cara membuat blog

Panduan Gratis Cara Membuat Blog | Website | Situs Langkah 1
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Langsung saja…..!!!!! Tutorial Di bawah ini bisa saja di pakai untuk belajar cara membuat blog / website / situs

Pastikan Anda sudah mempunyai E-mail Bisa email dari yahoo, ymail, rocketmail, in.com, hotmail, gmail dll.. Hanya 3 langkah untuk CARA MEMBUAT BLOG/WEB/SITUS Full GRATIS….

Pendaftaran Domain
Pendaftaran Hosting
Install Script

Contoh :

Buatsitus.co.cc
Bob85.co.cc
Membuat-web.co.cc

Ingat tutorial ini FULL GRATIS tanpa di pungut biaya apapun…
1. Jika tertarik langsung saja daftar melalui link di bawah ini untuk daftar DOMAIN GRATIS :
Daftar Klik Segera Disini




2. Tuliskan Nama Domain yang anda sukai atau anda inginkan. misalnya : namaku, buatsitus dll. Masukan Tanpa www
Kemudian Klik Tombol : Check Availability

Setelah itu jika anda beruntung anda dapat memperoleh domain gratis seperti dibawah ini:

www.bob85.co.cc is available
One year domain registration for $0
lanjutkan ke klik : Continue to registration

Tetapi jika yang muncul adalah pemberitahuan seperti ini :



www.membuatsitus.co.cc is available
One year domain registration for $3
Berarti kamu harus membayar $3, kalau memang kamu butuh nama domain tersebut, boleh kamu membelinya, menggunakan paypal atau credit card. Tapi jika tidak, ulangi masukan nama domain kamu dengan nama yang lain,
Dengan Klik Getting A New Domain.

Tetapi jika muncul pemberitahuan seperti ini :



www.buatsitus.co.cc is already registered
hal ini menandakan bahwa domain tersebut sudah dimiliki orang lain, namun jangan khawatir silakan coba ulangi masukan nama domain kamu dengan nama domain yang lain. atau dengan memilih / Klik domain yang disediakan di bawahnya seperti ilustrasi dibawah dengan harga FREE..

Silakan coba berulang-ulang kali jika masih tetap belum menemukan domain kesukaan anda yang gratis. Sampai anda menemukan bahwa domain tersebut “ is available dan $0…” Untuk mempermudah anda mendapatkan domain gratis di co.cc kami menyediakan beberapa tips GRATIS, silakan baca tulisan di bawah ini.

Tips daftar domain di co.cc:

Coba hindari kata2 berbahasa inggris seperti : website, home, backlink, bookmark, tool… (biasanya meskipun bisa, tapi pasti harus bayar $3)
Coba gunakan kata2 berbahasa indonesia : bikinwebgratis, anakbelajar, mencariilmu, belajarbuatblog… atau menggunakan strip (-) contoh : buat-web-gratis, belajar-blog-gratis, nama-sendiri, jualan-pulsa, download-mp3, komik-naruto, dll ( menurut saya jika kamu tetap tidak dapat domain yang kamu inginkan, coba gunakan nama domain asal-asalan misal : gajahfluburung, inginkayamendadak, siapakamu, googleku, juga bisa menggunakan kata2 kombinasi huruf dan angka : sepatu26, membuatsitus88, jokotingkir21, yuseprukmana25 dll, yang penting pada tahap ini kamu bisa dan tahu dulu cara mendapatkan domain dan hosting )

3. Kalau sudah dapat is available dan $0… Klik Continue to Registration :



4. Silahkan klik : Create An Acount Now

5. Lengkapi Data-data anda sesuai dengan indentitas, Harus di isi dengan benar ya :) .

Nama lengkap
Alamat Email
Tanggal Lahir
Password

(Data-data diatas Harus Dicatat di Notepad atau Ms Word Karena nanti akan sangat diperlukan) Username Password Langkah 1
Account Information
(kalau yang di bawah ini boleh asal tapi harus di isi)

Alamat rumah
Kota
Negara
No Tlp
Dll

6. Klik centang dan tombol CREATE AN ACCOUNT NOW


7. Masukan username dan password yg kamu buat kemudian masukan gambar tulisan seperti diatas..
SIGN IN >> ikuti sampai SETUP..


8. Setup lagi kemudian pilih nomor 1 (nameserver)
9. Masukan nameservernya dari Hostingforfree (karena nanti kita akan daftar hosting disini)

ns1.hostingforfree.us
ns2.hostingforfree.us

10. Kemudian klik SETUP, hati2 jangan salah masukan Nameserver ini karena salah satu huruf saja akan berakibat tidak akan ONLINE website kamu.
Kalo berhasil silahkan lanjutkan ke pendaftaran hosting, tp jika belum berhasil coba ulangi lagi tahapannya karena sebagian besar ternyata berhasil,, kira2 sekitar 1800 orang/bulan yg berhasil membuat DOMAIN dengan tutorial yg saya berikan ini.. SEMANGAT

Langkah ke 2 adalah Daftar Hosting Gratis

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cara membuat efek salju pada blog

, ia Salju,, Tapi Bukan Salju yang adda di Kutub, ini Salju yang yang terdapat pada Background, seperti anda Liat sekarang ini di Blog q,
Dengan Tujuan Memperindah Blog , Supaya Blog kita tidak terlihat monoton.. hhee..
Saya ingin sekali berbagi ilmu engan sobat, walawpun sedikit ilmu yang aq bisa berikan Untuk kalian,
Yawdah Ya Sob, Langsung aja Kita sikat Caranya :
Kalau mau, ini source codenya. Tapi sebelumnya yang perlu diingat, "download template" sobat dulu biar kalo ada eror ngga buat frustasi.

Nah sekarang cari , trus paste/ganti dengan code ini:





Bagaimana ??
indah Bukan ?

Mudah - Mudahan Selain Salju bisa turun di Blog, Salju Es bisa Turun di indonesia ia, biar kaya Luar Negri..
hhee..
Tapi hanya Khayalan!!

BlackBerry PlayBook

 Performa profesional
BlackBerry PlayBook Tablet merupakan computer dengan kemampuan penuh dalam bentuk tablet
Prosesor 1GHz dual-core
RAM 1GB
MultiprosesSimetrik
 Web tanpa batas
BlackBerry PlayBook cocok untuk permainan, media, aplikasi, dan semua yang bias diakses lewat Internet
Mendukungsepenuhnya Adobe® Flash® 10.1
ternal untuk HTML 5
Tampilan teks, grafis, dan video tanpak ompromi
 Pengalaman BlackBerry yang disempurnakan
Sambungkan smartphone BlackBerry secaranir ka


bel untuk akses real time ke: Email, kalender, buku alamat, daftar tugas, dan BBM
 BlackBerry tablet OS
BlackBerry PlayBook Tablet menggunakan teknologi QNX
yang mudah digunakan dan canggih:
Teknologi yang digunakan World Wide Web
Multi proses untuk multi tugas yang sebenarnya
 Konverensi video
Layar HD jernih
Dua kamera video
 Media terbaik
Kameradepan 3 MP definisitinggi
Kamerabelakang 5 MP definisitinggi
Mendukung codec untukpemutarandanpembuatan
media sertapanggilan video yang sempurna
Video HD 1080p; H.264, MPEG4, WMV output video HDMI
Port Micro USB dan Micro HDMI
 Sangatpraktis
Layar LCD 7", resolusilayar 1024 x 600
400g (0,9lbs)
Layar sentuh kapasitif
 Ekosistem aplikasi yang banyak
Lingkungan pengembangan aplikasi cepat
BlackBerry Tablet OS yang handal, dengan teknologi QNX
Mendukung POSIX OS, SMP, Open GL, WebKit, Adobe Flash, Java®, dan Adobe Mobile AIR
 Cocok untuk bisnis
BlackBerry PlayBook terhubung dengan BlackBerry Enterprise Server
Dapat dipasangkan dengan sempurna untuk jalur aman ke smartphone BlackBerry® Anda
Akses 3G melalui program layanan smartphone BlackBerry yang ada
Akses data perusahaan
Aman dan mudah dikelola

Daftar Pustaka
http://id.blackberry.com/playbook-tablet/#updates

BlackBerry Tablet


UI dan kinerja - Pengalaman pengguna adalah kejutan terbesar dari pedoman tersebut. Sangat mudah untuk belajar, halus untuk menavigasi, dan memiliki beberapa respons terbaik dan tercepat yang akan Anda temukan pada setiap smartphone atau tablet. Ini adalah pengalaman yang berbeda dari smartphone BlackBerry

fitur Web browsing-Full - Seperti yang telah kita bicarakan, pengalaman browsing Web pada pedoman yang sangat baik. Meskipun aku bukan penggemar Flash, itu masih merupakan bagian besar dari Web dan akan selama bertahun-tahun, sampai HTML5 menggantikan itu dan Playbook sudah menangani HTML5 cukup baik

Dapat digunakan pengolah kata - Salah satu keluhan terbesar saya dengan iPad isn'ta adalah bahwa ada aplikasi pengolah kata yang layak untuk mengambil catatan, menulis surat / memo, bangunan dokumen dasar, dll Apple aplikasi Halaman yang sedikit terlalu rumit daripada itu perlu dan aplikasi seperti iA Writer yang bagus tapi terlalu telanjang tulang hampir sedikit. Its Word To Go app adalah aplikasi pengolah kata terbaik saya digunakan pada tablet. Hal ini mati mudah digunakan dan memiliki fitur dasar yang paling penting untuk membangun sebuah dokumen yang baik. Plus, gratis dan diinstal secara default. Ini adalah tempat akuisisi RIM dari Davaviz - perusahaan di belakang Dokumen Go - telah benar-benar membantu.

