BAHAN KULIAH DAN MAKALAH KESEHATAN

ASUHAN KEPERAWATAN DENGAN POST HERNIOTOMY AKIBAT HERNIA INGUINALIS LATERAL

2011-09-01T13:02:00.000+07:00

ASUHAN KEPERAWATAN DENGAN POST HERNIOTOMY AKIBAT HERNIA INGUINALIS LATERAL

A. Konsep Dasar

1. Definisi

a. Hernia

1) Hernia adalah menonjolnya suatu organ atau struktur organ dari tempatnya yang normal melalui sebuah defek kongenital atau yang didapat (C.Long, Barbara, 1996 : 246 ).

2) Hernia adalah penonjolan isi perut dari rongga yang normal melalui suatu defek pada fasia muskuloaponeurotik dinding perut, baik secara kongenital atau didapat,yang memberi jalan keluar pada setiap alat tubuh selain yang biasa melalui dinding tersebut (Mansjoer dkk, 2002 : 313 ).

3) Hernia merupakan protrusi atau penonjolan isi suatu rongga melalui defek atau bagian lemah dari dinding rongga bersangkutan. Pada hernia abdomen, isi perut menonjol melalui defek atau bagian lemah dari lapisan muskulo-aponeurotik dinding perut (Sjamsuhidayat, 2004: 523 ).

Dari beberapa pengertian diatas dapat disimpulkan bahwa hernia adalah penonjolan suatu organ atau struktur organ yang normal melalui kongenital atau yang didapat karena kelemahan otot perut.

b. Hernia Inguinalis Lateral

1) Hernia inguinalis lateral adalah hernia yang melalui anulus inguinalis internus yang terletak disebelah lateral vasa epigastrika inferior, menyusuri kanalis inguinalis dan keluar kerongga perut melalui anulus inguinalis eksternus ( Mansjoer dkk, 2002 : 314 )

2) Hernia inguinalis lateral merupakan penonjolan yang keluar dari rongga peritoneum melalui anulus inguinalis internus yang terletak lateral dari pembuluh epigastrika inferior, kemudian hernia masuk kedalam kanalis inguinalis dan jika cukup panjang, menonjol keluar dari anulus inguinalis eksternus ( Sjamsuhidayat, 2004 : 527 ).

3) Hernia inguinalis yaitu berkenaan dengan lipat paha, saluran tubuler melalui bagian bawah dinding anterior abdomen dan letaknya sejajar serta sedikit diatas ligamentum inguinale.

Dari ketiga definisi diatas dapat disimpulkan bahwa yang dimaksud dengan Hernia inguinalis lateral adalah hernia yang melalui anulus inguinalis internus yang terletak lateral dari pembuluh epigastrika inferior kemudian hernia masuk ke dalam kanalis inguinalis dan jika cukup panjang, menonjol keluar dari anulus inguinalis eksternus.

c. Herniotomi

Herniotomi adalah pembesaran kantong hernia sampai ke lehernya, kantong dibuka dan isi hernia dibebaskan kalau ada perlekatan, kemudian direposisi kantong hernia dijahit-ikat setinggi mungkin lalu dipotong. (Sjamsuhidayat, 2004 : 531 )

d. Post herniotomi

Keadaan setelah dilakukan pembedahan hernia sampai kelehernya, kantong dibuka dan isi hernia dibebaskan kalau ada perlekatan, kemudian direposisi kantong hernia dijahit-ikat setinggi mungkin lalu dipotong

2. Anatomi fisiologi Region Inguinalis

Kanalis inguinalis dibatasi dikraniolateral oleh anulus inguinalis internus yang merupakan bagian terbuka dari fasia transpersalis dan aponeurosis m.tranversus abdominis. Dimedial bawah, diatas tuberkulum tubkum, kanal ini dibatasi oleh anulus inguinalis eksternus, bagian terbuka dari aponeurosis m.oblikus eksternus. Atapnya adalah aponeurosis m.oblikus eksternus, dan didasarnya terdapat ligamentum inguinale. Kanal berisi tali sperma pada lelaki, dan ligamentum rotundum pada perempuan.

Hernia inguinalis indirek, disebut juga hernia inguinalis lateralis, karena keluar dari peritonium melalui anulus inguinalis internus yang terletak lateral dari pembuluh epigastrika inferior, kemudian hernia masuk ke dalam kanalis inguinalis dan jika cukup panjang, menonjol keluar dari anulus inguinalis eksternus. Apabila hernia ini berlanjut, tonjolan akan sampai ke skrotum, ini disebut hernia skrotalis (Sjamsuhidayat, 2004 :526).

a. Pada Pria

1) Fenikulus spermaticus

2) Vasa spermatika

3) Proccesus vaginalis peritoni

b. Pada wanita

1) Ligamentum Rotundum

Gambar 2.1

Dinding abdomen dilihat dari depan/ (Region kanalis inguinalis)

(Sumber: Sjamsuhidayat, 2004: 527).

Kanalis inguinalis adalah kanal yang normal pada fetus. Pada bulan ke-8 kehamilan terjadi desensus testis melalui kanal tersebut. Penurunan testis tersebut akan menarik peritoneum kedaerah skrotum sehingga terjadi penonjolan peritoneum yang disebut dengan prosesus vaginalis peritonei. Pada bayi yang sudah lahir, umumnya prosesus ini telah mengalami obliterasi sehingga isi rongga perut tidak dapat melalui kanalis tersebut namun dalam beberapa hal, seringkali kanalis ini tidak menutup. Karena testis kiri turun terlebih dahulu, maka kanalis inguinalis kanan lebih sering terbuka.Bila kanalis kiri terbuka maka biasanya yang kanan juga terbuka. Dalam keadaan normal, kanalis yang terbuka ini akan menutup pada usia 2 bulan (Mansjoer dkk, 2002 : 314).

3. Etiologi

Hernia ingunalis dapat terjadi karena anomali kongenital atau karena sebab yang didapat. Pada bayi dan anak, hernia lateralis disebabkan oleh kelainan bawaan berupa tidak menutupnya prosesus vaginalis peritoneum sebagai akibat proses penurunan testis ke skrotum.Insiden hernia meningkat dengan bertambahnya umur mungkin karena meningkatnya penyakit yang meninggikan tekanan intra abdomen dan berkurangnya kekuatan jaringan penunjang.

Faktor yang dipandang berperan kausal adalah :

1). Adanya prosesus vaginalis yang terbuka

2). Peninggian tekanan didalam rongga perut

3). Kelemahan otot dinding perut karena usia.

4. Patofisiologi

Pada hernia inguinalis lateral bahwa apabila ada defek integritas dinding otot pada ligamen inguinal disertai dengan adanya tekanan intra abdominal (tekanan intra abdominal ini disebabkan kegemukan, hamil, mengangkat benda berat, mengejan saat defekasi, atau trauma benda tumpul.

Herniotomi harus dilakukan apabila cincin hernia memutuskan suplai darah pada segmen hernia. putusnya suplai darah ini karena cin cin hernia menjepit segmen hernia ( Luckman & Sorensens, 2000: 1658).

5. Manifestasi Klinis

Pasien mengatakan turun berok, burut, atau klingsir, atau mengatakan adanya benjolan diselangkangan atau kemaluan. Benjolan tersebut bisa mengecil atau menghilang pada waktu tidur, dan bila menangis, mengejan, atau mengangkat benda berat dan bila posisi pasien berdiri dapat timbul kembali.

Bila telah terjadi kompliksi dapat ditemukan nyeri. Keadaan umum pasien biasanya bak, bila benjolan tidak nampak, pasien dapat disuruh mengejan dengan menutup mulut dalam keadaan berdiri. bila ada hernia maka akan tampak benjolan. (Mansjoer et al, 2000: 314).

6. Manajemen medik secara umum

Penatalaksanaan medik secara umum pada hernia inguinalis yaitu :

a. Tindakan Non Bedah

1) Tindakan ini dilakukan untuk mengobati atau mengatakan keluhan (simptomatik) obat-obatan yang dapat diberikan pada klien hernia inguinal, biasanya :

a). Obat anti nyeri ( analgetik )

b). Obat anti mikrobial ( antibiotik )

c). Obat anti mual ( antiemetik )

d). Vitamin

2) Reposisi Bimanual

Teknik ini dilakukan dengan cara memegang isi hernia membentuk corong, sedangkan tangan kanan mendorongnya kearah cincin hernia dengan tekanan lambat tapi menetap sampai terjadi reposisi

3) Reposisi Spontan

Reposisi dilakukan dengan menidurkan anak dengan pemberian sedatif dan kompres es diatas hernia. Bila resposisi ini berhasil anak disiapkan untuk operasi pada hari berikutnya. Jika resposisi tidak berhasil, dalam waktu 6 jam harus dilakukan operasi segera.

b. Tindakan Bedah

Prinsip dasar operasi hernia terdiri dari :

1) Herniotomi

Merupakan suatu tindakan pembedahan dengan pembebasan kantong hernia sampai kelehernya, kantong dibuka dan isi hernia dibebaskan kalau ada perlengketan, kemudian direposisi. Kantong hernia dijahit dan diikat setinggi mungkin lalu dipotong (Sjamsuhidayat, 2004 : 531 )

2) Hernioplastik

Adalah suatu tindakan memperkecil annulus inguinalis internus dan memperkuat dinding belakang kanalis inguinalis (Sjamsuhidayat, 2004 : 531 ).

