VISI SURVEILAN DINKES TASIKMALAYA

MENJADI SDM SURVEILAN YANG PROFESIONAL DAN BERDEDIKASI TINGGI

Tuesday 26 October 2010

Basic Information about HIV and AIDS

What are HIV and AIDS?
Scanning electron microscope image of HIV virons on CD4 lymphocytes.
Electron microscope image of HIV, seen as small spheres on the surface of white blood cells.

HIV is the human immunodeficiency virus. It is the virus that can lead to acquired immune deficiency syndrome, or AIDS. CDC estimates that about 56,000 people in the United States contracted HIV in 2006.

There are two types of HIV, HIV-1 and HIV-2. In the United States, unless otherwise noted, the term “HIV” primarily refers to HIV-1.

Both types of HIV damage a person’s body by destroying specific blood cells, called CD4+ T cells, which are crucial to helping the body fight diseases.

Within a few weeks of being infected with HIV, some people develop flu-like symptoms that last for a week or two, but others have no symptoms at all. People living with HIV may appear and feel healthy for several years. However, even if they feel healthy, HIV is still affecting their bodies. All people with HIV should be seen on a regular basis by a health care provider experienced with treating HIV infection. Many people with HIV, including those who feel healthy, can benefit greatly from current medications used to treat HIV infection. These medications can limit or slow down the destruction of the immune system, improve the health of people living with HIV, and may reduce their ability to transmit HIV. Untreated early HIV infection is also associated with many diseases including cardiovascular disease, kidney disease, liver disease, and cancer. Support services are also available to many people with HIV. These services can help people cope with their diagnosis, reduce risk behavior, and find needed services.

AIDS is the late stage of HIV infection, when a person’s immune system is severely damaged and has difficulty fighting diseases and certain cancers. Before the development of certain medications, people with HIV could progress to AIDS in just a few years. Currently, people can live much longer - even decades - with HIV before they develop AIDS. This is because of “highly active” combinations of medications that were introduced in the mid 1990s.

No one should become complacent about HIV and AIDS. While current medications can dramatically improve the health of people living with HIV and slow progression from HIV infection to AIDS, existing treatments need to be taken daily for the rest of a person’s life, need to be carefully monitored, and come with costs and potential side effects. At this time, there is no cure for HIV infection. Despite major advances in diagnosing and treating HIV infection, in 2007, 35,962 cases of AIDS were diagnosed and 14,110 deaths among people living with HIV were reported in the United States.

Thursday 21 October 2010

DIFTERI


Penyakit Difteri disebabkan oleh Corynebacterium diphteri. Terdapat 3 tipe yaitu: mitis, intermedius, dan gravis. Masa inkubasi antara 2-5 hari, masa penularan penderita  2-4 minggu sejak masa inkubasi, sedangkan masa penularan carrier bisa sampai 6 bulan.
Gambaran klinis: demam 38 , pseudomembranputih ke abu-abuan yang tak mudah lepas dan mudah berdarah di faring, laring atau tonsil, sakit waktu menelan, leher membengkak seperti leher sapi (Bullneck) dan sesak napas disertai stridor. Diagnosis pasti jika didapatkan kuman difteri yang dilakukan melalui specimen apusan tenggorok (throat swab) yang di biakan.
Sumber penularan adalah manusia, baik sebagi penderita maupun sebagai carrier. Penyebaran melalui droplet infection dan difteri kulit yang mencemari tanah. Kekebalan diperoleh karena menderita sakit atau mendapat imunisasi. Kekebalan yang tinggi secara aktif melalui imunisasi DPT.
LANGKAH PENYELIDIKAN EPIDEMIOLOGI (PE)
a.      Dasar: adanya kasus tersangka Difteri segera lakukan PE
b.      Tujuan: penegakan diagnosis, mengetahui besaran kasus, identifikasi factor resiko, investigasi kasus lain, penentuan arah pencegahan dan penaggulangan.
c.       Langkah Penyelidikan: Koordinasi melalui Tim Investigasi, siapkan administrasi, pengumpulan data
d.      Pengolahan dan penyajian data
e.      Analisa data
f.        Membuat laporan hasil penyelidikan.