Brilliant untuk multimedia - Kinerja grafis dan layar LCD pada pedoman yang lain ditambah besar - dan lain kejutan menyenangkan karena BlackBerry tidak dikenal sebagai pusat multimedia Playbook ini luar biasa untuk menonton video dan melihat foto. Gambar-gambar tajam, warna-warna yang cerah, dan kinerja yang tajam.

Daftar Pustaka
http://www.wayantulus.com/harga-dan-spesifikasi-blackberry-playbook-tablet

KURVA PERTUMBUHAN BAKTERI

Kurva di atas disebut sebagai kurva pertumbuhan bakteri. Ada empat fase pada pertumbuhan bakteri sebagaimana tampak pada kurva, yaitu :

1. Fase lag
Fase Lag merupakan fase penyesuaian bakteri dengan lingkungan yang baru. Lama fase lag pada bakteri sangat bervariasi, tergantung pada komposisi media, pH, suhu, aerasi, jumlah sel pada inokulum awal dan sifat fisiologis mikroorganisme pada media sebelumnya. Ketika sel telah menyesuaikan diri dengan lingkungan yang baru maka sel mulai membelah hingga mencapai populasi yang maksimum. Fase ini belum terjadi pembelahan sel karena beberapa enzim mungkin belum disintesis. Jumlah sel pada fase ini mungkin tetap, tetapi kadang-kadang menurun. Lamanya fase ini bervariasi, dapat cepat atau lambat tergantung dari kecepatan penyesuaian dengan lingkungan di sekitarnya.

Lamanya fase adaptasi dipengaruhi oleh beberapa faktor, di antaranya adalah sebagai berikut:
(a) Medium dan lingkungan pertumbuhan. Sel yang ditempatkan pada medium dan lingkungan pertumbuhan sama seperti medium dan lingkungan sebelumnya, mungkin tidak diperlukan waktu adaptasi. Tetapi jika nutrien yang tersedia dan kondisi lingkungan yang baru sangat berbeda dengan sebelumnya, diperlukan waktu penyesuaian untuk mensintesis enzim-enzim yang dibutuhkan untuk metabolisme.
(b) Jumlah inokulum. Jumlah sel yang semakin tinggi akan mempercepat proses adaptasi. Fase adaptasi mungkin berjalan lambat karena beberapa sebab, misalnya : (1) kultur dipindahkan dari medium yang kaya nutrien ke medium yang kandungan nutriennya terbatas, (2) mutan yang baru terbentuk menyesuaikan diri dengan lingkungannya, (3) kultur yang dipindahkan dari fase statis ke medium baru dengan komposisi sama seperti sebelumnya.

2.Fase Eksponensial
Fase Eksponential ditandai dengan terjadinya periode pertumbuhan yang cepat. Setelah mikroba menyesuaikan diri dengan lingkungannya, yakni pada fase adaptasi dan fase permulaan pembiakan, maka sel jasad renik membelah dengan cepat, dimana pertambahan jumlahnya mengikuti kurva logaritmik. Pada fase ini kecepatan pertumbuhan sangat dipengaruhi oleh medium tempat tumbuhnya seperti Ph dan kandungan nutrien, suhu dan kelembapan udara. Pad fase ini sel membutuhkan energi lebih banyak dibandingkan dengan fase lainnya, selain itu sel paling sensitif terhadap keadaan lingkungan.Bila kita ingin mengadakan piaraan yang cepat tumbuh, maka bakteir pada fase ini baik sekali untuk diadakan inokulum.

3.Fase stasioner
Fase stasioner terjadi pada saat laju pertumbuhan bakteri sama dengan laju kematiannya, sehingga jumlah bakteri keseluruhan bakteri akan tetap. Keseimbangan jumlah keseluruhan bakteri ini terjadi karena adanya pengurangan derajat pembelahan sel. Hal ini disebabkan oleh kadar nutrisi yang berkurang dan terjadi akumulasi produk toksik sehingga menggangu pembelahan sel.
4.Fase Kematian
Fase Kematian ditandai dengan peningkatan laju kematian yang melampaui laju pertumbuhan, sehingga secara keseluruhan terjadi penurunan populasi bakteri. Pada fase ini sebagian populasi jasad renik mulai mengalami kematian karena sebab, yakni:
1. Nutrien di dalam medium sudah habis,
2. Energi cadangan di dalam sel habis. Jumlah sel yang mati semakin lama akan semakin banyak, dan kecepatan kematian dipengaruhi kondisi nutrie, lingkungan dan jenis jasad renik.



DAFTAR PUSTAKA
1. Waluyo,Lud.Drs.M.Kes.2004.Mikrobiologi Umum.Universitas Muhammadiyah Press : Malang.
2. Schlegel,H.G. dan Schmidt, K.1994. Mikrobiologi Umum. Gadjah Mada University Press : Yogyakarta.
3. Volk, W.A. dan Wheeler, M.F., 1993, Mikrobiologi Dasar, Jilid I, Ed ke-5, Erlangga, Jakarta.

SKIN PUNCTURE

Proses pengambilan darah dengan tusukan kulit. Spesimen darah diperoleh tusukan kulit.
.
Indikasi melakukan skin puncture:
1. pasien dengan luka bakar yang parah
2. pasien yang sangat gemuk (obesitas)
3. venipuncture sudah dipakai untuk tujuan terapi
4. usia lanjut
5. vena superficial tidak dapat diakses atau sangat rapuh
6. bila pasien mempunyai kecenderungan trombosis
7. apabila vena sulit ditemukan

Peralatan yang dipergunakan untuk skin puncture antara lain :
1. Lancet
2. Tabung penampung ukuran mikro
3. Kapas alkohol

Kulit merupakan campuran darah dari arteriol, venula, dan kapiler, dan intraseluler cairan interstisial.
Komposisinya dipengaruhi oleh beberapa faktor:
1. Aliran darah ke kulit pada saat pengumpulan spesimen.
2. Proporsi relatif dan vena darah arteri. Proporsi arteri
darah adalah lebih besar daripada darah vena karena tekanan arteriola dan
dahan arteri kapiler jauh lebih besar dari tekanan di venula
dan dahan vena dari kapiler.
3. Komposisi darah vena di kulit. Vena darah dalam kulit lebih
mirip dengan darah arteri daripada darah vena di bagian lain dari tubuh

Tindakan yang dilakukan sebelum melakukan skin puncture:
1. Menyapa dan Identifikasi pasien.
Konfirmasi pasien pertama dan terakhir nama. Minta pasien untuk mengeja namanya, jika diperlukan.
Jika seorang pasien tidak sadar, terlalu muda, mental tidak kompeten, mintalah seorang atau teman, kerabat untuk mengidentifikasi pasien dengan nama dan alamat. Pastikan bahwa nama pasien cocok dengan lembar permintaan pemeriksaan.
2. Pasang Perlengkapan
Pilih dan mengatur semua perlengkapan yang diperlukan untuk menggambar ini. Memanfaatkan khusus tabung koleksi mikro dirancang untuk digunakan dengan tusuk kulit. Pastikan tabung ekstra dalam jangkauan. Buka paket untuk kasa pad dan persiapan alkohol.
3. Cuci tangan dan memakai sarung tangan.
4. Posisi pasien
Mintalah pasien untuk duduk nyaman di kursi. Jika pasien adalah anak Anda mungkin perlu orang tua atau wali untuk menahan anak di kursi

5. Yakinkan pasien.
Phlebotomist harus meyakinkan pasien bahwa, meskipun fingerstick / heelstick akan sedikit menyakitkan, itu akan menjadi durasi pendek. Bijaksana untuk memberitahu pasien ketika lanset memasuki kulit sehingga pasien tidak takut. Jangan pernah memberitahukan pasien, "Ini tidak akan terluka."
6. Pilih lokasi
Sisi permukaan tumit, untuk bayi kurang dari satu tahun.
Permukaan sisi jari manis untuk anak-anak yang lebih tua dan orang dewasa.
Kulit daun telinga tidak dianjurkan.