7. Dampak Post Herniotomi Terhadap Sistem Tubuh

a. Sistem Gastrointestinal

Pembedahan traktus gastrointestinal sering kali mengganggu proses fisiologi normal pencernaan dan penyerapan. Mual, muntah dan nyeri dapat terjadi selama pmbedahan ketika digunakan anestesia spinal. Dan penurunan peristaltik usus ini mengakibatkan distensi abdomen dan gagal untuk mengeluarkan feses dan flatus. motalitas gastrointestinal dapat mengakibatkan distensi abdomen dan gagal untuk mengeluarkan feses dan flatus ( Brunner & Suddarth 2002 : 484 & 455 ).

b. Sistem Neurologi

Luka pembedahan mengakibatkan spasme otot dan pembuluh darah sehingga merangsang pelepasan mediator kimia ( seratonin, bradikinin, histamin ). Pross ini merangsang reseptor nyeri kemudian rangsangan ditransmisikan ke thalamus, kortek cerebri sehingga terasa nyeri. Nyeri akan merangsang RAS ( Retikular Activating Sistem ) stimulus ini menyebabkan sikap terjaga dan berkurangnya stimulus untuk mengantuk.

c. Sistem Pernapasan

Peningkatan frekuensi nafas dapat terjadi akibat nyeri pada luka operasi,hal ini merangsang sinyal dari sum-sum tulang belakang yang dihantarkan melalui dua jalur yaitu Spinal Thalamus Traktus ( STT ) ke Spinal Respiratory Traktus ( SRT ). Dari spinal thalamus traktus akan dihantarkan ke korteks cerebri sehingga nyeri dipersepsikan, sedangkan dari spinal respirator, traktus akan dihantarkan ke medula oblongata sehingga mengakibatkan neural inspiratory yang akan meningkatkan frekuensi pernapasan. Nyeri pada luka operasi dapat menekan pengembanahan rongga dada dan pasien dapat memerlukan sangat banyak dorongan untuk beergerak, ambulasi, dan bernafas dalam ( C.Long, Barbara, 1996 : 251 ).

d. Sistem Kardiovaskuler

Pada klien post herniotomi biasanya dapat terjadi peningkatan denyut nadi, hal ini disebabkan dari rasa nyeri akibat luka operasi sehingga mengakibatkan medula oblongata untuk meningkatkan frekuensi pernapasan dan merangsang epineprin sehingga menstimulasi jantung untuk memompa lebih cepat selain itu juga dapat terjadi akibat faktor metabolik, endokrin dan keadaan yang menghasilkan adrenergik sehingga dimanifestasikan peningkatan denyut nadi.

e. Sistem Integumen

Luka operasi akan mengakibatkan kerusakan kontinuitas jaringan dan keterbatasan gerak dapat mengakibatkan kerusakan kulit pada daerah yang tertekan karena sirkulasi perifer terhambat. Akibat dari keadaan post operatif seperti peradangan, edema dan perdarahan, sering terjadi pembekakan skrotum setelah perbaikan hernia inguinal lateral ( C.Long, Barbara, 1996 : 247 ).

f. Sistem Muskuloskeletal

Nyeri pada luka operasi timbul akibat terputusnya kontinuitas jaringan serta adanya spasme otot, terjadi penekanan pada pembuluh darah yang mengakibatkan metabolisme anaerob sehingga menghasilkan asam laktat, hal ini mengakibatkan terjadinya gangguan pergerakan ( otot persendian ) sehingga aktivitas sehari-hari dapat terganggu. Selain itu nyeri akibat luka operasi dapat mengakibatkan klien mengalami keterbatasan gerak.

g. Sistem Perkemihan

Terjadinya retensi urine dapat terjadi setelah prosedur pembedaha. Retensi terjadi paling sering setelah pembedahan pada rektum, anus, dan vagina setelah pembedahan pada abdomen bagian bawah, penyebabnya diduga adalah spasme spinkter kandung kemih ( Brunner & Suddarth 2002 : 484 ).

B. Proses Keperawatan

Proses Keperawatan pada klien dengan post herniotomi adalah metode sistematik dimana secara langsung perawat bersama klien secara bersama menentukan masalah keperawatan sehingga membutuhkan asuhan keperawatan, membuat perencanaan dan rencana implementasi, serta mengevaluasi hasil asuhan keperawatan.

Proses Keperawatan menurut Yura dan Walsh (1967) yang dikutip oleh Gaffar dalam buku asuhan keperawatan profesional terdiri dari 5 tahap, yaitu :

1. Pengkajian

Pengkajian adalah pendekatan sistematis untuk mengumpulkan data melalui wawancara, observasi, pemeriksaan fisik, pemeriksaan laboratorium dan diagnostik serta reviu catatan sebelumnya.

Untuk mengkaji klien dengan post herniotomi meliputi :

a. Pengumpulan Data

1) Identitas

a) Identitas klien mencakup : nama. Umur, jenis kelamin, pendidikan, pekerjaan, suku/bangsa, nomor medik, status, diagnosa medis, tanggal masuk rumah sakit, tanggal pengkajian dan alamat.

b) Identitas penanggung jawab meliputi : nama, umur, pekerjaan, agama, hubungan dengan klien dan alamat

2) Riwayat Kesehatan Sekarang

a) Alasan Masuk Perawatan

Disini menggambarkan tentang hal-hal yang menjadikan pasien di bawa ke rumah sakit dan dirawat.

b) Keluhan utama

Keluhan utama merupakan keluhan klien yang bersifat subyektif pada saat dikaji. Biasanya keluhan utama yang dirasakan klien post herniotomi adalah nyeri daerah luka operasi.

c) Riwayat Kesehatan sekarang

Bagian ini menguraikan keluhan pertama yang muncul secara kronologis meliputi faktor yang mencetuskan memperingan gejala, kualitas, lokasi / penyebaran, upaya yang dilakukan serta waktu dirasakannya keluhan, durasi dan frekuensi. Dengan menggunakan alat bantu yang mencakup PQRST :

P : Provokative / palliative

Merupakan hal atau faktor yang pencetus terjadinya penyakit, hal yang memperberat atau memperingan, nyeri yang dirasakan biasanya bertambah bila klien berjalan, bersin, batuk atau napas dalam.

Q : Quality / Quantity

Qualitas dari suatu keluhan atau penyakit yang dirasakan.

R : Region / Radition

Region adalah daerah atau tempat dimana keluhan dirasakan

S : SaveQuality / Quantity

Region / Radition

S :

ale

rity Scale

Severity scale adalah keganasan atau intensitas dari keluhan tersebut.

T : Time

Time adalah waktu dimana keluhan dirasakan.

d) Riwayat kesehatan yang lalu

Pada tahap ini dikaji mengenai latar belakang kehidupan klien sebelum masuk rumah sakit yang menjadi faktor predisposisi seperti riwayat bekerja mengangkat benda-benda berat, tanyakan juga tentang riwayat penyakit menular dan atau penyakit keturunan.

e) Riwayat keluarga

Pada tahap ini dikaji tentang riwayat kesehatan keluarga, adakah dalam keluarga yang mengalami penyakit sama dengan klien saat ini dan atau riwayat penyakit keturunan.

3) Data Biologis

a) Pola nutrisi

Pada aspek ini dikaji mengenai kebiasaan makan klien sebelum dan sesudah masuk rumah sakit. Dikaji mengenai riwayat diet klien. Bagaimana kebiasaan makan dalam sehari, jenis makan. Apakah dijumpai perubahan pada makan akibat penyakit, setelah itu dikaji tentang kebiasaan minum ( jenis, jumlah dalam sehari ) dan kebiasaan minum-minuman beralkohol.

b) Pola eleminasi

Dikaji mengenai frekuensi, konsistensi, warna dan kelainan eleminasi, kesulitan-kesulitan eliminasi dan keluhan-keluhan yang dirasakan klien pada saat bab dan bak.

c) Istirahat dan tidur

Dikaji mengenai kebutuhan istirahat dan tidur, apakah ada gangguan sebelum dan pada saat tidur, lama tidur dan kebutuhan istirahat tidur.

d) Personal hygiene

Dikaji mengenai kebiasaan mandi, gosok gigi, mencuci rambut dan dikaji apakah memerlukan bantuan orang lain atau secara mandiri.

e) Aktivitas dan latihan

Dikaji apakah aktivitas yang dilakukan klien dirumah dan dirumah sakit dibantu atau secara mandiri.

4) Pemeriksaan Fisik

Pemeriksaan fisik dilakukan dengan cara inspeksi, palpasi, perkusi dan auskultasi. Pemeriksaan fisik dilakukan head to toe tetapi hasilnya dituliskan persistem tubuh.

a) Keadaan umum

Keadaan klien dengan hernia biasanya mengalami kelemahan, dan periksa status gizinya serta tingkat kesadaran compos mentis.

b) Tanda-tanda vital

Pada tahap ini dilakukan pemeriksaan tanda-tanda vital biasanya pada pasien post herniotomi terjadi penurunan tekanan darah, peningkatan suhu dan demam, pernapasan cepat dan dangkal.

c) Tinjauan sistem

(1) Sistem respirasi

Dikaji dengan cara inspeksi, palpasi, auskultasi, perkusi.Dalam sistem ini perlu dikaji mengenai bentuk hidung, kebersihannya, adanya sekret, adanya pernafasan cuping hidung, bentuk dada, pergerakan dada apakah simetris atau tidak, bunyi nafas, adanya ronchi atau tidak, frekuensi dan irama nafas teratur.

(2) Sistem cardiovaskuler

Dikaji mulai dari warna konjungtiva, warna bibir, tidak ada peningkatan JVP, peningkatan frekuensi dan irama denyut nadi, bunyi jantung tidak disertai suara tambahan, penurunan tekanan darah.

(3) Sistem pencernaan

Sistem pencernaan dikaji mulai dari mulut sampai anus, dalam sistem ini perlu dikaji adanya stomatitis, jumlah gigi, caries, bau mulut, mukosa mulut, ada tidaknya pembesaran tonsil, bentuk abdomen datar, turgor kulit kembali lagi, fokus pada pemeriksaan dengan kasus hernia apakah ada distensi abdomen, nyeri tekan dan nyeri lepas. Adakah lesi pada daerah abdomen adanya massa, pada auskultasi dapat diperiksa peristaltik usus.

(4) Sistem perkemihan

Dikaji ada tidaknya pembengkakan dan nyeri pada daerah pinggang, observasi dan palpasi pada daerah abdomen untuk mengkaji adanya retensio urine, ada tidaknya nyeri tekan dan benjolan serta pengeluaran urine apakah ada nyeri pada waktu miksi atau tidak.

(5) Sistem neurologis

Secara umum pada kasus hernia inguinalis lateral tidak mengalami gangguan, namun gangguan terjadi dengan adanya nyeri sehigga perlu dikaji tingkat skala ( 0-5) serta perlu dikaji nilai GCS dan pemeriksaan fungsi syaraf kranial untuk mengidentifikasi kelainan atau komplikasi.

(6) Sistem integumen

Dalam sistem ini perlu dikaji keadaan kulit (turgor, kebersihan, pigmentasi, tekstur dan lesi), serta perlu dikaji kuku dan keadaan rambut, sekitar kulit atau ekstremitas adakah oedema atau tidak.