Sunday 17 October 2010

FILARIASIS

Di Indonesia berdasarkan survei tahun 2000-2004 terdapat lebih dari 8000 orang menderita klinis kronis Filariasis (Elephantiasis) yang tersebar di seluruh propinsi. Secara epidemiologi terindikasi lebih dari 60 juta penduduk Indonesia berada di daerah yanmg beresiko tinggi.
Perkembangan klinis Filariasis dipengaruhi oleh faktor kerentanan individu terhadap parasit, seringnya mendapat gigitan nyamuk, banyaknya larva infektif yang masuk ke dalam tubuh dan adanya infeksi sekunder oleh bakteri atau jamur.
Pada dasarnya perkembangan klinis Filariasis tersebut disebabkan oleh karena cacing dewasa yang tinggal dalam saluran limfe menimbulkan pelebaran (dilatasi) saluran limfe bukan penyumbatan (obstruksi), sehingga terjadi gangguan fungsi sistem limfatik.
GEJALA KLINIS

Terdiri dari gejala klinis Akut dan Kronis.
Akut: berupa limfadenitis, limfangitis, adenolimfangitis, yang disertai demam, sakit kepala, lemah dan timbulnya abses.
Kronis: Limfedema, lym scrotum, kiluria, dan hidrokel.
TATALAKSANA KASUS KLINIS FILARIASIS
A. Pengobatan Kasus Klinis
Setiap kasus klinis di daerah endemis atau non endemis mendapatkan pengobatan:
1. Diberikan DEC 3x1 tab 100 mg selama 10 hari berturut-turut.
2. Apabila penderita berada di daerah endemis, maka pada tahun berikutnya baru boleh diikutsertakan dalam pengobatan massal dengan DEC, albendazol dan parasetamol sekali setahun, minimal 5 tahun secara berturut-turut. Penderita yang tinggal di daerah non endemik tidak melaksanakan pengobatan massal.
B. Perawatan Kasus klinis
1. Gejala  Klinis Akut: Istirahat yang cukup, banyak minum, pembersihan luka, dean mengatasi symtomatiknya.
2. Gejala Kronis: perawatan kasus dilakukan berdasarkan kondisi medis masing-masing kasus.
PECATATAN & PELAPORAN
a. Perekaman Status
b. Pemeriksaan Kemajuan Perawatan.
c. Pencatatan dan Pelaporan Data Kasus Filariasis

Thursday 7 October 2010

CHIKUNGUNYA

Chikungunya is a mosquito-borne viral disease first described during an outbreak in southern Tanzania in 1952. It is an alphavirus of the family Togaviridae. The name ‘chikungunya’ derives from a root verb in the Kimakonde language, meaning "to become contorted" and describes the stooped appearance of sufferers with joint pain.
Signs and symptoms

Chikungunya is characterized by an abrupt onset of fever frequently accompanied by joint pain. Other common signs and symptoms include muscle pain, headache, nausea, fatigue and rash. The joint pain is often very debilitating, but usually ends within a few days or weeks. Most patients recover fully, but in some cases joint pain may persist for several months, or even years. Occasional cases of eye, neurological and heart complications have been reported, as well as gastrointestinal complaints. Serious complications are not common, but in older people, the disease can contribute to the cause of death. Often symptoms in infected individuals are mild and the infection may go unrecognized, or be misdiagnosed in areas where dengue occurs.
Transmission

The virus is transmitted from human to human by the bites of infected female mosquitoes. Most commonly, the mosquitoes involved are Aedes aegypti and Aedes albopictus, two species which can also transmit other mosquito-borne viruses, including dengue. These mosquitoes can be found biting throughout daylight hours, although there may be peaks of activity in the early morning and late afternoon. Both species are found biting outdoors, but Ae. aegypti will also readily feed indoors.