Jika Pasien bayi, daerah paling aman untuk membuat bayi adalah tumit atau neonatal adalah pada medial atau lateral bagian paling sebagian besar permukaan plantar .
1) Dengan bayi di bawah posisi berbaring, lokasi sayatan tumit dibersihkan dengan kapas antiseptik dan udara kering.Tusukan tidak lebih dari 2,4 mm. Jangan melakukan tusukan pada kelengkungan belakang tumit. Jangan tusukan sebelumnya situs. Kulit tusukan untuk memperoleh spesimen darah harus tidak dilakukan pada daerah pusat bayi kaki suatu (daerah dari arch). Hal ini dapat mengakibatkan cedera pada saraf, tendon, dan
tulang rawan dan menawarkan keuntungan tidak lebih dari menusuk tumit.
2) Kulit tusukan tidak boleh dilakukan pada jari bayi. Jarak dari permukaan kulit ke tulang di tebal bagian dari segmen terakhir dari masing-masing jari bayi baru lahir bervariasi 1,2-2,2 mm, dan dengan lancets tersedia tulang dengan mudah bisa terluka. bayi baru lahir, infeksi lokal dan gangrene merupakan potensi komplikasi dari tusukan jari.

Apabila pasien dewasa ,lokasi tusukan kulit harus hangat dan tidak boleh bengkak (Edema), karena akumulasi cairan dalam jaringan akan mencemari spesimen darah.
1) Bersihkan tusukan-situs kulit dengan persiapan alkohol komersial
Situs harus benar-benar kering dengan pad kasa sebelum tertusuk karena alkohol
menyebabkan hemolisis. Kesalahan dalam penentuan glukosa darah disebabkan oleh kontaminasi dengan preps alkohol. Betadine tidak boleh digunakan untuk membersihkan dan mensterilkan-tusuk situs kulit. Darah yang terkontaminasi dengan betadine palsu dapat meningkatkan kadar kalium, fosfor, atau urat asam.
2) Tusuk lokasi
Studi telah dilakukan untuk menentukan kedalaman optimal pungsi kulit dari mana sebuah spesimen darah dapat diperoleh tanpa menyebabkan cedera pada bayi baru lahir dan orang dewasa. Memanfaatkan teknik berikut untuk kulit menusuk:
 Pembuluh darah utama kulit terletak di persimpangan subkutan kulit,
yang pada bayi baru lahir tumit adalah 0,35 untuk 1.6mm di bawah permukaan kulit. Oleh karena itu, bahkan di bayi terkecil, pungsi 2,0-2,3 mm mendalam pada permukaan plantar tumit akan menembus pembuluh kulit besar dan tidak bocor risiko tulang.
 Tumit atau jari harus diadakan tegas untuk mencegah gerakan tiba-tiba.
 Jika jari digunakan, pegang jari tiga inci di bawah ujung. Lokasi yang ideal adalah ujung atau cincin jari keempat tangan non-dominan.


 Kumpulkan Spesimen
1. Tusuk kulit dan menghapus darah yang pertama keluar dengan kain kasa.
2. Tekan dengan lembut Terapkan untuk membuat jari atau tumit berdarah.
3. Pegang tabung microcollection pada sudut bawah horisontal dengan lubang atas dari setetes darah dengan koleksi-tabung mikro dan memungkinkan jumlah yang diinginkan darah mengalir ke tabung.
4. Tutup lokasi pengambilan dengan Band-Aid
5. Pelabelan pada spesimen
6. Buang sarung tangan dan cuci tangan.

ASAM ASETAT

Rumus kimia asam asetat adalah CH3COOH atau C2H4O2.. Asam asetat memiliki berat molekul sebesar 60,05. Asam asetat atau lebih dikenal dengan nama asam cuka adalah golongan asam karboksilat yang sering digunakan dalam kehidupan sehari-hari yaitu digunakan sebagai pemberi rasa asam pada makanan, selain itu asam cuka digunakan untuk menurunkan pH dan sebagai zat pengawet. Asam asetat biasa digunakan pada pembuatan serat selulosa asetat, plastik, zat warna, dan obat-obatan.

 Prosedur pemeriksaan Asam Asetat (Alkalimetri)
Penetapan kadar: timbang seksama lebih kurang 6 ml dalam labu bersumbat yang telah ditara. Ditambahkan 40 ml air dan titrasi dengan natrium hidroksida 1 N LV menggunakan indikator fenolftalein LP.
1 ml natrium hidroksida 1 N setara dengan 60,05 mg C2H4O2.

 Reaksi kimia CH3COOH dengan NaOH
CH3COOH + NaOH CH3COONa + H2O

Daftar Pustaka
Sutresna, Nana. 2007. Cerdas Belajar Kimia. Bandung: Grafindo Media Pratama. Halaman: 229.
Anonym.1995.Farmakope Indonesia, edisi IV.Jakarta:Departemen Kesehatan RI. Halaman: 45-46.

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Iodometri dan Iodimetri

Reaksi-reaksi kimia yang melibatkan oksidasi reduksi dipergunakan secara luas oleh analisis
titrimetrik. Ion-ion dari berbagai unsur dapat hadir dalam kondisi oksidasi yang berbeda-beda,
menghasilkan kemungkinan banyak reaksi redoks. Banyak dari reaksi-reaksi ini memenuhi
syarat untuk dipergunakan dalam analisi titrimetrik dan penerapan-penerapannya cukup banyak.
Iodometri adalah analisa titrimetrik yang secara tidak langsung untuk zat yang bersifat oksidator
seperti besi III, tembaga II, dimana zat ini akan mengoksidasi iodida yang ditambahkan
membentuk iodin. Iodin yang terbentuk akan ditentukn dengan menggunakan larutan baku
tiosulfat .
Oksidator + KI → I2 + 2e
I2 + Na2 S2O3 → NaI + Na2S4O6

Sedangkan iodimetri adalah merupakan analisis titrimetri yang secara langsung digunakan untuk zat reduktor atau natrium tiosulfat dengan menggunakan larutan iodin atau dengan penambahan larutan baku berlebihan. Kelebihan iodine dititrasi kembali dengan larutan tiosulfat.
Reduktor + I2 → 2I-
Na2S2 O3 + I2 → NaI +Na2S4 O6

Untuk senyawa yang mempunyai potensial reduksi yang rendah dapat direksikan secara
sempurna dalam suasana asam. Adapun indikator yang digunakan dalam metode ini adalah
indikator kanji.
Sedangkan bromometri merupakan metode oksidasi reduksi dengan dasar reaksi aksidasi dari ion
bromat .
BrO3- + 6H+ + 6e → Br- + 3H2O
Adanya kelebihan KBrO3 dalam larutan akan menyebabkan ion bromida bereaksi dengan ion
bromat
BrO3 + Br- + H+ → Br2 +H2O

Bromine yang dibebaskan akan merubah warna larutan menjadi kuning pucat (warna merah ),
jika reaksi antara zat dan bromine dalam lingkungan asam berjalan cepat maka titrasi dapat
secara langsung dilakukan. Namun bila lambat maka dapat dilakukan titrasi tidak langsung yaitu
larutan bromine ditambah berlebih dan kelebihan bromine ditentukan secar iodometri. Bromin
dapat diperoleh dari penambahan asam kedalam larutan yang mengandung kalium bromat dan
kalium bromide.
Substansi-substansi penting yang cukup kuat sebagai unsur-unsur reduksi untuk dititrasi
langsung dengan iodin adalah tiosulfat, arseni dan entimon, sulfida dan ferosianida. Kekuatan
reduksi yang dimiliki oleh dari beberapa substansi ini adalah tergantung dari pada konsentrasi
ion hydrogen, dan reaksi dengan iodin baru dapat dianalisis secara kuantitatif hanya bila kita
melakukan penyesuaian ph yang sulit.
Dalam menggunakan metode iodometrik kita menggunakan indikator kanji dimana warna dari
sebuah larutan iodin 0,1 N cukup intens sehingga iodin dapat bertindak sebagai indikator bagi
dirinya sendiri. Iodin juga memberikan warna ungu atau violet yang intens untuk zat-zat pelarut seperti karbon tetra korida dan kloroform. Namun demikan larutan dari kanji lebih umum
dipergunakan, karena warna biru gelap dari kompleks iodin–kanji bertindak sebagai suatu tes
yang amat sensitiv untuk iodin.
Dalam beberapa proses tak langsung banyak agen pengoksid yang kuat dapat dianalisis dengan
menambahkan kalium iodida berlebih dan mentitrasi iodin yang dibebaskan. Karena banyak agen
pengoksid yang membutuhkan larutan asam untuk bereaksi dengan iodin, Natrium tiosulfat
biasanya digunakan sebagai titrannya. Titrasi dengan arsenik membutuhakn larutan yang sedikit
alkalin.
Dalam larutan yang sedikit alkalin atau netral, oksidasi menjadi sulfat tidak muncul terutama jika
iodin dipergunakan sebagai titran. Banyak agen pengoksid kuat, seperti garam permanganat,
garam dikromat yang mengoksid tiosulfat menjadi sulfat, namun reaksinya tidak kuantitatif.
Pada penentuan iodometrik ada banyak aplikasi proses iodometrik seperti tembaga banyak
digunakan baik untuk biji maupun paduannya metode ini memberikan hasil yang lebih sempurna
dan cepat daripada penentuan elektrolit tembaga.
Pada metode bromometri, kalium bromat merupakan agen pengoksid yang kuat dengan potensial
standar dari reaksinya
BrO3 + 6H+ + 6e → Br- + 3H2O