Pada klien dengan post herniotomi akan didapatkan kelamaan integumen karena adanya luka insisi pada daerah abdomen, sehingga perlu dikaji ada atau tidaknya tanda radang didaerah terkena adalah ada tidaknya tanda lesi dan kemerahan, pengukuran suhu untuk mengetahui adanya infeksi.

(7) Sistem penglihatan

Pada post herniotomi sistem ini tidak mengalami gangguan. Untuk mengetahui keadaan kesehatan maka harus diperiksa tentang fungsi penglihatan, kesimetrisan mata kiri dan kanan, oedema atau tidak.

(8) Sistem Endokrin

Dalam sistem ini perlu dikaji adanya pembesaran kelenjar tiroid dan kelenjar getah bening.

(9) Sistem Muskuloskeletal

Pada hernia inguinalis lateral biasanya post operasi secara umum tidak mengalami gangguan,tapi perlu dikaji kekuatan otot ekstremitas atas dan bawah, dengan nilai kekuatan otot (0-5). Diperiksa juga adanya kekuatan pergerakan, atau keterbatasan gerak.

5) Data psikologis

Data psikologis yang perlu dikaji adalah status emosional, konsep diri, mekanisme koping klien dan harapan serta pemahaman klien tentang kondisi kesehatan sekarang.

a) Status emosional

Kemungkinan ditemukan emosi klien jadi gelisah dan labil, karena proses penyakit yang tidak di ketahui/ tidak pernah diderita sebelumnya.

b) Konsep diri

Konsep diri didefinisikan sebagai semua pikiran, keyakinan dan kepercayaan yang membuat orang mengetahui tentang dirinya dan mempengaruhi hubungannya dengan orang lain. (Stuart and Sundeen, 1997 : 227).

Konsep diri terdiri atas komponen-komponen berikut ini ( keliat, Budi Anna : 2001).

1) Citra tubuh

Kumpulan dari sikap individu yang disadari dan tidak disadari terhadap tubuhnya. Termasuk persepsi masa lalu dan sekarang serta perasaan tentang ukuran, fungsi, penampilan dan potensi.

2) Ideal diri

Persepsi individu tentang bagaimana dia seharusnya berperilaku berdasarkan standar, aspirasi, tujuan, atau nilai personal tertentu.

3) Harga diri

Penilaian individu tentang nilai personal yang diperoleh dengan menganalisa seberapa baik prilaku seseorang sesuai ideal diri.

4) Penampilan peran

Serangkaian pola perilaku yang dihapkan oleh lingkungan sosial berhubungan dengan fungsi individu diberbagai kelompok sosial

5) Identitas personal

Pengorganisasian perinsip dari kepribadian yang bertanggung jawab terhadap kesatuan, kesinambungan, konsistensi, dan keunikan individu

c) Stressor

Stressor adalah faktor-faktor yang menambah beban klien baik dari pelayanan kesehatan ataupun pribadi dan keluarga.

Seseorang yang mempunyai stressor akan mempersulit dalam proses suatu penyembuhan penyakit.

d) Koping Mekanisme

Koping mekanisme ini merupakan suatu cara bagaimana seseorang untuk mengurangi atau menghilangkan stress yang dihadapi

e) Harapan dan pemahaman klien tentang kondisi kesehatan yang dihadapi.

Hal ini perlu dikaji agar tim kesehatan dapat memberikan bantuan dengan efisien.

Pengkajian psikososial post herniotomi meliputi bagaimana status emosi klien, harapan klien tentang penyakit yang dideritanya, gaya komunikasi, sosialisasi klien dengan keluarga atau masyarakat, interaksi klien dirumah sakit, gaya hidup klien sehari-hari, serta kepuasan pelayanan keperawatan yang klien rasakan dirumah sakit.

6) Aspek Sosial dan Budaya

Pengkajian ini menyakit pada pola komunikasi dan interaksi interpersonal, gaya hidup, faktor sosial serta support sistem yang ada pada klien.

7) Data Spiritual

Data spiritual menyangkut keyakinan terhadap Tuhan Yang Maha Esa, harapan terhadap kesembuhan serta kegiatan spiritual yang dilakukan saat ini.

8) Pemeriksaan Penunjang

Pemeriksaan laboratorium dan atau radiologi perlu dilakukan untuk memvalidasi dalam menegakkan diagnosa sebagai pemeriksaan penunjang.

9) Data Pengobatan

Data ini digunakan untuk mengetahui jenis obat apa saja yang digunakan pada kasus hernia inguinalis lateral. Untuk mengetahui keefektifan penyembuhan penyakit.

b. Analisa Data

Setelah dilakukan pengkajian secara lengkap, maka tahap selanjutnya adalah menganalisa data untuk menentukan diagnosa keperawatan.

2. Diagnosa Keperawatan

Diagnosa keperawatan adalah penyataan yang status atau masalah kesehatan aktual atau potensial. Tujuannya adalah mengidentifikasi adanya masalah aktual berdasarkan respon klien terhadap masalah atau penyakit, penyebab adanya masalah, kemampuan klien untuk mencegah atau menghilangkan masalah (Gaffar, 1999 : 61)

Diagnosa keperawatan yang mungkin muncul pada post herniotomi adalah :

a Nyeri berhubungan dengan terputusnya kontinuitas jaringan akibat pembedahan.

b Risiko tinggi terhadap komplikasi, Atelektasis, Ileus Paralitik, Dehisens, Infeksi, Kekurangan cairan dan biokimia, Tromboflebitis berhubungan dengan pembedahan.

c Kurang perawatan diri berhubungan dengan keterbatasan mobilitas fisik sekunder terhadap pembedahan

d Risiko tinggi terhadap kerusakan penatalaksanaan pemeliharaan dirumah berhubungan dengan kurangnya pengetahuan tentang perawatan diri saat pasien pulang.

e Risiko tinggi terhadap infeksi berhubungan dengan retensi perkemihan akut, insisi pembedahan, dan inflamasi skrotum sekunder terhadap herniorafi.

3. Perencanaan Keperawatan

Setelah merumuskan diagnosa keperawatan maka perlu dibuat perencanaan intervensi keperawatan dan aktivitas keperawatan. Tujuan perencanaan adalah untuk mengurangi, menghilangkan dan mencegah masalah keperawatan klien. Tahapan perencanaan keperawatan adalah penentuan prioritas diagnosa keperawatan,penetapan sasaran (goal) dan tujuan (objective), penetapan kriteria evaluasi dan merumuskan intervensi keperawatan ( Gaffar, 1999:63 )

Perencanaan keperawatan pada tahap ini dibahas rencana tindakan keperawatan berikut rasionalnya :

a. Nyeri berhubungan dengan terputusnya kontinuitas jaringan akibat pembedahan.

Tujuan : Nyeri berkurang sampai dengan hilang, dengan kriteria :

- Klien tampak tenang

- Skala nyeri 0 ( 0-5)

INTERVENSI

RASIONAL

1. Pantau :

- Tekanan darah, nadi dan pernapasan setiap 4 jam.

- Intensitas nyeri

- Tingkat kesadaran

2. Informasikan ke dokter jika nyeri diberikan sampai pemberian obat respon terhadap analgetik yang bertambah buruk atau tidak ada selanjutnya.

3. Bantu pasien untuk mengambil posisi yang nyaman. Tinggikan ekstremitas yang terasa sakit. Tekuk lutut dengan menggunakan bantal atau penyokong lutut ditempat tidur untuk menurunkan ketegangan otot-otot perut setelahtindakan bedah atau bila ada nyeri dipunggung.

4. Ajarkan pasien teknis bernapas berirama untuk nyeri yang ringan sampai sedang dalam hubungannya deengan nyeri yang lain meringankan intervensi :

- Instrusikan pasien untuk memelihara kontak mata pada suatu objek sambil menarik napas perlahan melalui mulut dan mengeluarkan napas melalui bibir yang dikerutkan.

5. Berikan istirahat sampai nyeri hilang. Kurangi kebisingan dan sinar yang terang. Jaga kehangatan pasien dengan selimut ekstra.

1. Untuk mengenal indikasi kemajuan atau penyimpangan dari hasil yang diharapkan.

2. Ini merupakan indikasi bahwa perlu analgetik yang lebih keras atau mulai ada komplikasi.

3. Tempatkan tubuh pada posisi yang nyaman untuk mengurangi penekanan dan mencegah otot-otot tegang membantu menurunkan rasa tidak nyaman.

4. Distraksi mengganggu stimulus nyeri dengan mengurangi rasa nyeri. Distraksi tidak mengubah intensitas nyeri. Paling baik digunakan untuk periode pendek pada nyeri ringan sampai sedang.

5. Istirahat menurunkan pengeluaran energi. Vasokontriksi perifer terjadi pada nyeri hebat dan menyebabkan pasien merasa dingin. Biasanya rangsangan lingkungan yang kuat, memperhebat persepsi nyeri.

b. Risiko tinggi terhadap komplikasi, Atelektasis, Ileus Paralitik, Dehisens, Infeksi, Kekurangan cairan dan biokimia, Tromboflebitis berhubungan dengan pembedahan.

Tujuan : Mendemonstrasikan tidak adanya komplikasi.

INTERVENSI

RASIONAL

Atelektasis :

1. Pantau bunyi paru-paru tiap 4 jam selama 24 jam, kemudian 8 jam sekali terutama pada orang yang berisiko tinggi ateletaksis pascaoperasi (perokok,lansia,dan orang-orang yang mempunyai penyakit paru kronis).

2. Ubah posisi tiap 2 jam. Biarkan pasien melakukannya sesering mungkin. Melakukan ambulasi sesuai perintah.

3. Pastikan rasa sakit dapat dikontrol

Paralitic ileus :

1. Pantau :

- Selang nasogastrik (warna dan jumlah drainase setiap 8 jam).

- Status abdomen (mengauskultasi bising usus, menanyakan tentang flatus) setiap 8 jam.