After the bite of an infected mosquito, onset of illness occurs usually between four and eight days but can range from two to 12 days.
Diagnosis

Several methods can be used for diagnosis. Serological tests, such as enzyme-linked immunosorbent assays (ELISA), may confirm the presence of IgM and IgG anti-chikungunya antibodies. IgM antibody levels are highest three to five weeks after the onset of illness and persist for about two months. The virus may be isolated from the blood during the first few days of infection. Various reverse transcriptase–polymerase chain reaction (RT–PCR) methods are available but are of variable sensitivity. Some are suited to clinical diagnosis. RT–PCR products from clinical samples may also be used for genotyping of the virus, allowing comparisons with virus samples from various geographical sources.
Treatment

There are no specific drugs to cure the disease. Treatment is directed primarily at relieving the symptoms, including the joint pain. There is no commercial chikungunya vaccine.
Prevention and control

The proximity of mosquito vector breeding sites to human habitation is a significant risk factor for chikungunya as well as for other diseases that these species transmit. Prevention and control relies heavily on reducing the number of natural and artificial water-filled container habitats that support breeding of the mosquitoes. This requires mobilization of affected communities. During outbreaks, insecticides may be sprayed to kill flying mosquitoes, applied to surfaces in and around containers where the mosquitoes land, and used to treat water in containers to kill the immature larvae.

For protection during outbreaks of chikungunya, clothing which minimizes skin exposure to the day-biting vectors is advised. Repellents can be applied to exposed skin or to clothing in strict accordance with product label instructions. Repellents should contain DEET (N, N-diethyl-3-methylbenzamide), IR3535 (3-[N-acetyl-N-butyl]-aminopropionic acid ethyl ester) or icaridin (1-piperidinecarboxylic acid, 2-(2-hydroxyethyl)-1-methylpropylester). For those who sleep during the daytime, particularly young children, or sick or older people, insecticide treated mosquito nets afford good protection. Mosquito coils or other insecticide vaporizers may also reduce indoor biting.
Disease outbreaks

Chikungunya occurs in Africa, Asia and the Indian subcontinent. Human infections in Africa have been at relatively low levels for a number of years, but in 1999-2000 there was a large outbreak in the Democratic Republic of the Congo, and in 2007 there was an outbreak in Gabon.

Starting in February 2005, a major outbreak of chikungunya occurred in islands of the Indian Ocean. A large number of imported cases in Europe were associated with this outbreak, mostly in 2006 when the Indian Ocean epidemic was at its peak. A large outbreak of chikungunya in India occurred in 2006 and 2007. Several other countries in South-East Asia were also affected. In 2007 transmission was reported for the first time in Europe, in a localized outbreak in north-eastern Italy.
More about disease vectors

Both Ae. aegypti and Ae. albopictus have been implicated in large outbreaks of chikungunya. Whereas Ae. aegypti is confined within the tropics and sub-tropics, Ae. albopictus also occurs in temperate and even cold temperate regions. In recent decades Ae. albopictus has spread from Asia to become established in areas of Africa, Europe and the Americas.

The species Ae. albopictus thrives in a wider range of water-filled breeding sites than Ae. aegypti, including coconut husks, cocoa pods, bamboo stumps, tree holes and rock pools, in addition to artificial containers such as vehicle tyres and saucers beneath plant pots. This diversity of habitats explains the abundance of Ae. albopictus in rural as well as peri-urban areas and shady city parks. Ae. aegypti is more closely associated with human habitation and uses indoor breeding sites, including flower vases, water storage vessels and concrete water tanks in bathrooms, as well as the same artificial outdoor habitats as Ae. albopictus.

In Africa several other mosquito vectors have been implicated in disease transmission, including species of the A. furcifer-taylori group and A. luteocephalus. There is evidence that some animals, including non-primates, may act as reservoirs.