Adalah +1,44 V. Reagen dapat digunakan dalam dua cara yaitu sebagai sebuah oksdasi langsung
untuk agen-agen pereduksi tertentu dan untuk membangkitkan sejumlah bromin yang
kuantitasnya diketahui.
Sejumlah agen pereduksi pada titrasi langsung metode bromometri sepertyi arsenik, besi (II) dan
sulfida serta disulfida organik tertentu dapat dititrasi secara langsung dengan sebuah larutan
kalium bromat .
Kehadiran bromin terkadang cocok untuk menentukan titik akhir titrasi,
beberapa indikator organik yang bereaksi dengan bromin untuk memberikan perubahan warna.
Perubahan warna ini biasanya tidak reversibel dan kita harus hati-hati agar kita mendapatkan
hasil yang lebih baik .
Reaksi brominasi senyawa-senyawa organik larutan standar seperti kalium bromat dapat
dipergunakan untuk menghasilkan sejumlah bromin dengan kuantitas yang diketahui. Bromin
tersebut kemudian dapat digunakan untuk membrominasi secara kuantitatif berbagai senyawa
organik. Bromide berlebih hadir dalam kasus-kasus semacam ini, sehingga jumlah bromin yang
dihasilkan dapat dihitung dari jumlah KBrO3 yang diambil. Biasanya bromin yang dihasilkan
apabila terdapat kelebihan pada kuantitas yang dibutuhkan untuk membrominasi senyawa
organik tersebut untuk membantu memaksa reaksi ini agar selesai sepenuhnya.
Reaksi bromin dengan senyawa organiknya dapat berupa subtitusi atau bisa juga reaksi adisi

Translasi (genetik)

Translasi dalam genetika dan biologi molekular adalah proses penerjemahan urutan nukleotida yang ada pada molekul mRNA menjadi rangkaian asam-asam amino yang menyusun suatu polipeptida atau protein. Transkripsi dan Translasi merupakan dua proses utama yang menghubungkan gen ke protein.Translasi hanya terjadi pada molekul mRNA, sedangkan rRNA dan tRNA tidak ditranslasi. Molekul mRNA yang merupakan salinan urutan DNA menyusun suatu gen dalam bentuk kerangka baca terbuka.mRNA membawa informasi urutan asam amino.

Proses
Proses translasi berupa penerjemahan kodon atau urutan nukleotida yang terdiri atas tiga nukleotida berurutan yang menyandi suatu asam amino tertentu. Kodon pada mRNA akan berpasangan dengan antikodon yang ada pada tRNA.Setiap tRNA mempunyai antikodon yang spesifik.Tiga nukleotida di anti kodon tRNA saling berpasangan dengan tiga nukleotida dalam kodon mRNA menyandi asam amino tertentu. Proses translasi dirangkum dalam tiga tahap, yaitu inisiasi, elongasi (pemanjangan) dan terminasi (penyelesaian).Translasi pada mRNA dimulai pada kodon pertama atau kodon inisiasi translasi berupa ATG pada DNA atau AUG pada RNA. Penerjemahan terjadi dari urutan basa molekul (yang juga menyusun kodon-kodon setiap tiga urutan basa) mRNA ke dalam urutan asam amino polipeptida. Banyak asam amino yang dapat disandikan oleh lebih dari satu kodon.Tempat-tempat translsasi ini ialah ribosom, partikel kompleks yang memfasilitasi perangkaian secara teratur asam amino menjadi rantai polipeptida. Asam amino yang akan dirangkaikan dengan asam amino lainnya dibawa oleh tRNA. Setiap asam amino akan dibawa oleh tRNA yang spesifik ke dalam kompleks mRNA-ribosom. Pada proses pemanjangan ribosom akan bergerak terus dari arah 5'3P ke arah 3'OH sepanjang mRNA sambil merangkaikan asam-asam amino. Proses penyelesaian ditandai denga bertemunya ribosom dengan kodon akhir pada mRNA

Translasi prokariot dan eukariot
Walaupun mekanisme dasar trskripsi dan translasi serupa untuk prokariot dan eukariot, terdapat suatu perbedaan dalam aliran informasi genetik di dalam sel tersebut. Karena bakteri tidak memiliki nukleus (inti sel), DNA-nya tidak tersegregasi dari ribosom dan perlengkapan pensintesis protein lainnya. Transkripsi dan translasi dipasangkan dengan ribosom menempel pada ujung depan molekul mRNA sewaktu transkripsi masih terus berlangsung. Pengikatan ribosom ke mRNA membutuhkan situs yang spesifik.Sebaliknya, dalam sel eukariot selubung nukleus atau membran inti memisahkan transkripsi dari translasi dalam ruang dan waktu. Transkripsi terjadi di dalam inti sel dan mRNA dikirim ke sitoplasma tempat translasi terjadi.

Sindrom Progeria

Progeria merupakan penyakit kesalahan kode genetik (terjadi mutasi), tepatnya kelainan protein (Lamin A) di sekitar inti sel atau menurut para ahli lainnya kesalahan terdapat di kromosom nomor 1, pada seseorang yang mengakibatkan penuaan dini sebelum waktunya.
Progeria terdiri atas dua jenis yaitu sindrom Hutchinson-Gliford (progeria masa kanak-kanak) dan sindrom Werner (progeria masa dewasa)
Progeria masa kanak-kanak atau yang disebut sebagai sindroma Hutchinson-Gliford ditandai dengan adanya kegagalan pertumbuhan pada tahun pertama kehidupan. Tampak dengan jelas adanya ketidakseimbangan ukuran tubuh (kecil atau cenderung kurus), kulit terlihat keriput, pertumbuhan gigi terlambat atau bahkan tidak ada sama sekali, kemampuan bergerak sangat terbatas, dan beberapa ciri-ciri lainnya. Biasanya, penderita hanya sanggup bertahan hidup sampai awal usia remaja, rata-rata hingga usia 13-14 tahun.
Para penderita seringkali mengalami aterosklerosis progresif (kelainan penyumbatan pembuluh darah) seperti yang biasa tampak pada individu lanjut usia. Hal ini dapat mengakibatkan stroke atau serangan jantung yang berujung pada kematian. Hingga saat ini belum ditemukan pengobatan dan pencegahan yang tepat untuk penanganan kasus progeria ini.
Di Indonesia pun, penyakit Progeria sangatlah langka. Baru ditemukan seorang anak Indonesia yang mengalami nasib kurang beruntung itu. Anak itu bernama Wiradianty yang akrab dipanggil Ranti, yang saat ini telah beristirahat dengan tenang di pangkuan Tuhan Yang Maha Esa.
Eriyati Indrasanto, ahli genetika anak pada Rumah Sakit Harapan Kita, merupakan salah satu dokter yang menangani Ranti ketika masih hidup. Saat mulai berobat, Ranti kecil berusia tujuh tahun tiga bulan. Beratnya 10 kg dan tinggi 94 cm. Menurut Eriyati, di dunia hanya ditemui satu penderita Progeria di antara 250.000 kelahiran hidup. Meski begitu, ditemukan pula sebuah keluarga dengan lima orang anak yang seluruhnya adalah penderita Progeria. "Saat ini, di dunia baru tercatat 60 kasus," ujarnya. Penyakit ini pertama kali ditemukan di London, Inggris, pada 1752.
Anak penderita Progeria, pada umumnya, baru ‘disadari’ ketika melihat kondisi fisik anak tersebut setelah berumur setahun. Gejala utamanya, rambut rontok hingga botak, tubuhnya mengecil, dan ada kelainan serta perkembangan tulang yang tak sempurna. Indikasi lain, pembuluh darah di batok kepala terlihat jelas, kulit tak mulus, kuku menjadi rapuh, melengkung, dan kekuning-kuningan. Kaki pun mengalami pengeroposan. Selain itu, gigi tumbuh jarang. Bahkan, dalam beberapa kasus, gigi sama sekali tak tumbuh, seperti yang telah disampaikan sebelumnya. Pada kasus Ranti, sang penderita pun mengalami gangguan pendengaran, katarak, serta gangguan pada limfa.
"Yang perlu mendapat perhatian adalah adanya penumpukan kolesterol di pembuluh darah, terutama di jantung dan usus," kata Eriyati.
Meski begitu, perkembangan otak dan kemampuan inteligensianya tak mengalami gangguan. "Kemampuannya sama dengan anak-anak lain seusianya," kata Eriyati. Hanya saja, kondisi tubuh Ranti tak memungkinkan penderita melakukan aktivitas sebanyak rekan sebayanya.
Menurut Eriyati, sampai sekarang masih belum ada terapi efektif untuk progeria. "Saat ini, penanganannya berdasar keluhan saja," katanya. Pengobatan memang masih jadi masalah. Hal ini dikarenakan penyebab penyakit Progeria sendiri pun masih jadi tanda tanya.
Sejumlah literatur menyebutkan, stroke bisa menyerang anak-anak progeria pada usia empat hingga lima tahun. Eriyati juga mengingatkan pentingnya perhatian terhadap jantung. "Tersumbatnya aliran darah ke jantung adalah penyebab utama kematian si penderita," ujarnya. Hingga saat ini, harapan hidup penderita "hanya" sampai 14 tahun. Lantaran keburu meninggal, barangkali ini alasannya mengapa para ahli genentika kesulitan melacak kaitan penyakit ini dengan faktor keturunan
Sangat disayangkan, ketika individu lain melewati penuaan secara perlahan sembari menikmati waktu hidup mereka, para penderita Progeria justru merasakan suatu hal yang di mana jam penuaan berputar dengan kecepatan amat tinggi, sehingga proses penguzuran berlangsung jauh lebih cepat daripada yang normal terjadi.
Asumsi yang diambil Krawetz yaitu semua gen yang berkaitan dengan proses penuaan adalah bagian dari respons normal karena suatu mekanisme kontrol telah hilang. Maka bila semua gen serempak “dipadamkan”, sehingga responsnya tadi terhenti, untuk dibiarkan berkembang normal, proses penuaan tidak akan terjadi.
Bila penanda progeria dapat ditemukan, Krawets akan mampu mencari jalan mematikan proses penuaan cepat akibat progeria. Jika berhasil, berarti telah ditemukan pula cara menghentikan semua jenis penuaan. Demikianlah, kiprah manusia dalam ilmu yang satu ini tak urung mengundang decak kagum.
Hanya saja, seperti yang tertulis di atas, Progeria belum dapat dicegah maupun diobati. Yang bisa kita lakukan bila dihadapkan dengan kasus seperti itu adalah tetap mendampingi dan memberi semangat kepada sang penderita. Bimbingan untuk membangun rasa percaya diri pun sangat dibutuhkan. Tak ketinggalan, satu hal yang utama dalam menghadapi kasus Progeria yaitu kesabaran, karena para penderita Progeria memiliki emosi yang cenderung tidak stabil. Sehingga emosi kita pun bisa saja ikut tidak stabil ketika kita menghadapi mereka.