2. Ukur dan catat besarnya lingkaran perut setiap 8 jam jika diperkirakan terjadi distensi abdomen.

3. Berikan makan melalui mulut jika bising usus telah ada, keluar flatus dan distensi abdomen berkurang.

Dehisens :

1. Pantau keadaan tepi luka ketika mengganti perban.

2. Agar pasien menahan insisi abdomen ketika batuk.

3. Berikan perawatan luka dengan menggunakan teknik aseptik yang ketat.

Infeksi :

Pantau :

- Suhu badan setiap 4 jam

- Keadaan luka ketika melakukan perawatan luka

- Hasil laporan JDL terutama jumlah leukosit (terutama SDP ).

Berikan antibiotik yang diresepkan.Berikan paling sedikit 2 liter cairan setiap hari ketika melaksanakan terapi antibiotik
Ganti perban sesuai aturan dengan menggunakan tekhnik aseptik.

Kekurangan cairan dan biokimia :

Pantau :

- Masukan dan haluaran setiap 8 jam.

- Hasil elektrolit serum

- Status umum setiap 8 jam

Lakukan terapi yang ditentukan untuk mengatasi retensi cairan :

- Diet natrium dibatasi

- Masukan cairan dibatasi

- Terapi diuretik.

Evaluasi keefektifan terapi :resolusi manifestasi kelebihan volume cairan, natrium serum kembali kerentang normal.

Tromboflebitis :

1. Bantu sirkulasi pada anggota badan bawah setiap 8 jam sampai dimulai ambulasi :denyut nadi telapak kaki, tanda-tanda Homan's, betis nyeri tekan, pengisian kapiler,warna dan badan.

2. Anjurkan latihan gerak ditempat tidur setiap 2 jam. Ketika ambulasi dimulai,pastikan pasien melakukannya secara progresif paling sedikit 3 kali sehari.

1. Untuk mengidentifikasi kemajuan atau penyimpangan dari hasil yang diharapkan.

2. Aktivitas mendorong bernapas dalam.

3. Individu melakukan pernapasan cepat dan dangkal bila mengalami nyeri hebat, yang membatasi ekspansi penuh dari alveoli.

1. Untuk mengidentifikasi indikasi kemajuan atau penyimpangan dari hasil yang diharapkan.

2. Untuk memperoleh data yang objektif.

3. Keadaan tersebut mengindikasikan adanya peristaltik dan fungsi usus normal.

1. Untuk mengidentifikasi kemajuan atau penyimpangan dari hasil yang diharapkan.

2. Untuk mencegah tegangan pada jahitan.

3. Infeksi luka adalah penyebab utama dehisens.

1. Untuk mengidentifikasi kemajuan atau penyimpangan dari hasil yang diharapkan.

2. Terapi antibiotik diperlukan untuk mencegah dan mengatasi infeksi. Cairan membantu menyebarkan obat kejaringan tubuh.

3. Perban yang lembab merupakan media kultur untuk pertumbuhan bakteri. Dengan mengikuti teknik aseptik akan mengurangi risiko kontaminasi bakteri.

1. Untuk mengidentifikasi indikasi kemajuan atau penyimpangan dari hasil yang diharapkan

2. Natrium menahan air. Diuretik membantu membuang kelebihan air tubuh.

1. Untuk mengidentifikasi kemajuan atau penyimpangan dari hasil yang diharapkan.

2. Latihan merangsang sirkulasi.

c. Kurang perawatan diri berhubungan dengan keterbatasan mobilitas fisik sekunder terhadap pembedahan

Tujuan : Perawatan diri terpenuhi dengan kriteria :

- Klien dapat memenuhi kebutuhan aktifitas

- Perawatan diri terpenuhi scara mandiri

INTERVENSI

RASIONAL

1. Tentukan tingkat bantuan yang diperlukan.Berikan bantuan AKS sesuai keperluan. Membiarkan pasien melakukan sebanyak mungkin untuk dirinya.

2. Berikan waktu yang cukup bagi pasien untuk melaksanakan aktifitas.

3. Instruksikan pasien adaptasi yang diperlukan untuk melaksanakan AKS. Dimulai dengan tugas yang mudah dilakukan dan berlanjut sampai tugas yang sulit. Berikan pujian untuk keberhasilan tersebut.

4. Menaruh bel ditempat yang mudah dijangkau.

1. Untuk mendorong kemandirian

2. Membebani pasien dengan aktifitas menyebabkan frustasi.

3. Untuk mendorong kemandirian. Pujian memotivasi untuk terus belajar.

4. Untuk memberikan rasa aman.

d. Risiko tinggi terhadap kerusakan penatalaksanaan pemeliharaan dirumah berhubungan dengan kurangnya pengetahuan tentang perawatan diri saat pasien pulang.

Tujuan : Kerusakan penatalaksanaan dirumah tidak terjadi dengan kriteria hasil :

- Klien dan keluarga mengerti tentang penatalaksanaan dirumah.

- Klien dan keluarga mengatakan akan melaksanakan perawatan, aktifitas yang baik dirumah.

- Mengidentifikasi bagian-bagian yang memerlukan perawatan.

INTERVENSI

RASIONAL

1. Pastikan pasien memiliki instruksi tertulis tentang perawatan diri dan perjanjian tertulis untuk kunjungan evaluasi.

2. Ajarkan dan biarkan pasien merawat luka jika penggantian perban perlu dilakukan dirumah. Tekankan pentingnya mencuci tangan sebelum dan sesudah merawat luka.

3. Evaluasi kebutuhan bantuan perawatan dirumah dan tersedianya sistem pendukung yang memadai untuk memberikan bantuan yang diperlukan. Hubungi perencana atau bagian pemulangan pasien untuk mengatur bantuan perawatan dirumah jika pasien memerlukan bantuan tetapi tidak mempunyai sistem pendukung dirumah.

4. Instruksikan pasien untuk memberitahu dokter jika terjadi infeksi luka : kemerahan, nyeri tekan, drainase, demam.

5. Pastikan pasien mempunyai persediaan yang cukup untuk perawatan luka dan resep untuk analgetik.

6. Instruksikan agar pasien beristirahat sepanjang hari, secara bertahap melakukan aktivitas serta menghindari mengangkat benda-benda berat dan latihan yang berlebihan.

1. Instruksi verbal akan mudah terlupakan.

2. Praktik akan membantu pasien mengembangkan keyakinannya dalam perawatan diri. Juga memungkinkan perawat mengevaluasi kemampuan pasien melaksanakan keterampilan tersebut sendiri dan menentukan apakah diperlukan bantuan. Tindakan untuk mencegah infeksi harus dilanjutkan sampai luka benar-benar sembuh.

3. Layanan sosial atau perencana pemulangan pasien berfungsi sebagai penghubung yang penting untuk pemindahan pasien kelingkungan rumah atau fasilitas perawatan luar untuk memastikan kelanjutan penyembuhan atau rehabilitasi.

4. Diperlukan antibiotik untuk mengatasi infeksi.

5. Persediaan penting untuk mengurangi kecemasan yang pada umumnya berhubungan dengan pemulangan pasien. Analgesik memberi kenyamanan dan mendorong untuk tidur.

6. Pembedahan adalah stresor.

e. Risiko tinggi terhadap infeksi berhubungan dengan pembedahan

Tujuan : Risiko tinggi terhadap infeksi tidak terjadi dengan kriteria :

- Suhu tubuh normal 37⁰C

- Tanda-tanda infeksi tidak terjadi

INTERVENSI

RASIONAL

1. Pantau :

- Suhu badan setiap 4 jam

- Keadaan luka ketika melakukan perawatan luka

- Hasil laporan JDL terutama jumlah leukosit.

2. Tetap pada fasilitas kontrol infeksi, sterilisasi dan prosedur/kebijakan aseptik.

3. Identifikasi gangguan pada teknik aseptik dan atasi dengan segera pada waktu terjadi.

4. Sediakan pembalut yang steril

5. Berikan antibiotik sesuai petunjuk

1. Untuk mengidentifikasi kemajuan atau penyimpangan dari hasil yang diharapkan

2. Tetapkan mekanisme yang dirancang untuk untuk mencegah infeksi.

3. Kontaminasi dengan lungkungan/ kontak personal akan menyebabkan daerah yang steril menjadi tidak steril sehingga dapat meningkatkan risiko infeksi.

4. Mencegah kontaminasi lingkungan pada luka yang baru.

5. Dapat diberikan secara profilaksis bila dicurigai terjadinya infeksi atau kontaminasi.

3. Implementasi

Implementasi merupakan pelaksanaan perencanaan keperawatan oleh perawat dan klien. Hal-hal yang harus diperhatihan ketika melakukan implementasi adalah intervensi dilaksanakan sesuai dengan rencana setelah dilakukan validasi (Gaffar, 1999:65 ).

Perencanaan tindakan keperawatan akan dapat dilaksanakan dengan baik, jika klien mempunyai keinginan untuk berpartisipasi dalam pelaksanaan tindakan keperawatan. Selama tahap pelaksanaan, perawat terus melakukan pengumpulan data dan memilih tindakan perawatan yang paling sesuai dengan kebutuhan klien.

4. Evaluasi

Evaluasi adalah fase akhir dari proses keperawatan. Evaluasi menyediakan nilai informasi mengenai pengaruh intervensi yang telah direncanakan dan merupakan perbandingan dari hasil yang diamati dengan kriteria hasil yang telah dibuat pada tahap perencanaan, disamping itu evaluasi juga digunakan sebagai alat ukur suatu tujuan yang mempunyai kriteria tertentu yang memberikan tujuan tercapai, tidak tercapai atau tercapai sebagaian (Hidayat, 2002 : 41)

Terdapat 2 tipe dokumentasi evaluasi yaitu evaluasi formatif yang menyatakan evaluasi yang dilakukan pada saat memberikan intervensi dengan respon segera dan evaluasi sumatif yang merupakan rekapitulasi dari hasil observasi dan analisis status pasien pada waktu tertentu.

Evaluasi sumatif dapat dilakukan dengan menggunakan pendekatan SOAP, sebagai berikut :

S : Respon Subjektif klien terhadap tindakan keperawatan yang telah dilaksanakan

O : Respon objektif klien terhadap tindakan keperawatan yang telah dilaksanakan

A : Analisa ulang atas subjektif dan objektif untuk menyimpukan apakah masalah masih tetap atau muncul. Masalah baru atau data yang kontradiksi dengan masalah yang ada.

P : Perencanaan atau tindak lanjut berdasarkan hasil analisa pada respon klien

Selanjutnya setelah evaluasi dilakukan pada hari berikutnya dituliskan dalam catatan perkembangan.

