelaskan pada 9A4 di atas).

6) Investigasi kontak dan sumber infeksi: Lakukan investigasi dan identifikasi wanita hamil yang kontak dengan penderita, terutama wanita hamil pada trimester pertama. Mereka yang pernah kontak dengan penderita ini sebaiknya dilakukan pemeriksaan serologis untuk melihat tingkat kerentanannya atau untuk melihat apakah ada infeksi awal (antibodi IgM) dan terhadap mereka diberi nasihat seperlunya.

7) Pengobatan spesifik: Tidak ada.



C. Penanggulangan wabah

1) Untuk menanggulangi KLB rubella, laporkan segera seluruh penderita dan tersangka rubella dan seluruh kontak dan mereka yang masih rentan diberi imunisasi.

2) Petugas dan praktisi kesehatan serta masyarakat umum sebaiknya diberi informasi tentang adanya KLB rubella agar dapat mengidentifikasi dan melindungi wanita hamil yang rentan.



D. Implikasi bencana: Tidak ada.

E. Tindakan Internasional: Tidak ada.

ABOUT CYTOMEGALO VIRUS (CMV)

Cytomegalovirus (CMV)

What Is CMV?

Cytomegalovirus (CMV) is an opportunistic infection. The virus is very common. Between 50% and 85% of the US population tests positive for CMV by the time they are 40 years old. A healthy immune system keeps this virus in check.

When the immune defenses are weak, CMV can attack several parts of the body. This can be caused by various diseases including HIV. Combination antiviral therapy has reduced the rate of CMV in people with HIV by 75%. However, about 5% of people with HIV still develop CMV disease.

The most common illness caused by CMV is retinitis. This is the death of cells in the retinas, the back of the eye. It can quickly cause blindness unless treated. CMV can spread throughout the body and infect several organs at once. The risk of CMV is highest when CD4 cell counts are below 50. It is rare in people with 100 or more T-cells.

The first signs of CMV retinitis are vision problems such as moving black spots. These are called "floaters." They may indicate an inflammation of the retina. Patients may also notice light flashes, decreased or distorted vision, or blind spots. Some doctors recommend eye exams to catch CMV retinitis. The exams are done by an ophthalmologist (an eye specialist). If your CD4 count is below 100 and you experience any vision problems, tell your doctor immediately.

Some patients who have recently started using anti-HIV medications can get inflammation in their eyes, causing loss of vision. This is called immune restoration syndrome (see Fact Sheet 473).


How Is CMV Treated?

The first treatments for CMV required daily intravenous infusions. Most people had a permanent medication "port" inserted into their chest or arm. People had to keep taking anti-CMV drugs for life.

CMV treatments have improved dramatically over the past several years. There are now seven CMV treatments approved by the FDA.

Strong HIV medications can improve the immune system. Patients can stop taking CMV drugs if their CD4 cell count goes over 100 to 150 and stays there for at least three months. However, there are two special cases:
Immune restoration syndrome can cause severe inflammation in the eyes of people with HIV even if they didn't have CMV before. The usual treatment is to add anti-CMV drugs to the patient's anti-HIV drugs.
If the CD4 count drops below 50, there is an increased risk of developing CMV disease.


Can CMV Be Prevented?

Ganciclovir was approved for prevention (prophylaxis) of CMV. However, many physicians don't prescribe it. They don't want to add up to 12 capsules a day for their patients. Also, it's not clear that it does any good. Two large studies came to different conclusions. Finally, strong antiviral medications keep most people's CD4 counts high enough so that they won't get CMV.


How Do I Choose a Treatment for CMV?

There are several issues to consider when choosing a treatment for active CMV disease.

Is your vision at risk? You may need to take quick action to save your eyesight.

How effective is it? Intravenous ganciclovir is the most effective overall CMV treatment. Implants are very good at stopping retinitis. However, they only work in the eye with the implant.

How is it administered? Pills are the easiest to manage. Intravenous (IV) medication involves needle sticks or a medication line that might become infected. Ocular injections mean inserting a needle directly into the eye. Implants, which last six to eight months, take about an hour to insert in an office procedure.

Is it a local therapy or systemic? Local therapies affect just the eyes. CMV retinitis can progress rapidly and lead to blindness. For this reason, it is treated aggressively when it first shows up. The newer injections or implants put medication directly into the eye and have the greatest impact on retinitis.

CMV can also show up in other places in the body. To control CMV in the rest of the body, you need a systemic (whole-body) therapy. Intravenous medication can be used, or valganciclovir pills.

What are the side effects? Some CMV drugs can damage your bone marrow or kidneys. This may require additional medications. Other drugs require infusions that can take a long time. Discuss the side effects of any CMV treatment with your health care provider.

What do the guidelines say? Recently, several sets of professional guidelines have recommended valganciclovir as the preferred treatment for patients who are not at immediate risk of losing their sight.