Sumber: http://id.shvoong.com/medicine-and-health/genetics/1942233-penyakit-langka-progeria-progeria-merupakan/#ixzz1MrDtdT5o

Urinary Tract Infection (UTI)

What is a urinary tract infection (UTI)?

The urinary tract is comprised of the kidneys, ureters, bladder, and urethra (see Figure 1). A urinary tract infection (UTI) is an infection caused by pathogenic organisms (for example, bacteria, fungi, or parasites) in any of the structures that comprise the urinary tract. However, this is the broad definition of urinary tract infections; many authors prefer to use more specific terms that localize the urinary tract infection to the major structural segment involved such as urethritis (urethral infection), cystitis (bladder infection), ureter infection, and pyelonephritis (kidney infection). Other structures that eventually connect to or share close anatomic proximity to the urinary tract (for example, prostate, epididymis, and vagina) are sometimes included in the discussion of UTIs because they may either cause or be caused by UTIs. Technically, they are not UTIs and will be only briefly mentioned in this article.

UTIs are common, more common in women than men, leading to approximately 8.3 million doctor visits per year. Although some infections go unnoticed, UTIs can cause problems that range from dysuria (pain and/or burning when urinating) to organ damage and even death. The kidneys are the active organs that, during their average production of about 1.5 quarts of urine per day, function to help keep electrolytes and fluids (for example, potassium, sodium, water) in balance, assist removal of waste products (urea), and produce a hormone that aids to form red blood cells. If kidneys are injured or destroyed by infection, these vital functions can be damaged or lost.

While some investigators state that UTIs are not transmitted from person to person, other investigators dispute this and say UTIs may be contagious and recommend that sex partners avoid relations until the UTI has cleared. There is no dispute about UTIs caused by sexually transmitted disease (STD) organisms; these infections (gonorrhea, chlamydia) are easily transmitted between sex partners and are very contagious.
Picture of the urinary tract structures
Figure 1: Picture of the urinary tract structures
What causes a UTI?

The most common causes of UTI infections (about 80%) are Escherichia coli bacterial strains that usually inhabit the colon. However, many other bacteria can occasionally cause an infection (for example, Klebsiella, Pseudomonas, Enterobacter, Proteus, Staphylococcus, Mycoplasma, Chlamydia, Serratia and Neisseria spp) but are far less frequent causes than E. coli. In addition, fungi (Candida and Cryptococcus spp) and some parasites (Trichomonas, Schistosoma) also may cause UTIs; Schistosoma causes other problems, with bladder infections as only a part of its complicated infectious process. In the U.S., most infections are due to Gram-negative bacteria with E. coli causing the majority of infections.

What are UTI risk factors?

There are many risk factors for UTIs. In general, any interruption or impedance of the usual flow of urine (about 50 cc per hour in normal adults) is a risk factor for a UTI. For example, kidney stones, urethral strictures, enlarged prostate, or any anatomical abnormalities in the urinary tract increases infection risk. This is due in part to the flushing or wash-out effect of flowing urine; in effect the pathogens have to "go against flow" because the majority of pathogens enter through the urethra and have to go retrograde (against a barrier, urine flow) to reach the bladder, ureters, and eventually the kidneys. Many investigators suggest that women are far more susceptible than men to UTIs because their urethra is short and its exit (or entry for pathogens) is close to the anus and vagina, which can be sources for pathogens.

People who require catheters have an increased risk (about 30% of patients with indwelling catheters get UTIs) as the catheter has none of the protective immune systems to eliminate bacteria and offers a direct connection to the bladder.

There are reports that suggest that women who use a diaphragm or who have partners that use condoms with spermicidal foam are at increased risk for UTIs. In addition, females who become sexually active seem to have a higher risk of UTI; some investigators term these UTIs as "honeymoon cystitis."

Men over 60 have a higher risk for UTIs because many men at or above that age develop enlarged prostates that may cause slow and incomplete bladder emptying.

Occasionally, people with bacteremia (bacteria in the bloodstream) have the infecting bacteria lodge in the kidney; this is termed hematogenous spread. Similarly, people with infected areas that are connected to the urinary tract (for example, prostate, epididymis, or fistulas) are more likely to get a UTI. Additionally, patients who undergo urologic surgery also have and increased risk of UTIs. Pregnancy does not apparently increase the risk of UTIs according to some clinicians; others think there is an increased risk between weeks six through 26 of the pregnancy. However, most agree that if UTIs occur in pregnancy, the risk of the UTI progressing in seriousness to pyelonephritis is increased according to several investigators. In addition, their baby may be premature and have a low birth weight. Patients with chronic diseases such as diabetics or those who are immunosuppressed (HIV or cancer patients) also are at higher risk for UTIs.
What are UTI symptoms and signs in women, men, and children?

The UTI symptoms and signs may vary according to age, sex, and location of the infection in the tract. Some individuals will have no symptoms or mild symptoms and may clear the infection in about two to five days. Many people will not spontaneously clear the infection; some of the most frequent signs and symptoms experienced by most patients is a frequent urge to urinate, accompanied by pain or burning on urination. The urine often appears cloudy and occasionally reddish if blood is present. The urine may develop an unpleasant odor. Women often have lower abdominal discomfort or feel bloated and experience sensations like their bladder is full. Women may also complain of a vaginal discharge, especially if their urethra is infected, or if they have an STD. Although men may complain of dysuria, frequency, and urgency, other symptoms may include rectal, testicular, penile, or abdominal pain. Men with a urethral infection, especially if it is caused by an STD may have a pus-like drip or discharge from their penis. Toddlers and children with UTIs often show blood in the urine, abdominal pain, fever, and vomiting along with pain and urgency with urination.

Symptoms and signs of a UTI in the very young and the elderly are not as diagnostically helpful as they are for other patients. Newborns and infants may develop fever or hypothermia, poor feeding, jaundice, vomiting, and diarrhea. Unfortunately, the elderly often have mild symptoms or no symptoms of a UTI until they become weak, lethargic, or confused

Location of the infection in the urinary tract usually gives certain symptoms. Urethral infections usually have dysuria (pain or discomfort when urinating). STD infections may cause a pus-like fluid to drain or drip from the urethra. Cystitis (bladder infection) symptoms include suprapubic pain, usually without fever and flank pain. Ureter and kidney infections often have flank pain and fever as symptoms. These symptom and signs are not highly specific, but they do help the physician determine where the UTI may be located.
How is a urinary tract infection diagnosed?