Catatan perkembangan merupakan catatan tentang perkembangan keadaan klien yang didasarkan pada setiap masalah yang ditemui pada klien (Hidayat, 2002 : 46)

S : Data Subjektif

Perkembangan keadaan didasarkan pada apa yang dirasakan, dikeluhkan, dan dikemukakan klien.

O : Data objektif

Perkembangan yang bisa diamati dan diukur oleh perawat atau tim kesehatan lain.

A : Analisis

Data subjektif dan objektif dinilai dan dianalisis, apakah berkembang ke arah perbaikan atau kemunduran. Hasil analisis dapat menguraikan sampai dimana masalah yang ada dapat diatasi atau adakah perkembangan masalah baru yang menimbulkan diagnosa keperawatan baru.

P : Perencanaan

Rencana penangan klien dalam hal ini didasarkan pada hasil analisis diatas yang berisi melanjutkan rencana selanjutnya apabila keadaan atau masalah belum teratasi dan membuat rencana baru bila rencana awal tidak efektif.

I : Implementasi

Tindakan yang dilakukan berdasarkan rencana

E : Evaluasi

Evaluasi berisikan penilaian sejauh mana tindakan dan evaluasi telah dilaksanakan dan sejauh mana masalah bisa teratasi

R : Reassement

Bila hasil evaluasi menunjukkan masalah belum teratasi, pengkajian ulang perlu dilakukan kembali melalui proses pengumpulan data subjektif, data objektif dan proses analisisnya.

a Nyeri berhubungan dengan terputusnya kontinuitas jaringan akibat pembedahan.

Kriteria hasil : Menyatakan tidak nyeri, intensitas nyeri berkurang, tanda-tanda vital stabil, ekspresi muka dan postur tubuh rileks.

b Risiko tinggi terhadap komplikasi, Atelektasis, Ileus Paralitik, Dehisens, Infeksi, Kekurangan cairan dan biokimia, Tromboflebitis berhubungan dengan pembedahan.

Kriteria hasil : tidak ada infeksi, bunyi napas bersih, penyembuhan luka, dan tidak ada perdarahan.

c Kurang perawatan diri berhubungan dengan keterbatasan mobilitas fisik sekunder terhadap pembedahan

Kriteria hasil : Mengidentifikasi area kebutuhan, mengungkapkan aktifitas terprnuhi.

d Risiko tinggi terhadap kerusakan penatalaksanaan pemeliharaan dirumah berhubungan dengan kurangnya pengetahuan tentang perawatan diri saat pasien pulang.

Kriteria hasil : Klien dan keluarga mengerti tentang penatalaksaan di rumah.

e Risiko tinggi terhadap infeksi berhubungan dengan retensi perkemihan akut, insisi pembedahan, dan inflamasi skrotum sekunder terhadap herniorafi.

Kriteria hasil : Mendemonstrasikan tidak ada tanda-tanda infeksi

VIROLOGICAL COMPLIANCE

2011-08-26T09:25:00.001+07:00

7.1 Introduction

7.2 Health significance of human viruses in drinking-water

7.3 Occurrence of human viruses in source waters

7.4 Risk management

7.4.1 International approaches

7.4.2 Virus removal by current water treatment processes

7.5 Sampling, testing and data interpretation

7.6 C.t values

http://bahankuliahkesehatan.blogspot.com/

REFERENCES

Figures and Tables

Table 7.1: UV dose requirements for virus inactivation credit

Table 7.2: C.t values for inactivation of viruses by free chlorine, pH 6 – 9

Table 7.3: C.t values for inactivation of viruses by chloramine

Table 7.4: C.t values for inactivation of viruses by chlorine dioxide, pH 6 – 9

Table 7.5: C.t values for inactivation of viruses by ozone

7.1 INTRODUCTION

No maximum acceptable values (MAVs) have been set for human viruses in the Drinking-water Standards for New Zealand (2005). It is likely that a MAV or MAVs will be established in a future edition. This chapter foreshadows such developments.

In the absence of any MAVs for viruses in the current DWSNZ it should be understood that if they are specifically sought, they should not be detected. If detected, advice should be sought from the relevant health authorities.

There are more than 140 different types of human enteric viruses that may contaminate potable source waters. These include several important groups: Hepatitis A virus, Hepatitis E virus, norovirus, enterovirus and adenovirus, that have been associated with waterborne illness and are capable of causing severe, and in some cases fatal, infections.

Human viruses are obligate intracellular parasites, which means they cannot grow or multiply outside their host. Viruses consist of a nucleic acid genome surrounded by a protein capsid and, in some cases, a lipoprotein envelope. These viruses are very small, ranging from 20 – 70 nm in diameter.

Human enteric viruses are shed in the gut, respiratory tract and occasionally urine of an infected person, and are discharged with body wastes into wastewater. Infected people do not always show signs of illness (asymptomatic) but they will still produce virus in their wastes. Specific viruses or strains of viruses are not always present in a community at any one time, but representatives of the large groups (e.g. adenovirus or enterovirus) are generally present on most occasions.

Enteric viruses may be found in high numbers in domestic wastewater. Recent New Zealand studies have shown adenovirus and enteroviruses to be present in concentrations greater 10,000 infectious virus units per litre of wastewater (Watercare Services Surrogate Study 2002). The numbers of viruses in wastewater varies with the level of virus infection in the community but, in general, human viruses will always be present in wastewater, even of small communities, (average human virus load 100 – 1000 infectious viruses/L) and will occasionally reach very high levels (>10,000 infectious virus/L) (Lewis et al 1986). Wastewater treatment processes that do not include a disinfection step are often inefficient in removing viruses (<90% removal) and some viruses may reach potable water supplies.

Human enteric viruses cannot multiply in the environment once outside the host. The viruses are characterised by the ability to survive for days, weeks or more, in the environment depending on the type of water, season and other factors (Hunter 1997).

A large proportion of the human viruses present in source drinking-waters will normally be removed or inactivated by well-operated standard drinking-water treatment processes.

Routine monitoring for viruses in treated water and source water is currently impractical in most situations in New Zealand because of the high cost of sampling and analysis, and problems of detection of a full range of the viruses occurring.

7.2 Health significance of human viruses in drinking-water

Hepatitis A virus, Hepatitis E virus, norovirus, enterovirus and adenovirus may occur in drinking-water where they are present in the source water and when water treatment does not remove them completely. Very few human enteric viruses (1 – 50 virus particles depending on type) are required to produce an infection in a susceptible person (Hunter 1997). The symptoms generally attributed to enteric viruses are gastroenteritis and diarrhoea but they can also cause respiratory, central nervous system, liver, muscular and heart infections. Some waterborne viruses have also been associated with some forms of diabetes, chronic fatigue syndrome and dementia (Nwachcuku and Gerba 2004). The major groups of viruses contaminating water are discussed below but may not represent all the viruses likely to be transmitted by water. It is reasonable to expect that further important groups of waterborne viruses will be detected in the future and that these will most likely cause atypical waterborne disease (Nwachcuku and Gerba 2004).

Norovirus: this group of caliciviruses includes the Norwalk and Norwalk-like viruses. Members of this group are strongly associated with waterborne outbreaks in many parts of the world. Symptoms of infection are mild and self-limiting and include vomiting, diarrhoea and nausea over 24 – 48 hours. Norovirus is quite prevalent in New Zealand and is responsible for a large proportion of viral gastroenteritis reported to health authorities (ESR 2004). This virus is one of the easiest to link to a common source outbreak as the symptoms occur rapidly after contact with the virus (approximately 24 hours).

Hepatitis A and E: Hepatitis A and E have a relatively low occurrence in New Zealand (ESR 2004) but induce quite significant symptoms including fever, malaise anorexia and jaundice. The disease is generally self-limiting but has a 2 percent mortality rate. The infectious doses for these viruses are relatively low (10 – 100 viruses) and symptoms do not occur until 10 – 50 days after infection. Internationally Hepatitis A and E outbreaks have frequently been associated with water.

Enteroviruses and adenoviruses: these two different groups represent the viruses that are most commonly found in contaminated surface water. These viruses produce a very broad range of symptoms including respiratory, skin and eye, nervous system, liver, heart and muscular involvement. Gastroenteritis with vomiting and diarrhoea is a less common outcome of infection with these viruses and is limited to only a few adenovirus and enterovirus types. Reported waterborne outbreaks of these viruses, other than in swimming pools, are very infrequent. It is not clear whether lack of reporting is because the dominant symptoms produced by these viruses are not those traditionally associated with water or food borne disease, or because such outbreaks are indeed rare (Hunter 1997).

Virus infections resulting from treated water have not been reported in New Zealand (ESR 2004) in recent years although internationally such outbreaks are recognised (Hunter 1997). Human viruses have been reported to occur at very low levels (0.1 – 1/100 L) in conventionally treated drinking-water in many countries (Vivier et al 2004) including New Zealand (Kim 2005).

Estimations of viral disease risk using standard risk assessment techniques with a high infectivity virus predict the surprisingly high annual risk of infection of between 1:3 and 1:25 from conventionally treated drinking-water contaminated by viruses at low levels (~1 virus per 100 litres) (Gerba and Rose 1992).

7.3 Occurrence of Human viruses in Source waters

The New Zealand freshwater microbiology study (McBride et al 2002) is the most significant study of human viruses occurrence in surface water in New Zealand to date. This study carried out in collaboration between the Ministries for the Environment, Agriculture and Forestry, and Health tested recreational water locations on 25 rivers and lakes every 2 weeks for 15 months.

Human adenovirus and/or enterovirus were detected, by qualitative molecular methods, in more than 50% of the 275 samples collected. This data suggests that human virus occurs quite frequently in surface waters and in a wide range of source water locations and types.

Subsequent culture based studies of virus occurrence in the Waikato River show that adenovirus and enterovirus levels are generally low, less than 5 per 100 L, but on some occasions may be as high as 10 per 100 L (Watercare Waikato River Monitoring studies 2003 - 2004).

Studies using sensitive qualitative molecular-based virus detection methods suggest that adenovirus occurrence may be 10 times higher than this level on some occasions in the Waikato River (Kim et al 2005) although it is not clear whether all of these viruses are able to produce infections.