The Bottom Line

Strong anti-HIV drugs are the best way to prevent CMV. If your T-cell count is below 100, talk with your doctor about CMV prevention and a regular schedule of eye exams. If you have a low T-cell count and experience ANY unusual vision problems, see your doctor immediately!

Treatments directly in the eye make it possible to control CMV retinitis. With the newer drugs to treat CMV, you can avoid implanted medication lines and daily infusions.

Most people can safely stop taking CMV medication if their T-cell counts go up and stay above 100 to 150 when they take anti-HIV drugs.





You Can Prevent CMV (Cytomegalovirus)
A Guide for People With HIV Infection


CMV infection is very common; between 50 and 85 percent of all Americans have CMV by age 40.

In people with HIV, CMV can cause retinitis (ret-in-I-tis), which can cause blindness.

You can take steps to reduce your chance of infection with CMV and to protect yourself from CMV-related diseases.


What is CMV?

CMV, or cytomegalovirus (si-to-MEG-a-lo-vi-rus), is a virus that is found in all parts of the world. For someone with HIV or AIDS, CMV can cause retinitis (blurred vision and blindness), painful swallowing, diarrhea, and pain, weakness, and numbness in the legs.


How is CMV spread?

CMV spreads from one person to another in saliva (spit), semen, vaginal secretions, blood, urine, and breast milk. You can get CMV when you touch these fluids with your hands, then touch your nose or mouth. People can also get CMV through sexual contact, breastfeeding, blood transfusions, and organ transplants.





How can I protect myself from CMV?

You may already have CMV. However, you can take steps to avoid CMV, such as:

washing your hands frequently and thoroughly
using condoms (However, no protective method is 100 percent effective, and condom use cannot guarantee absolute protection against any sexually transmitted disease)
talking to your doctor if you expect to receive a blood transfusion. Most blood banks don't screen blood for CMV.

If you work in a day care center, you should take these special precautions:

wash your hands thoroughly after contact with urine or saliva
avoid oral contact with saliva or objects covered with saliva (such as cups, pacifiers, toys, etc.)
talk with your doctor about whether you should continue to work in a day care center.


How do I know if I have CMV?

A blood test can tell you if you have CMV, but this test is not commonly performed. CMV doesn't always cause symptoms. Some people have fatigue, swollen glands, fever, and sore throat when they first get CMV. But these are also symptoms of other illnesses, so most people don't know it when they get CMV.


How is CMV different for someone with HIV?

Once CMV enters a person's body, it stays there. Most people with CMV never get CMV-related diseases. However, in people with HIV or AIDS, the virus can cause severe disease.


How can I prevent CMV disease?

The most important thing you can do is to get the best care you can for your HIV infection. Take your antiretroviral medicine just the way your doctor tells you to. If you get sick from your medicine, call your doctor for advice. CMV disease mostly affects HIV-infected people whose CD4 cell counts are below 100. Oral (taken by mouth) ganciclovir (gan-CY-clo-veer) may be used to prevent CMV disease, but it is expensive, has side effects, and may not work for all people. Normally, ganciclovir is not recommended, but you may want to talk with your doctor about it.

ABOUT CYTOMEGALO VIRUS (CMV)

Cytomegalovirus (CMV)




What Is CMV?

Cytomegalovirus (CMV) is an opportunistic infection. The virus is very common. Between 50% and 85% of the US population tests positive for CMV by the time they are 40 years old. A healthy immune system keeps this virus in check.

When the immune defenses are weak, CMV can attack several parts of the body. This can be caused by various diseases including HIV. Combination antiviral therapy has reduced the rate of CMV in people with HIV by 75%. However, about 5% of people with HIV still develop CMV disease.

The most common illness caused by CMV is retinitis. This is the death of cells in the retinas, the back of the eye. It can quickly cause blindness unless treated. CMV can spread throughout the body and infect several organs at once. The risk of CMV is highest when CD4 cell counts are below 50. It is rare in people with 100 or more T-cells.

The first signs of CMV retinitis are vision problems such as moving black spots. These are called "floaters." They may indicate an inflammation of the retina. Patients may also notice light flashes, decreased or distorted vision, or blind spots. Some doctors recommend eye exams to catch CMV retinitis. The exams are done by an ophthalmologist (an eye specialist). If your CD4 count is below 100 and you experience any vision problems, tell your doctor immediately.

Some patients who have recently started using anti-HIV medications can get inflammation in their eyes, causing loss of vision. This is called immune restoration syndrome (see Fact Sheet 473).


How Is CMV Treated?

The first treatments for CMV required daily intravenous infusions. Most people had a permanent medication "port" inserted into their chest or arm. People had to keep taking anti-CMV drugs for life.

CMV treatments have improved dramatically over the past several years. There are now seven CMV treatments approved by the FDA.

Strong HIV medications can improve the immune system. Patients can stop taking CMV drugs if their CD4 cell count goes over 100 to 150 and stays there for at least three months. However, there are two special cases:
Immune restoration syndrome can cause severe inflammation in the eyes of people with HIV even if they didn't have CMV before. The usual treatment is to add anti-CMV drugs to the patient's anti-HIV drugs.
If the CD4 count drops below 50, there is an increased risk of developing CMV disease.