The caregiver should obtain a detailed history from the patient, and if a UTI is suspected, a urine sample is usually obtained. The best sample is a midstream sample of urine placed in a sterile cup because it usually contains only the pathogenic organisms instead of the transient organisms that may be washed from adjacent surfaces when the urine stream begins. Male patients with foreskin should retract the foreskin before providing a midstream urine sample. In some patients who cannot provide a midstream sample, a sample can be obtained by a catheter. The urine sample is then sent for urinalysis. Patients with a "discharge" or possibility of having an STD usually will have the discharge tested for STD organisms (for example, Neisseria, Chlamydia). A positive urinalysis is usually detection of about two to five leukocytes (white blood cells), about 15 bacteria per high-power microscopic field, and a positive nitrite test and/or positive leukocyte esterase test. Some clinicians and labs consider a positive test at least two of the above findings; still others report a positive for bacteria as > 1,000 bacteria cultured per milliliter of urine. At best, the initial urinalysis, depending on the various criteria used by clinicians and labs provide a presumptive positive test for a UTI. Most clinicians believe this presumptive test is adequate enough to begin treatment. A definitive test is usually considered to be isolation and identification of the infecting pathogen at a level of about 100,000 bacteria per cc of urine with genus of pathogen identified and antibiotic sensitivity determined by lab studies. This test takes 24-48 hours to obtain the results and your health-care provider will usually start treatment before this result is available.

In young children, infants, and some elderly patients, the best urine specimen is obtained by catheterization. Urine can also be collected from "bags" placed over the urethral outlet (genital area), but these bagged specimens are only used for presumptive urinalysis as they are unreliable for culture. Some investigators consider any bagged urine samples as unreliable. Urine samples not processed within an hour of collection should either be discarded or be refrigerated before an hour passes because bacterial growth in urine at room temperature can yield false-positive tests. Special culture media and other tests are done for the infrequent or rare pathogens (for example, fungi and parasites).

Other tests may be ordered to further define the extent of a UTI. They may include blood cultures, a complete blood count (CBC), intravenous pyelogram, a CT scan, or other specialized tests.
What is the treatment for a urinary tract infection?

Treatment for a UTI should be designed for each patient individually and is usually based on how sick the patient is, what pathogen(s) are causing the infection, and the susceptibility of the pathogen(s) to treatments. Patients who are very ill usually require IV antibiotics and admission to a hospital; they usually have a kidney infection (pyelonephritis) that may be spreading to the bloodstream. Other people may have a milder infection (cystitis) and may get well quickly with oral antibiotics. Still others may have a UTI caused by pathogens that cause STDs and may require more than a single oral antibiotic. The caregivers often begin treatment before the pathogenic agent and its antibiotic susceptibilities are known, so in some individuals, the antibiotic treatment may need to be changed. In addition, pediatric patients and pregnant patients should not use certain antibiotics that are commonly used in adults. For example, ciprofloxacin (Cipro) and other related quinolones should not be used in children or pregnant patients due to side effects. However, penicillins and cephalosporins are usually considered safe for both groups if the individuals are not allergic to the antibiotics. Patients with STD-related UTIs usually require two antibiotics to eliminate STD pathogens. The less frequent or rare fungal and parasitic pathogens require specific antifungal or antiparasitic medications; these more complicated UTIs should often be treated in consultation with an infectious-disease expert.

All antibiotics prescribed should be taken even if the person's symptoms disappear early. Reoccurrence of the UTI and even antibiotic resistance of the pathogen may happen in individuals who are not adequately treated.

Over-the-counter medicines offer relief from the pain and discomfort of UTIs but they don't cure UTIs. Over-the-counter products like AZO or Uristat contain the medicine phenazopyridine (Pyridium, Urogesic), which works in the bladder to relieve pain. This medication turns urine an orange-red color, so patients should not be worried when this occurs. This medication can also turn other body fluids orange, including tears, and can stain contact lenses.
Are there any home remedies for a UTI?

The best "home remedy" for a UTI is prevention (see section below). However, although there are many "home remedies" available from web sites, holistic medicine publications, and from friends and family members; there is controversy about them in the medical literature as few have been adequately studied. However, a few remedies will be mentioned because there may be some positive effect from these home remedies. The reader should be aware while reading about these remedies (the term means to correct, relieve, or cure), they should not to overlook the frequent admonition that UTIs can be dangerous and if no relief is given or the person's symptoms worsen over one to two days, the person should seek medical care. In fact, many of the articles about UTI remedies actually describe ways to reduce or prevent UTIs. Examples of home treatments that may help to prevent UTIs, that may have some impact on an ongoing infection, and are unlikely to harm people are as follows:

Increase fluid intake may work by washing out organisms in the tract, making it more difficult for pathogens to adhere or stay in close proximity to human cells.


Do not delay in emptying the bladder (urination): has the same effects of increased fluid intake and helps the bladder reduce the number of pathogens that may reach the bladder


Eating cranberries or blueberries or drinking their unsweetened juice: These berries contain antioxidants that may help the immune system, and some investigators suggest they contain compounds that reach the urine and reduce adherence of pathogens to human cells.


Eating pineapple: Pineapple contains bromelain that has anti-inflammatory properties that may reduce UTI symptoms.


Vitamin C may function to increase urine acidity to reduce bacterial growth
.

Yogurt, Echinacea, baking soda, Oregon grape root, and aromatherapy have had people claim effectiveness in treating UTIs but the mechanisms are not clear

The problem with these remedies is that standard testing data and results with known amounts or concentrations of these compounds are usually not available. For example, how much cranberry juice is effective for a woman with known cystitis? Most publications do not answer this simple question, and some say that sweetened cranberry juice may aggravate the infection. In addition, it pays to read the entire label for these products as many have a caveat at the end of the ad that says the product does not claim it will cure UTIs. If people elect to try home remedies, they should clearly understand that if symptoms are not reduced or if they get worse, medical care should be sought.

There are over-the-counter tests available for detecting presumptive evidence for a UTI (for example, AZO test strips). These tests are easy to use and can provide a presumptive diagnosis if the test instructions are carefully followed; a positive test should encourage the person to seek medical care.
What are possible complications of a urinary tract infection?

Most UTIs cause no complications if they spontaneously resolve quickly (a few days) or if treated early in the infection with appropriate medications. However, there are a number of complications that can occur if the UTI becomes chronic or rapidly advances. Chronic infections may result in urinary strictures, abscesses, fistulas, and kidney damage. Rapid advancement of UTIs can lead to dehydration, kidney failure, sepsis, and death. Pregnant females with untreated UTIs may develop premature delivery and a low birth weight for the infant and run the risks of rapid advancement of the infection.

What is the prognosis for a UTI?

A good prognosis is usual for spontaneously resolved and quickly treated UTIs. Even patients that have rapidly developing symptoms and early pyelonephritis can have a good prognosis if quickly and adequately treated. The prognosis begins to decline if the UTI is not quickly recognized or treated. Elderly and immunodepressed patients may not have the UTI recognized early; their prognosis may range from fair to poor, depending on how much damage is done to the urinary tract or if complications like sepsis occur. Like adults, most adequately treated children will have a good prognosis. Children and adults with recurrent UTIs may develop complications and a worse prognosis; recurrent UTIs may be a symptom of an underlying problem with the urinary tract structure. These patients should be referred to a specialist (urologist) for further evaluation.

Is it possible to prevent recurrent UTIs with a vaccine?

Currently, there are no commercially available vaccines for UTIs, either recurrent or first-time infections. One of the problems in developing a vaccine is that so many different organisms can cause infection, a single vaccine would be difficult to synthesize to cover them all. Even with E. coli causing about 80% of all infections, the subtle changes in antigenic structures that vary from strain to strain further complicates vaccine development even for E. coli. Researchers are still investigating ways to overcome the problems in UTI vaccine development; injected, oral, mucosal, and nasal preparations are being investigated.
Can a UTI be prevented?

Many methods have been suggested to reduce or prevent UTIs. Some of these are considered home remedies and have been discussed (see above home remedies section). There are other suggestions that may help prevent UTIs. Good hygiene for males and females is useful; for females, wiping from front to back helps keep pathogens that may reside or pass through the anal opening away from the urethra; for males, retracting the foreskin before urinating reduces the chance of urine lingering at the urethral opening and acting as a culture media for pathogens. Incomplete bladder emptying and resisting the normal urge to urinate can allow pathogens to survive and replicate easier in a non-flowing system. Some clinicians recommend washing before and urinating soon after sex to reduce the chance of urethritis/cystitis. Many clinicians suggest that anything that causes a person irritation in the genital area (for example, tight clothing, deodorant sprays, or other feminine products like bubble bath) may encourage UTI development. Wearing underwear that is somewhat adsorptive (for example, cotton) may help wick away urine drops that otherwise may be areas for pathogen growth.