International data collated by WHO suggest that typical surface source waters may contain 0 - 10 viruses per litre (WHO 2004).

7.4 Risk management

Potential for disease outbreaks associated with human virus contamination of source waters, and the potential for carry over to treated drinking-water is recognised throughout the developed world. Approaches to controlling the risks are largely through protection of source water quality by control of human activity in reservoir catchments, and through adequate treatment and disinfection of drinking-water. It is now well accepted that bacterial indicators such as E. coli are not adequate surrogates of viral occurrence. Human viruses tend to be more resistant to environmental stresses and water treatment mechanisms than are bacterial indicators, so the absence of the indicator may not equate with absence of the virus contaminant.

7.4.1 International approaches

The paucity of knowledge on the specific occurrence of human viruses in source waters, and the problems of virus detection and regular monitoring, mean that most guideline documents include only the qualitative requirement that, if tested for, human viruses should not be detected in treated drinking-water.

Where virus guidelines or standard requirements are in place these are stated either in terms of virus occurrence, or as water treatment plant virus removal efficiency. Such values are either derived from acceptable levels of health risk or, pragmatically, reflect virus detection capability.

Recent standard and guideline recommendations have moved towards risk-based evaluation of water treatment requirements. The USEPA Surface Water Treatment Rule includes a virus treatment requirement and requires that treatment of both filtered and unfiltered water sources is sufficient to remove or inactivate 99.99% (4 log) of viruses (USEPA 1994). This requirement is principally based on the acceptable (USEPA 1994) level of waterborne illness in a community (1 case per 10,000 consumers) and the likely level of viruses in surface water. Recent US proposals for surface water disinfection (USEPA 2003a) use the adenovirus group as the target virus.

The WHO Guidelines recognise that water treatment requirements will differ for different communities, and propose a risk-based approach for setting performance targets for surface water treatment plants (WHO 2004).

The risk-based approach takes into account a broad range of factors including virus occurrence and infectivity, water type, community health status and treatment characteristics. Such an approach requires a detailed knowledge of the water supply, water treatment performance and community activities and health status.

Approaches to managing viruses in treated water also recognise that the greatest health risk to a community occurs when water treatment conditions are atypical such as when source water condition is unusual, very high levels of virus occur, or through poor performance, or even failure, within the water treatment process.

7.4.2 Virus removal by current Water treatment processes

Reduction of virus numbers in water as a result of treatment can occur through either virus removal or virus inactivation. Each virus type may react somewhat differently to particular water treatment methods, but the bulk of research to-date suggests that some broad generalisations can be made.

Virus removal can occur by physical association of a virus with other particles. Particle flocs containing viruses are then removed by settlement or filtration. Virus association with particles and flocs may be enhanced by addition of coagulants and certain salts. The extremely small size of viruses means that they are unlikely to be removed if they are not associated with other particles. Water treatment processes such as flocculation, sand filtration, microfiltration and ultrafiltration, and prolonged standing in reservoirs, will result in physical removal of particle-associated viruses. Only reverse osmosis and dialysis membranes have pore sizes small enough to trap virus particles that are not associated with larger particles or flocs.

The effectiveness of virus removal is affected by those factors that act against particle association or floc formation including water condition and pH (LeChevelier and Au 2004).

Virus inactivation occurs through disruption of the external protein coat (capsid), modification of specific surface sites needed for infection (host receptor recognition sites) or major change to the nucleic acid (RNA or DNA). Disinfectants such as chlorine, chlorine dioxide, and ozone will cause disruption of the virus coat and of the exposed nucleic acids (Shin and Sobsey 2003, Tree et al 2003). Ultraviolet light in the range of 200 – 310 nm (antimicrobial range) will disrupt the nucleic acids by causing cross-linking that leaves them unable to replicate.

Viruses can also be inactivated by prolonged holding in reservoirs exposed to sunlight, elevated temperature and extremes of pH (e.g. lime treatment) (Sobsey 1989). Different virus types and strains will show different levels of resistance to chemical or physical inactivation. Adenoviruses are considered to be the most resistant virus group to many disinfection treatments, because of its structure and nucleic acid makeup, and have been used by the USEPA as a model virus for designing UV criteria for surface water treatment (USEPA 2003a).

The potential for virus inactivation by disinfectants is reduced by the presence of other particles or organic matter that will consume disinfectants or of light adsorbing or blocking materials that reduce UV penetration (LeChevelier and Au 2004).

Repair of disinfection damage is unlikely to occur in viruses as they do not have repair mechanisms as such. It has been suggested that some viruses (e.g. adenovirus) may be able to repair their DNA if there is no damage to the virus coat and they are able to infect a human cell (Nwachcuku and Gerba 2004).

Water treatment plants will normally include both virus removal and virus inactivation processes that act as multiple barriers.

Virus removal and inactivation efficiencies for a range of water treatment processes are reviewed in the WHO (2004) Guidelines (chapter 7), and by LeChevallier and Au (2004).

7.5 Sampling, testing and data Interpretation

The determination of virus removal efficiency within a water treatment plant, or occurrence in treated water, is dependant on the ability to reliably detect and enumerate the viruses. Determination of the health risk that viruses pose to the community using the water further depends on the ability to demonstrate or infer that the viruses detected are capable of causing human infection.

Virus detection and enumeration. No single method allows detection of all virus types and strains. Traditionally viruses have been concentrated from water samples using filtration or adsorption based techniques with subsequent detection by culture in a permissive human or primate cell line. Many of the virus concentration techniques were developed using poliovirus or other enterovirus types and it is not clear how effectively these work for other virus types particularly norovirus.

Virus concentration from large volumes of water is laborious and time consuming and adds significantly to the cost of virus analysis. Not all virus types are culturable in cell lines, again norovirus has not been cultured routinely and is not detectable using traditional methods.

Viruses (culturable and non-culturable) can be detected at very low levels using polymerase chain reaction (PCR) based molecular methods that target novel DNA or RNA sequences in the genetic information of the virus. Virus assay using PCR can target individual viruses or groups of viruses and multiple analyses would be required to investigate all the relevant viruses in a particular sample (Greening et al 2002). Recent advances in real-time PCR have made these methods both rapid and quantitative and potentially quite routine. PCR based methods are around 10-fold less sensitive that culture based methods for virus detection (Lewis et al 2000). Quantitative PCR based molecular methods are also significantly less expensive than traditional culture methods. It is unusual for a virus concentration and detection method to consistently recover more than 50 - 60% of the virus present in a sample (Lee and Jeong 2004).

Virus sampling strategies. Relatively few viruses are needed for an infection to occur in a susceptible person so low numbers of viruses must be quantified in relatively large volumes of finished water. For example, if source waters contain 5000 viruses per 100 L it would be necessary to sample and analyse at very least 200 L of finished water to demonstrate a 4 log reduction in viruses. Typically, source water sample volumes should be 10 – 100 L, partially treated waters 50 – 200 L, and finished, disinfected water sample volumes 100 – 200 L.

The current cost of virus analysis may make regular monitoring beyond the means of many groups responsible for drinking-water treatment.

Specific short-term studies of virus occurrence and inactivation/removal within a plant are feasible but should be designed carefully to allow adequate interpretation of the data.

Determination of virus infectivity. Molecular methods for virus detection do not specifically show whether viruses are still infectious. Detection of viruses using a cell-culture based technique shows that the viruses are infectious and pose a risk of illness to water consumers. Infectivity of a virus can however be inferred for certain RNA viruses (norovirus, enteroviruses, Hepatitis A and E) from molecular detection data where the viruses are subjected to chemical disinfection, but not UV disinfection (Greening et al 2002). Virus viability is inferred whenever virus nucleic acid is detected because the nucleic acids (single stranded RNA) are extremely susceptible to degradation in the environmental.

Interpretation of virus detection and occurrence data. Where viruses are detected in finished drinking-water the response to the data should be based, in consultation with relevant health authorities, on a risk evaluation incorporating the type and number of virus detected, the reproducibility of the result, and the health status and vulnerability of the community.

7.6 C.t VALUES

Appendix C of the LT1ESWTR Disinfection Profiling and Benchmarking Technical Guidance Manual (USEPA 2003b) includes C.t tables for disinfection of viruses by various disinfectants. These tables are referenced to AWWA (1991) but in the text of USEPA (1991) it would appear that it was a USEPA publication. Because the 2003 publication still uses the 1991 tables it is assumed that the data the 1991 tables were based on is still the latest information!

The USEPA Surface Water Treatment Rule required (inter alia) that treatment of both filtered and unfiltered sources remove or inactivate 4 log (99.99%) of viruses. This requirement was enacted in 1989. Presumably the 1991 tables were developed to assist water suppliers assess the degree of disinfection of viruses.

USEPA’s LT2ESWTR (2003a) includes a table showing the C.t values for disinfecting viruses using UV light. The proposed UV doses for inactivation of viruses were based on the dose-response of adenovirus because, among viruses that have been studied, it appears to be the most UV resistant and is a widespread waterborne pathogen. Health effects of adenovirus are described in Embrey (1999).

It is doubtful that this same approach was used in developing the 1991 tables; viruses are simply referred to collectively, and viruses are not defined in the 1991 information provided. Some viruses require a much higher C.t than others. Nor is it explained whether the data relate to studies in single virions or cell-associated virions – the latter require a higher C.t.

Table 7.1 shows the UV doses that water suppliers must apply to receive credit for up to 4 log inactivation of viruses. This is Table IV – 21 in USEPA (2003a).

Table 7.1: UV dose requirements for virus inactivation credit

Log Credit	Virus¹ UV Dose (mJ/cm²)
0.5	39
1.0 (90% removal)	58
1.5	79
2.0 (99% removal)	100
2.5	121
3.0 (99.9% removal)	143
3.5	163
4.0 (99.99% removal)	186

¹based on adenovirus studies

Tables 7.2, 7.3, 7.4, 7.5 have been taken from Appendix C of USEPA (2003b) and copied from the 1991 publication, i.e. they refer to undefined viruses.

Based on Table 7.2, a free available chlorine content of 0.20 mg/L after 30 minutes retention time is equivalent to a C.t of 6. This would achieve 4 log inactivations at 10°C. At 5°C the minimum retention time should be 40 minutes, or if that cannot be achieved, the residual free chlorine content should be increased to 0.30 mg/L.