Friday 1 October 2010

PENDEKATAN KLINIK ACUTE ONSET OF FLACCID PARALYSIS

1. Pendahuluan
Diiperlukan suatu surveilans untuk menentukan apakah masih ada kasus klinik kelumpuhan karena virus polioliar. Untuk itu, dilakukan deteksi terhadap seluruh kasus yang mengalami Acute Onset of Flaccid Paralysis yang sering disebut dengan akronim AFP atau lumpuh layu Akut. AFP merupakan sindroma yang disebabkan oleh berbagai macam penyebab. Secara klinis, kasus AFP yang berat dapat dikenal dengan mudah, sedangkan kasus yang ringan lebih sulit dikenal.
2. Kelumpuhan : flasid dan spastik
Kelumpuhan adalah berkurangnya kekuatan otot untuk menggerakkan anggota badan dan kelumpuhan total disebut sebagai paralisis, sedangkan kelumpuhan parsial disebut sebagai paresis. Kekuatan otot harus ditentukan derajat kekuatannya dan menurut Lovetts digunakan skala Council sebagai berikut:
5 : kekuatan otot normal, tidak ada kelumpuhan, mampu melawan beban maksimal(Normal)
4 : kekuatan otot tersebut mampu melawan gaya gravitasi dan beban (Good)
3 : terdapat kontraksi otot yang mampu menggerakkan sendinya dan mampu melawan
gravitasinya (Fair)
2 : terdapat pergerakan sendi seluas gerak sendinya akibat kontraksi otot penggerak utama
sendi yang bersangkutan, tetapi dengan menghilangkan gaya gravitasinya (Poor)
1 : tidak ada pergerakan sendi tetapi teraba/tampak adanya kontraksi otot (Trace)
0 : tidak ada kontraksi sama sekali (Zero)
AFP adalah sindroma klinik dengan berbagai penyebab. Para klinisi harus dapat mendeteksi
kelumpuhan / kelemahanyang menjadi dasar kasus AFP

Pendekatan Klinik AFP
Pemeriksaan Manual Muscle Test [MMT] sangat bermanfaat didalam penentuan diagnosa derajat kelumpuhan apapun sebabnya.
Tonus
Tonus otot adalah tahanan muskuler ( diluar pengertian penyakit sendi dan gaya gravitasi); yang dirasakan oleh pemeriksa bila melakukan manipulasi berupa gerakan sendisecara aktif pada seorang penderita . Tonus otot dikatakan normal apabila hanya dijumpai sedikit sekali tahanan pada
seluruh pergerakan sendi. Tonus otot yang berkurang bila tahanan gerakan yang dilakukan pemeriksa berkurang. Hilangtnya tonus otot yang jelas disebut sebagai tonus otot yang
flasid atau layu. Sedangkan hipertonia dikatakan bila tahanan otot meningkat, dapat berupa spastisitas atau rigiditas.
Kelumpuhan Lower Motor Neuron
Pada AFP didapatkan kelumpuhan yang flasid; yang kita kenal sebagai kelumpuhan lower motor neuron yang disebabkan lesi mulai dari motor neuron kornu anterior sampai ke saraf perifer. Kita kenal pula kelumpuhan upper motor neuron yang disebabkan kelainan pada jaras piramidalis dari kortek motorik
sampai dengan kornu anterior medulla spinalis.
III. Manifestasi Klinis AFP
Anak anak.
Beberapa pemeriksaan dapat dilalukan untuk rnembantu
menetapkan kondisi klinik penderita:
􀂙 Dapat disertai demam atau tidak
􀂙 Dapat disertai rasa nyeri atau tidak
􀂙 Mintalah anak berjalan dan perhatikan apakah ia pincang atau tidak.
􀂙 Mintalah anak berjalan pada ujung jari dan pada tumit, anak yang mengalami kelurnpuhan tidak dapat
melakukannya.
􀂙 Mintalah anak berjongkok atau duduk dilantai, kemudian bangun kembali. Anak yang mengalami
kelumpuhan akan menunjukkan adanya tanda dari Gower yaitu rnencoba berdiri dengan
berpegangan dan merambat pada tungkainya.
􀂙 Bila anak berbaring di tempat tidur, mintalah dia mengangkat kaki kemudian menahan tungkai diudara.
Dan mintalah untuk menggerakan pergelangan kaki & jari-jari kaki, pergerakan ujung jari ke arah
kepala.
􀂙 Tungkai yang mengalami lumpuh layu mengecil. Bila tidak yakin ukurlah lingkar betis kanan dan kiri
pada ketinggian yang sama.
􀂙 Refleks lutut dan pergelangan kaki berkurang atau negative demikian juga tidak dijumpai adanya retlek
patologis.
􀂙 Kadang dapat disertai gangguan miksi dan defekasi.