Jaundice

What is jaundice?

Jaundice is not a disease but rather a sign that can occur in many different diseases. Jaundice is the yellowish staining of the skin and sclerae (the whites of the eyes) that is caused by high levels in blood of the chemical bilirubin. The color of the skin and sclerae vary depending on the level of bilirubin. When the bilirubin level is mildly elevated, they are yellowish. When the bilirubin level is high, they tend to be brown.

What causes jaundice?

Bilirubin comes from red blood cells. When red blood cells get old, they are destroyed. Hemoglobin, the iron-containing chemical in red blood cells that carries oxygen, is released from the destroyed red blood cells after the iron it contains is removed. The chemical that remains in the blood after the iron is removed becomes bilirubin.

The liver has many functions. One of the liver's functions is to produce and secrete bile into the intestines to help digest dietary fat. Another is to remove toxic chemicals or waste products from the blood, and bilirubin is a waste product. The liver removes bilirubin from the blood. After the bilirubin has entered the liver cells, the cells conjugate (attaching other chemicals, primarily glucuronic acid) to the bilirubin, and then secrete the bilirubin/glucuronic acid complex into bile. The complex that is secreted in bile is called conjugated bilirubin. The conjugated bilirubin is eliminated in the feces. (Bilirubin is what gives feces its brown color.) Conjugated bilirubin is distinguished from the bilirubin that is released from the red blood cells and not yet removed from the blood which is termed unconjugated bilirubin.

Jaundice occurs when there is 1) too much bilirubin being produced for the liver to remove from the blood. (For example, patients with hemolytic anemia have an abnormally rapid rate of destruction of their red blood cells that releases large amounts of bilirubin into the blood), 2) a defect in the liver that prevents bilirubin from being removed from the blood, converted to bilirubin/glucuronic acid (conjugated) or secreted in bile, or 3) blockage of the bile ducts that decreases the flow of bile and bilirubin from the liver into the intestines. (For example, the bile ducts can be blocked by cancers, gallstones, or inflammation of the bile ducts). The decreased conjugation, secretion, or flow of bile that can result in jaundice is referred to as cholestasis: however, cholestasis does not always result in jaundice.
What problems does jaundice cause?

Jaundice or cholestasis, by themselves, causes few problems (except in the newborn, and jaundice in the newborn is different than most other types of jaundice, as discussed later.) Jaundice can turn the skin and sclerae yellow. In addition, stool can become light in color, even clay-colored because of the absence of bilirubin that normally gives stool its brown color. The urine may turn dark or brownish in color. This occurs when the bilirubin that is building up in the blood begins to be excreted from the body in the urine. Just as in feces, the bilirubin turns the urine brown.

Besides the cosmetic issues of looking yellow and having dark urine and light stools, the symptom that is associated most frequently associated with jaundice or cholestasis is itching, medically known as pruritus. The itching associated with jaundice and cholestasis can sometimes be so severe that it causes patients to scratch their skin "raw," have trouble sleeping, and, rarely, even to commit suicide.

It is the disease causing the jaundice that causes most problems associated with jaundice. Specifically, if the jaundice is due to liver disease, the patient may have symptoms or signs of liver disease or cirrhosis. (Cirrhosis represents advanced liver disease.) The symptoms and signs of liver disease and cirrhosis include fatigue, swelling of the ankles, muscle wasting, ascites (fluid accumulation in the abdominal cavity), mental confusion or coma, and bleeding into the intestines.

If the jaundice is caused by blockage of the bile ducts, no bile enters the intestine. Bile is necessary for digesting fat in the intestine and releasing vitamins from within it so that the vitamins can be absorbed into the body. Therefore, blockage of the flow of bile can lead to deficiencies of certain vitamins. For example, there may be a deficiency of vitamin K that prevents proteins that are needed for normal clotting of blood to be made by the liver, and, as a result, uncontrolled bleeding may occur.
What diseases cause jaundice?

Increased production of bilirubin

There are several uncommon conditions that give rise to over-production of bilirubin. The bilirubin in the blood in these conditions usually is only mildly elevated, and the resultant jaundice usually is mild and difficult to detect. These conditions include: 1) rapid destruction of red blood cells (referred to as hemolysis), 2) a defect in the formation of red blood cells that leads to the over-production of hemoglobin in the bone marrow (called ineffective erythropoiesis), or 3) absorption of large amounts of hemoglobin when there has been much bleeding into tissues (e.g., from hematomas, collections of blood in the tissues).

Acute inflammation of the liver

Any condition in which the liver becomes inflamed can reduce the ability of the liver to conjugate (attach glucuronic acid to) and secrete bilirubin. Common examples include acute viral hepatitis, alcoholic hepatitis, and Tylenol-induced liver toxicity.

Chronic liver diseases

Chronic inflammation of the liver can lead to scarring and cirrhosis, and can ultimately result in jaundice. Common examples include chronic hepatitis B and C, alcoholic liver disease with cirrhosis, and autoimmune hepatitis.

Infiltrative diseases of the liver

Infiltrative diseases of the liver refer to diseases in which the liver is filled with cells or substances that don't belong there. The most common example would be metastatic cancer to the liver, usually from cancers within the abdomen. Uncommon causes include a few diseases in which substances accumulate within the liver cells, for example, iron (hemochromatosis), alpha-one antitrypsin (alpha-one antitrypsin deficiency), and copper (Wilson's disease).

Inflammation of the bile ducts

Diseases causing inflammation of the bile ducts, for example, primary biliary cirrhosis or sclerosing cholangitis and some drugs, can stop the flow of bile and elimination of bilirubin and lead to jaundice.

Blockage of the bile ducts

The most common causes of blockage of the bile ducts are gallstones and pancreatic cancer. Less common causes include cancers of the liver and bile ducts.

Drugs

Many drugs can cause jaundice and/or cholestasis. Some drugs can cause liver inflammation (hepatitis) similar to viral hepatitis. Other drugs can cause inflammation of the bile ducts, resulting in cholestasis and/or jaundice. Drugs also may interfere directly with the chemical processes within the cells of the liver and bile ducts that are responsible for the formation and secretion of bile to the intestine. As a result, the constituents of bile, including bilirubin, are retained in the body. The best example of a drug that causes this latter type of cholestasis and jaundice is estrogen. The primary treatment for jaundice caused by drugs is discontinuation of the drug. Almost always the bilirubin levels will return to normal within a few weeks, though in a few cases it may take several months.

Genetic disorders

There are several rare genetic disorders present from birth that give rise to jaundice. Crigler-Najjar syndrome is caused by a defect in the conjugation of bilirubin in the liver due to a reduction or absence of the enzyme responsible for conjugating the glucuronic acid to bilirubin. Dubin-Johnson and Rotor's syndromes are caused by abnormal secretion of bilirubin into bile.

The only common genetic disorder that may cause jaundice is Gilbert's syndrome which affects approximately 7% of the population. Gilbert's syndrome is caused by a mild reduction in the activity of the enzyme responsible for conjugating the glucuronic acid to bilirubin. The increase in bilirubin in the blood usually is mild and infrequently reaches levels that cause jaundice. Gilbert's syndrome is a benign condition that does not cause health problems.

Developmental abnormalities of bile ducts

There are rare instances in which the bile ducts do not develop normally and the flow of bile is interrupted. Jaundice frequently occurs. These diseases usually are present from birth though some of them may first be recognized in childhood or even adulthood. Cysts of the bile duct (choledochal cysts) are an example of such a developmental abnormality. Another example is Caroli's disease.

Jaundice of pregnancy

Most of the diseases discussed previously can affect women during pregnancy, but there are some additional causes of jaundice that are unique to pregnancy.

Cholestasis of pregnancy. Cholestasis of pregnancy is an uncommon condition that occurs in pregnant women during the third trimester. The cholestasis is often accompanied by itching but infrequently causes jaundice. The itching can be severe, but there is treatment (ursodeoxycholic acid or ursodiol). Pregnant women with cholestasis usually do well although they may be at greater risk for developing gallstones. More importantly, there appears to be an increased risk to the fetus for developmental abnormalities. Cholestasis of pregnancy is more common in certain groups, particularly in Scandinavia and Chile, and tends to occur with each additional pregnancy. There also is an association between cholestasis of pregnancy and cholestasis caused by oral estrogens, and it has been hypothesized that it is the increased estrogens during pregnancy that are responsible for the cholestasis of pregnancy.