Table 7.2: C.t values for inactivation of viruses by free chlorine, pH 6 – 9

Log inactivation	1°C	5°C	10°C	15°C	20°C	25°C
2	5.8	4.0	3.0	2.0	1.0	1.0
3	8.7	6.0	4.0	3.0	2.0	1.0
4	11.6	8.0	6.0	4.0	3.0	2.0

Table 7.3: C.t values for inactivation of viruses by chloramine

Log inactivation	1°C	5°C	10°C	15°C	20°C	25°C
2	1243	857	643	428	321	214
3	2063	1423	1067	712	534	356
4	2883	1988	1491	994	746	497

Table 7.4: C.t values for inactivation of viruses by chlorine dioxide, pH 6 – 9

Log inactivation	1°C	5°C	10°C	15°C	20°C	25°C
2	8.4	5.6	4.2	2.8	2.1	1.4
3	25.6	17.1	12.8	8.6	6.4	4.3
4	50.1	33.4	25.1	16.7	12.5	8.4

Table 7.5: C.t values for inactivation of viruses by ozone

Log inactivation	1°C	5°C	10°C	15°C	20°C	25°C
2	0.9	0.6	0.5	0.3	0.25	0.15
3	1.4	0.9	0.8	0.5	0.40	0.25
4	1.8	1.2	1.0	0.6	0.50	0.30

REFERENCES

Embrey, M. (1999). Adenovirus in drinking water, literature summary. Final report. Prepared by The George Washington University School of Public Health and Health Services, Department of Environmental and Occupational Health, Washington, DC.

ESR (2004). Annual Summary of Outbreaks in New Zealand: 2003. Report to Ministry of Health ISSN 1176-3485.

Gerba C. P. and J. Rose (1992). Estimating viral risk from drinking-water: in Comparative Environmental Risk Assessment. Ch. 9, pp 117 – 137. CR Conthern Lewis Publishers.

Greening G., J. Hewitt and G. Lewis (2002). Evaluation of integrated cell culture-PCR (C-PCR) for virological analysis of environmental samples. Journal of Applied Microbiology, 93, pp 745 – 750.

Hunter, P. (1997). Viral gastroenteritis. in waterborne disease. Epidemiology and Ecology. Chapter 28, pp 222-231. John Wiley and Sons.

Kim J. (2005). Human adenovirus in the Waikato River: Implication for water supply and public health. MSc thesis. University of Auckland Library.

LeChevelier M., K-K. Au (2004). Water treatment and pathogen control: Process efficiency in achieving safe drinking-water. WHO Drinking-Water Quality Series. WHO, Geneva.

Lee, H. K. and Y.S. Jeong (2004). Comparison of total culturable virus assay and multiplex integrated cell culture-PCR for reliablity of waterborne virus detection. Applied & Environmental Microbiology, 70, pp 3632-3636.

Lewis, G. D., F. J. Austin, M. W. Loutit and K. Sharples (1986). Enterovirus removal from sewage - the effectiveness of four different treatment plants. Water Research, 20, pp 1291 - 1297.

Lewis G., S. L. Molloy, G. E. Greening and J. Dawson (2000). Influence of environmental factors on virus detection by RT-PCR and cell culture. Journal of Applied Microbiology, 88, pp 633-640.

McBride, G., D. Till, T. Ryan, A. Ball, G. Lewis, S. Palmer and P. Weinstein (2002). Freshwater Microbiology Research Programme Report: Pathogen Occurrence and Human Health Risk Assessment Analysis. Ministry of Health, Wellington.

Ministry of Health (2005). Drinking-water Standards for New Zealand 2005. Ministry of Health, Wellington.

Nwachcuku N. and C. P. Gerba (2004). Emerging waterborne pathogens: can we kill them all? Current Opinion in Biotechnology, 15, pp 175-180.

Shin G-A and M. D. Sobsey (2003). Reduction of Norwalk Virus, Poliovirus 1, and Bacteriophage MS2 by ozone disinfection of water. Appl. Environ. Microbiol., 69 (7), pp 3975-3978.

Sobsey M. D. (1989). Inactivation of health-related microorganisms in water by disinfection processes. Water Science and Technology, 21 (3), pp 179-195.

Tree J. A., M. R. Adams, D. N. Lees (2003). Chlorination of indicator bacteria and viruses in primary sewage effluent. Applied & Environmental Microbiology, 69 (4), pp 2038-43.

USEPA (1994). National Primary Drinking Water Regulations: Enhanced Surface Water Treatment Regulations. 59 FR 38832; July 29.

USEPA (2003a). Long Term 2 Enhanced Surface Water Treatment Rule; Proposed Rule. National Primary Drinking Water Regulations: 40 CFR Parts 141 and 142, August 11, 2003.

USEPA (2003b). LT1ESWTR Disinfection Profiling and Benchmarking Technical Guidance Manual. EPA 816-R-03-004, Office of Water, May 2003. Available at: http://www.epa.gov/safewater/mdbp/pdf/profile/lt1profiling.pdf

Vivier J. C., M. M. Ehlers and W. O. Grabow (2004). Detection of enteroviruses in treated drinking-water. Water Research, 38 (11), pp 2699-705, 2004.

Watercare Services Ltd (personal communication): Surrogate study: Mangere wastewater treatment plant 2002.

Watercare Services Ltd (personal communication): Adenovirus and enterovirus monitoning data, Waikato River at Mercer, 2003, 2004.

World Health Organisation (2004). Guidelines for drinking-water quality, 3rd edition. Volume 1: recommendations. ISBN 92 4 154638 7. World Health Organisation, Geneva.

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HUMAN IMMUNODEFICIENCY VIRUS: VIROLOGY AND VACCINE DEVELOPMENT

2011-08-26T09:04:00.001+07:00

Elizabeth A. Cahill

Abstract. Figures from 2004 suggest that as many as 42.3 million people, 1.1 percent of the world’s population, are currently infected with the human immunodeficiency virus (HIV). In Sub-Saharan Africa, the region suffering most from this pandemic, it is estimated that one in four adults will be killed by acquired immune deficiency syndrome (AIDS) (deWaal, 2004). HIV is a Lentivirus that infects T-helper cells, macrophages and monocytes. The host immune system reacts by removing its own infected T-cells, making the patient more susceptible to opportunistic infection. Chemotherapeutic drugs may drastically reduce morbidity and mortality of patients. These are available to less than 2% of persons with advanced AIDS. Despite much research into various types of vaccines, an effective vaccine against HIV has yet to be developed.

http://bahankuliahkesehatan.blogspot.com/

15 September 2004

Research sponsored by DARPA Grant DAAD19-02-1-0288, P00001

1 September 2004

Reed College, Portland, OR

DARPA Grant

Introduction

Just under twenty five years have passed since the Human Immunodeficiency Virus (HIV) was first described (Barre-Sinoussi et al., 1983) and already twenty million people have died (UNAIDS global report, 2004), approximately 14 times the population of the island of Manhattan (US Census data 2000). Despite the enormous amount of research that has gone into vaccine and therapy development, no cure has been found and the number of people with HIV continues to grow. At the close of the year 2003, UNAIDS estimated that 42.3 million people were currently infected. Of the twenty million people dead, approximately 2.9 million died last year alone (Steinbrook, 2004). This pandemic is changing the face of the world.

The enormity of these numbers makes them difficult to comprehend. Some more staggering numbers help to make this figure more accessible. Among adults aged 15-49, 1.1 percent are currently infected (Steinbrook, 2004). Each day approximately 14,000 new infections are established; 95% of new infections occur in developing countries (Emini and Koff, 2001). Every country in southern Africa reports HIV infection rates ranging from 20%-35% (deWaal, 2004). In sub-Saharan Africa approximately 1/3 of children (under age 15) have lost one or both of their parents. In some countries in Africa, there are more than one million orphans (Lewis, 2004). Reversing these trends will be an enormous struggle but is tremendously important. The implications of these numbers and the social challenges surrounding this epidemic cannot be discussed in this paper. However, it is important to consider the macroscopic reality of the HIV crisis when considering the virology of the disease. This virus has created a crisis that demands a global effort. For scientists, politicians and individual citizens it must simultaneously be treated as a pressing crisis and a long-term reality. Both types of strategies are essential.

Basic virology

Human Immunodeficiency Virus (HIV) is an infection of the immune system. Other immune system infections include Lupus, asthma and Crohn’s disease. To date, no human has been able to overcome an infection with HIV, although some persons have been able to force viral loads to below the level of detection. The most common modes of HIV infection are direct blood exchange (intravenous drug use or blood transfusion), sexual contact and mother to child transmission. Each of these infection routes can be dampened with appropriate protection strategies.

An understanding of the basic virology of HIV is necessary for discussions of vaccine and chemotherapeutic developments and challenges. HIV is a retrovirus. This indicates that it is an enveloped RNA virus that uses the enzyme reverse transcriptase (RT) to convert its viral RNA into a complementary DNA (cDNA). The resultant cDNA, during a successful infection, is inserted into the host chromosomal DNA where it is able to utilize host machinery, and energy, to further replication and infection. One important feature of RT is that it is error-prone. This serves to increase the virus’ genetic variability and the rate of variant evolution. Retroviral infection can cause numerous diseases, malignancies and cancer. HIV belongs to the genus Lentivirus (“slow virus”), a subset of the family Retroviridae. Lentiviruses are generally larger than other retroviruses and, as their name suggests, have long incubation periods. Every lentivirus causes immune deficiencies and nervous system dysfunctions (Flint et al., 2000) and can be responsible for malignancies such as arthritis or autoimmune disorders.

For an infection to be established the virus must adsorb to the host cell surface. Therefore, the availability of surface receptors determines the host and tissue specificity of any viral infection. In HIV the major viral receptor is a cell surface CD4 protein found on T-helper cells, macrophages and monocytes (Prescott et al., 2001). The humoral and cellular host immune systems both respond to the new infection. The humoral immune system is responsible for the production of antibodies again HIV-1. Antibodies bind to the virus, targeting them for destruction. The cellular immune response is activation of cytotoxic T lymphocytes (CTLs) that directly remove cells presenting viral antigens. The combined efforts of these two limbs of the immune system are insufficient to clear the virus. The continued viral replication in the cells of the lymph nodes ultimately leads to the destruction of the host lymph node structure (Prescott et al., 2001).