Bayi
􀂙 Dapat didahului dengan demam atau tidak. Rasa nyeri sulit diketahui.
􀂙 Seringkali sulit mendeteksi apakah seorang bayi sedang mengalami kelumpuhan. Pendekatan Klinik
AFP
􀂙 Perhatikan posisi saat tidur terlentang. Bayi normal menunjukkan tingkah
dalam posisi fleksi di dan di panggul. Bayi lumpuh menunjukkan frog leg position. Tungkai terkulai
lemas dan lutut menyentuh tempat tidur.
􀂙 Perhatikan gerakan kedua tungkai. Bila terdapat kelumpuhan gerakan sisi tersebut kurang bila
Dibandingkan sisi yang sehat. Bila kelumpuhan terjadi pada kedua tungkai gerakan kedua tungkai
berkurang
􀂙 Untuk merangsang gerakan dapat digelitik pada telapak kaki atau ditusuk
perlahan dengan benda yang agak tajam misalnya pensil. Bayi yang normal akan menarik kakinya.
􀂙 Pegang kedua pergelangan dan gerakan kedua tungkai ke depan dan kebelakang. Rasakan perbedaan
ketegangan otot.
􀂙 Angkat kedua tungkai dari permukaaan tempat tidur lalu lepaskan. Bayi normal akan memperlihatkan
sedikit tahanan sebelum tungkai jatuh ketempat tidur atau bahkan dapat menahan tungkai di udara.
Pada kelumpuhan, tungkai akan jatuh ke tempat tidur tanpa tahanan.
􀂙 Lakukan uji pendulum. Pegang bayi pada ketiak dan ayunkan Bayi normal memperlihatkan gerakan
simetris tungkai disertai sedikit f1eksi lutut dan pangkal paha. Bayi yang lumpuh memperlihatkan
tungkai tergantung lemas tanpa gerakan.
􀂙 Lihatlah apakah dijumpai atrofi otot. Atrofi yang ringan sulit dilihat, gunakanlah pengukur untuk
mengukur lingkar betis pada ketinggian yang sama.
􀂙 Reflek Iutut dan pergelangan kaki berkurang atau negatif; reflek Babinsky pada bayi < 18 bulan
kadang masih timbul.
IV. Penyebab AFP
AFP dapat terjadi pada:
-Acute anterior poliomyelitis
+Disebabkan karena virus polio
+Disebabkan karena virus neurotrophik lainnya: coxsackie virus, echovirus dan enterovirus 70 dan71
-Acute myopathy
+Proses Desak Ruang:pembuntuan mielum; misalnya akibat abses paraspinal; tumor atau hematoma
+Mielopati transvesus idiopati yang akut
-Peripheral neuropathy
+Guillain Barre syndroma
+Neuropati demielinating yang akut
+Neuropati aksonal yang akut
+Pasca pemberian vaksin rabies
+Neuropati dalam perjalanan penyakit seperti difteria, rabies, Lyme, borrelios, intoksikasi logam berat,
toksin biologis
AFP dapat terjadi akibat berbagai penyakit Penyakit sistemik
+Porpiria intermiten akuta +Neuropatia pada penyakit yang kritis
-Kelainan transmisi neuron akibat
+Miastenia gravis +Gigitan ular +Botulisrne +Intoksikasi insectisida +Tick paralisa
-Kelainan otot
+Miopathia Inflamasi yang Idiopatis +Trichinosis +Hipokalemia dan hiperkalernia paralisa, termasuk familial periodic paralysa.