Can CMV Be Prevented?

Ganciclovir was approved for prevention (prophylaxis) of CMV. However, many physicians don't prescribe it. They don't want to add up to 12 capsules a day for their patients. Also, it's not clear that it does any good. Two large studies came to different conclusions. Finally, strong antiviral medications keep most people's CD4 counts high enough so that they won't get CMV.


How Do I Choose a Treatment for CMV?

There are several issues to consider when choosing a treatment for active CMV disease.

Is your vision at risk? You may need to take quick action to save your eyesight.

How effective is it? Intravenous ganciclovir is the most effective overall CMV treatment. Implants are very good at stopping retinitis. However, they only work in the eye with the implant.

How is it administered? Pills are the easiest to manage. Intravenous (IV) medication involves needle sticks or a medication line that might become infected. Ocular injections mean inserting a needle directly into the eye. Implants, which last six to eight months, take about an hour to insert in an office procedure.

Is it a local therapy or systemic? Local therapies affect just the eyes. CMV retinitis can progress rapidly and lead to blindness. For this reason, it is treated aggressively when it first shows up. The newer injections or implants put medication directly into the eye and have the greatest impact on retinitis.

CMV can also show up in other places in the body. To control CMV in the rest of the body, you need a systemic (whole-body) therapy. Intravenous medication can be used, or valganciclovir pills.

What are the side effects? Some CMV drugs can damage your bone marrow or kidneys. This may require additional medications. Other drugs require infusions that can take a long time. Discuss the side effects of any CMV treatment with your health care provider.

What do the guidelines say? Recently, several sets of professional guidelines have recommended valganciclovir as the preferred treatment for patients who are not at immediate risk of losing their sight.




The Bottom Line

Strong anti-HIV drugs are the best way to prevent CMV. If your T-cell count is below 100, talk with your doctor about CMV prevention and a regular schedule of eye exams. If you have a low T-cell count and experience ANY unusual vision problems, see your doctor immediately!

Treatments directly in the eye make it possible to control CMV retinitis. With the newer drugs to treat CMV, you can avoid implanted medication lines and daily infusions.

Most people can safely stop taking CMV medication if their T-cell counts go up and stay above 100 to 150 when they take anti-HIV drugs.





You Can Prevent CMV (Cytomegalovirus)
A Guide for People With HIV Infection


CMV infection is very common; between 50 and 85 percent of all Americans have CMV by age 40.

In people with HIV, CMV can cause retinitis (ret-in-I-tis), which can cause blindness.

You can take steps to reduce your chance of infection with CMV and to protect yourself from CMV-related diseases.


What is CMV?

CMV, or cytomegalovirus (si-to-MEG-a-lo-vi-rus), is a virus that is found in all parts of the world. For someone with HIV or AIDS, CMV can cause retinitis (blurred vision and blindness), painful swallowing, diarrhea, and pain, weakness, and numbness in the legs.


How is CMV spread?

CMV spreads from one person to another in saliva (spit), semen, vaginal secretions, blood, urine, and breast milk. You can get CMV when you touch these fluids with your hands, then touch your nose or mouth. People can also get CMV through sexual contact, breastfeeding, blood transfusions, and organ transplants.





How can I protect myself from CMV?

You may already have CMV. However, you can take steps to avoid CMV, such as:

washing your hands frequently and thoroughly
using condoms (However, no protective method is 100 percent effective, and condom use cannot guarantee absolute protection against any sexually transmitted disease)
talking to your doctor if you expect to receive a blood transfusion. Most blood banks don't screen blood for CMV.

If you work in a day care center, you should take these special precautions:

wash your hands thoroughly after contact with urine or saliva
avoid oral contact with saliva or objects covered with saliva (such as cups, pacifiers, toys, etc.)
talk with your doctor about whether you should continue to work in a day care center.


How do I know if I have CMV?

A blood test can tell you if you have CMV, but this test is not commonly performed. CMV doesn't always cause symptoms. Some people have fatigue, swollen glands, fever, and sore throat when they first get CMV. But these are also symptoms of other illnesses, so most people don't know it when they get CMV.


How is CMV different for someone with HIV?

Once CMV enters a person's body, it stays there. Most people with CMV never get CMV-related diseases. However, in people with HIV or AIDS, the virus can cause severe disease.


How can I prevent CMV disease?

The most important thing you can do is to get the best care you can for your HIV infection. Take your antiretroviral medicine just the way your doctor tells you to. If you get sick from your medicine, call your doctor for advice. CMV disease mostly affects HIV-infected people whose CD4 cell counts are below 100. Oral (taken by mouth) ganciclovir (gan-CY-clo-veer) may be used to prevent CMV disease, but it is expensive, has side effects, and may not work for all people. Normally, ganciclovir is not recommended, but you may want to talk with your doctor about it.