The fact that the virus targets both regulatory and antigen presenting immune system cells partially explains the virus’ total ability to avoid destruction by the host immune system (Emini and Koff, 2004). A coreceptor is necessary for viral fusion to the host membrane; it is the binding ability of the coreceptor that determines the tropism of the HIV strain (Flint et al., 2000). During the initial stages of HIV infection the corecptor to the moncyte or macrophage CD4 (M-tropic), CCR5, is essential. Persons homozygous for a mutated, and therefore nonfunctional, CCR5 receptor are impervious to HIV infection (Sullivan et al., 2001). Those heterozygous for the CCR5 receptor maintain a lower viral load during the pre-AIDS course of the disease and appear to progress to AIDS more slowly (Prescott et al., 2001). Mutations in the CCR5 receptor are extremely rare in many regions, such as sub-Saharan Africa and Asia, a fact that may alter the face of HIV/AIDS epidemiology in those regions (Sullivan et al., 2001). After the virus has been established in the host system, the T-cell tropic fusin (CXCR-4) protein is the coreceptor that determines the success of the virus (Prescott et al., 2001). Fusion facilitates the formation of syncitia. This is not seen in M-tropic strains.

All retroviruses have three common structural proteins Gag, Pol, and Env, which code for the core proteins and structural components of the virion, the reverse transcriptase and the envelope glycoprotein, respectively (Flint et al., 2004). Once the HIV-1 virus gains access to the host system, the viral gp120 Env protein binds the CD4 plasma membrane receptor on a host T lymphocyte. The gp120 protein is inaccessible to the host antibodies when it is unattached. It is able to bind CD4 only after a structural adjustment that exposes part of the gp120 to a chemokine receptor, such as CCR5 (Emini and Koff, 2004). The exposed part of the gp120 remains protected from antibodies by either steric hinderance or extensive glycosylation (Emini and Koff, 2004). Every fusion event is followed by the release of the virion core and RNA strands into the cytoplasm of the host T lymphocyte cell. The viral RNA is translated by viral RT into a single-stranded DNA (ssDNA). The RNA strand is then degraded; the ssDNA is used as a template to create a double-stranded DNA (dsDNA). At this point the virus either becomes latent in the cell or forces the cell to transcribe viral mRNAs. The formation of new virions within a host cell will ultimately destroy it, facilitating the release of thousands of new virions into the host system.

Because infected T cells are removed by the host’s own immune response, the patient’s immune response is necessarily compromised. As the loss of T cells becomes more advanced, the infected person becomes increasingly vulnerable to opportunistic infections because their immune system is less functional. These opportunistic infections are often the cause of patient mortality. The progression of HIV infection may be more aggressive in developing countries such as those in sub-Saharan Africa because of chronic infections with pathogens and parasites. Growing antibiotic resistance compounds this problem, making the treatment of other infections more challenging. However, the success of CTLs in removing the infected cells is not wholly destructive. The ability of the patient to clear infected cells, and therefore set the level of viremia during the asymptomatic phase, is a determinant of long-term HIV control. Therefore, the CTLs exert a strong selective pressure, which drives the formation of viral escape mutations (Leslie et al., 2004). HIV is also believed to carry oncogenes; cancer is another common demise of HIV patients. The central nervous system (CNS) can also be damaged because the virus is small enough to cross the blood-brain barrier.

There are roughly four stages described for the average course of an HIV infection. During the primary stage of infection the body produces an acute response to the introduction of the virus. Clinically, this period is best described by a general malaise but HIV antibodies can be detected in the body at this point and the patient is now infectious for the remainder of their lives. Normally, the host system manages to gain control over viral replication at this point and the viremia falls. The virus is not cleared but evades the host immune response and establishes a persistent infection (Emini and Koff, 2004). The patient is often asymptomatic during this phase, which lasts for a variable amount of time. Only approximately 10% of HIV positive adults exhibit disease progression in the first two or three years of infection. After ten years, 80% of HIV positive adults have signs of disease progression (Ho, 1997). During this period of clinical latency, destruction of the lymphoid tissues continues as the virus replicates (Fauci, 2003). The length of the asymptomatic phase poses an enormous challenge for disease control and epidemic modeling (Anderson and May, 1990). Eventually, the virus does overcome the host immune system and the symptoms of HIV/AIDS begin to emerge, the number of host T-cells drops and the patient historically will progress to AIDS at this point (T-cell count below 200 units). No survivors of AIDS have yet been recorded. The symptoms of AIDS are variable but can often include: fever, weight loss, skin rashes, diarrhea, dementia, myelopathy, peripheral neuropathy and increased susceptibility to any opportunistic pathogen (Fauci, 2003). More rare symptoms include Kaposi sarcoma, oral hairy leukoplakia and lymphomas (Flint et al., 2004).

Chemotherapeutic drugs have changed the quality and quantity of life that can be expected for HIV-positive persons who can afford to take them. The three general types of palliative drugs are RT inhibitors that are nucleoside analogs, nonnucleoside inhibitors of RT, fusion inhibitors and protease inhibitors (Prescott et al., 2002). The first effective treatment used to combat HIV was azidovudine (AZT), which is a RT inhibitor (McCleod and Hammer, 1992). A combination of these three types of drugs is most effective and results in greatly reduced morbidity and mortality in countries where they are available (Fauci, 2003). However, the virus does remain latent in T-helper cells and treatment must be continued indefinitely to avoid activation of the virus.

Vaccine development

In addition to the continued arms race for improved chemotherapeutic agents, a vaccine will be a necessary step towards slowing down the spread of this virus. Despite great efforts an effective vaccine remains elusive. Vaccines have historically been most effective in blocking diseases that have a period of acute illness such as smallpox, polio or tetanus. The fact that the host immune response has never been effective in clearing this virus indicates the challenge that biologists face in vaccine development. However, with approximately 14,000 new infections each day (Emini and Koff, 2004) it is a task of enormous importance.

An effective vaccine will have to induce, upon introduction of the virus, an immune response that is different, not just stronger or faster, than the naïve immune response. An obvious target in vaccine development is the Env surface protein, which is integral in establishing HIV infection, as discussed above. A vaccine based on the humoral arm of the immune system would produce antibodies to block new infections. A trimeric Env complex, which includes gp120 and gp41, triggers fusion when complexed with the CD4 receptor and an appropriate coreceptor. Neutralizing monoclonal antibodies (mAbs) have been developed for gp120 that interfere with binding to the CD4 receptor. Similarly mAbs designed for gp41 seem to block fusion. Neutralizing antibodies have been developed for many distinct regions in these glycoproteins but have not been effective in vivo (Burton et al., 2004). Gp120 quickly adapts to immune pressure forming variable surface proteins and gp41, although considered to be more stable, is kinetically inaccessible (Burton et al., 2004). Fortunately, there is a simian immunodeficiency virus (SIV) that is almost identical to HIV. Unfortunately, an effective vaccine has not yet been developed to withstand an SIV challenge (Desrosiers, R.C. 2004).

Another notable obstacle in the vaccine development effort is the sequence variability of the HIV-1 viruses to which humans are exposed. Goulder and Walker (2002) described cases where patients already infected with one strain of HIV-1 became infected again when exposed to a different strain. This has serious consequences for treatment as well as vaccination. In cases of superinfection, the same drug regime that is effective for one strain may not be effective for the other. The antiretroviral drugs used for treating HIV have severe side effects for many patients and increasing the drug dosage or number of drugs may not be possible. A fully effective vaccine would have to protect against many different strains of HIV.

A vaccine designed for a cellular immune response would create anti-HIV-1 CD4+ memory and CD8+ CTLs (Emini and Koff, 2004). The humoral response would, theoretically, be more important to block the establishment of an infection. However, a stronger, faster cellular immune response could help to establish a lower viral load. This is important both for the morbidity of individuals and epidemiologically (Emini and Koff, 2004). This should not be undervalued. The fact that teenagers in every country in sub-Saharan Africa have a 50% chance of being infected with HIV (deWaal, 2002) makes it important to use realistic triage tactics in addition to seeking out a totally effective vaccine.

Microbicides are another strategy being pursued. An entirely effective microbicide (non-toxic, contraceptive or non-contraceptive, fully effective) is many years away (Lewis, 2003). Yet even a partially effective microbicide could save millions of lives. Vaccine and microbicide development can be seen as an important strategy for protecting women (Lewis, 2003). In many cultures women have neither the ability to protect themselves from exposure to this virus nor the power to handle the consequences of the illness. Both a vaccine and a microbicide could give a woman the ability to protect herself without the necessary consent of her partner.

Conclusions

This epidemic is unlike any the human race has encountered before and must be handled as such. In 1981, during the conservative years under President Reagan, when doctors in New York and California began to note this remarkable and horrible illness in young, gay men, the reaction was slow (Shilts, R., 1987). Public fear and indifference to the gay community made the work of the doctors dedicated to uncovering the root of this disease a battle (Shilts, R., 1987). Similarly, in September 2001, President Mbeki of South Africa questioned the link between HIV and AIDS and decided that zidovudine was too toxic to distribute in clinics. This ignored substantial research demonstrating that zidovudine could dramatically reduce the mother to child transmission of HIV (Lallemant et al., 2004). This trend of insistent ignorance and cruelty is seen repeatedly. In Russia, a group of medical school graduates wrote, in 1997, "We are . . . categorically opposed to combatingthe `new disease' AIDS! We intend . . . to impede the search. . . to combat this `noble' epidemic. We are certain that .. . AIDS will destroy all drug addicts, homosexuals, and prostitutes.. . . Long live AIDS!" (Field, 2004). Despite all of this, there is great cause, and need, for optimism. The pandemic has reached such staggering levels that honest discussions and massive changes are beginning. Education programs, condom and needle distribution programs and health care programs are growing. The World Health Organization aims to have 3 million people in treatment by the year 2005. This is a step towards the ultimate goal of total access to antiretroviral medications. HIV introduces a nontraditional security threat in addition to the massive human tragedy. Countries with high incidence of HIV infection are experiencing severe economic crises along with enormous demographic changes. The effects of the epidemic in regions such as sub-Saharan Africa will be felt globally. There is a constant call for the change in the behavior of those in high-risk populations. For health considerations, this is valid. However, an equally substantial change in behavior is needed in the general population to make the necessary funding and support available.

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