Pre-eclampsia. Pre-eclampsia, previously called toxemia of pregnancy, is a disease that occurs during the second half of pregnancy and involves several systems within the body, including the liver. It may result in high blood pressure, fluid retention, and damage to the kidneys as well as anemia and reduced numbers of platelets due to destruction of red blood cells and platelets. It often causes problems for the fetus. Although the bilirubin level in the blood is elevated in pre-eclampsia, it usually is mildly elevated, and jaundice is uncommon. Treatment of pre-eclampsia usually involves delivery of the fetus as soon as possible if the fetus is mature.

Acute fatty liver of pregnancy. Acute fatty liver of pregnancy (AFLP) is a very serious complication of pregnancy of unclear cause that often is associated with pre-eclampsia. It occurs late in pregnancy and results in failure of the liver. It can almost always be reversed by immediate delivery of the fetus. There is an increased risk of infant death. Jaundice is common, but not always present in AFLP. Treatment usually involves delivery of the fetus as soon as possible.
What is neonatal jaundice (jaundice in newborn infants)?

Neonatal jaundice is jaundice that begins within the first few days after birth. (Jaundice that is present at the time of birth suggests a more serious cause of the jaundice.) In fact, bilirubin levels in the blood become elevated in almost all infants during the first few days following birth, and jaundice occurs in more than half. For all but a few infants, the elevation and jaundice represents a normal physiological phenomenon and does not cause problems.

The cause of normal, physiological jaundice is well understood. During life in the uterus, the red blood cells of the fetus contain a type of hemoglobin that is different than the hemoglobin that is present after birth. When an infant is born, the infant's body begins to rapidly destroy the red blood cells containing the fetal-type hemoglobin and replaces them with red blood cells containing the adult-type hemoglobin. This floods the liver with bilirubin derived from the fetal hemoglobin from the destroyed red blood cells. The liver in a newborn infant is not mature, and its ability to process and eliminate bilirubin is limited. As a result of both the influx of large amounts of bilirubin and the immaturity of the liver, bilirubin accumulates in the blood. Within two or three weeks, the destruction of red blood cells ends, the liver matures, and the bilirubin levels return to normal.

There is another uncommon syndrome associated with neonatal jaundice, referred to as breast-milk or breast feeding jaundice. In this syndrome, jaundice appears to be caused by or at least accentuated by breast feeding. Although the cause of this type of jaundice is unknown, it has been hypothesized that there is something in breast milk that reduces the ability of the liver to process and eliminate bilirubin. With breast-milk jaundice, the bilirubin levels rise and reach peak levels in approximately two weeks, remain elevated for a week or so, and then decline to normal over several weeks or months. This timing of the elevation in bilirubin and jaundice is different than normal physiological jaundice described previously and allows the two causes of jaundice to be differentiated. The real importance of the more prolonged jaundice associate with breast-milk jaundice is that it raises the possibility that there is a more serious cause for the jaundice that needs to be sought, for example, biliary atresia (destruction of the bile ducts). Breast-milk jaundice alone usually does not cause problems for the infant.

Physiologic jaundice and breast-milk jaundice usually do not cause problems for the infant; however, there is a concern that high or prolonged elevations in levels of unconjugated bilirubin (the type of bilirubin that is not attached to glucuronic acid and the main type of bilirubin that is present in physiologic and breast-milk jaundice) will cause neurologic damage to the infant. Therefore, when unconjugated bilirubin levels are high or prolonged, treatment usually is started to lower the levels of bilirubin. Treatment may be started earlier in infants who are born prematurely since their livers take longer to mature, and the risk of higher and more prolonged elevations of bilirubin is greater. Treatment involves phototherapy with artificial or natural sunlight and, if phototherapy is not successful, exchange transfusion in which the infant's blood is exchanged for normal blood from blood donors.

The benign nature of physiologic and breast-milk allergy need to be distinguished from hemolytic disease of the newborn, a much more serious, even life-threatening cause of jaundice in newborns that is due to blood group incompatibilities between mother and fetus, for example Rh incompatibility. The incompatibility results in an attack by the mother's antibodies on the babies red blood cells leading to hemolysis. Fortunately, because of modern management of pregnancy, this cause of jaundice is rare.
How is the cause of jaundice diagnosed?

Many tests are available for determining the cause of jaundice, but the history and physical examination are important as well.

History

The history can suggest possible reasons for the jaundice. For example, heavy use of alcohol suggests alcoholic liver disease, whereas use of illegal, injectable drugs suggests viral hepatitis. Recent initiation of a new drug suggests drug-induced jaundice. Episodes of abdominal pain associated with jaundice suggests blockage of the bile ducts usually by gallstones.

Physical examination

The most important part of the physical examination in a patient who is jaundiced is examination of the abdomen. Masses (tumors) in the abdomen suggest cancer infiltrating the liver (metastatic cancer) as the cause of the jaundice. An enlarged, firm liver suggests cirrhosis. A rock-hard, nodular liver suggests cancer within the liver.

Blood tests

Measurement of bilirubin can be helpful in determining the causes of jaundice. Markedly greater elevations of unconjugated bilirubin relative to elevations of conjugated bilirubin in the blood suggest hemolysis (destruction of red blood cells). Marked elevations of liver tests (aspartate amino transferase or AST and alanine amino transferase or ALT) suggest inflammation of the liver (such as viral hepatitis). Elevations of other liver tests, e.g., alkaline phosphatase, suggest diseases or obstruction of the bile ducts.

Ultrasonography

Ultrasonography is a simple, safe, and readily-available test that uses sound waves to examine the organs within the abdomen. Ultrasound examination of the abdomen may disclose gallstones, tumors in the liver or the pancreas, and dilated bile ducts due to obstruction (by gallstones or tumor).

Computerized tomography (CT or CAT scans)

Computerized tomography or CT scans are scans that use x-rays to examine the soft tissues of the abdomen. They are particularly good for identifying tumors in the liver and the pancreas and dilated bile ducts, though they are not as good as ultrasonography for identifying gallstones.

Magnetic resonance imaging (MRI)

Magnetic Resonance Imaging scans are scans that utilize magnetization of the body to examine the soft tissues of the abdomen. Like CT scans, they are good for identifying tumors and studying bile ducts. MRI scans can be modified to visualize the bile ducts better than CT scans (a procedure referred to as MR cholangiography), and, therefore, are better than CT for identifying the cause and location of bile duct obstruction.

Endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasound

Endoscopic retrograde cholangiopancreatography (ERCP) provides the best means for examining the bile duct. For ERCP an endoscope is swallowed by the patient after he or she has been sedated. The endoscope is a flexible, fiberoptic tube approximately four feet in length with a light and camera on its tip. The tip of the endoscope is passed down the esophagus, through the stomach, and into the duodenum where the main bile duct enters the intestine. A thin tube then is passed through the endoscope and into the bile duct, and the duct is filled with x-ray contrast solution. An x-ray is taken that clearly demonstrates the contrast-filled bile ducts. ERCP is particularly good at demonstrating the cause and location of obstruction within the bile ducts. A major advantage of ERCP is that diagnostic and therapeutic procedures can be done at the same time as the x-rays. For example, if gallstones are found in the bile ducts, they can be removed. Stents can be placed in the bile ducts to relieve the obstruction caused by scarring or tumors. Biopsies of tumors can be obtained.

Ultrasonography can be combined with ERCP by using a specialized endoscope capable of doing ultrasound scanning. Endoscopic ultrasound is excellent for diagnosing small gallstones in the gallbladder and bile ducts that can be missed by other diagnostic methods such as ultrasound, CT, and MRI. It also is the best means of examining the pancreas for tumors and can facilitate biopsy through the endoscope of tumors within the pancreas.

Liver biopsy

Biopsy of the liver provides a small piece of tissue from the liver for examination under the microscope. The biopsy most commonly is done with a long needle after local injection of the skin of the abdomen overlying the liver with anesthetic. The needle passes through the skin and into the liver, cutting off a small piece of liver tissue. When the needle is withdrawn, the piece of liver comes with it. Liver biopsy is particularly good for diagnosing inflammation of the liver and bile ducts, cirrhosis, cancer, and fatty liver.

How is jaundice treated?

With the exception of the treatments for specific causes of jaundice mentioned previously, the treatment of jaundice usually requires a diagnosis of the specific cause of the jaundice and treatment directed at the specific cause, e.g., removal of a gallstone blocking the bile duct.

Malaria

What is malaria?

Malaria is an infectious disease caused by a parasite, Plasmodium, which infects red blood cells. Malaria is characterized by cycles of chills, fever, pain, and sweating. Historical records suggest malaria has infected humans since the beginning of mankind. The name "mal aria" (meaning "bad air" in Italian) was first used in English in 1740 by H. Walpole when describing the disease. The term was shortened to "malaria" in the 20th century. C. Laveran in 1880 was the first to identify the parasites in human blood. In 1889, R. Ross discovered that mosquitoes transmitted malaria. Of the four common species that cause malaria, the most serious type is Plasmodium falciparum malaria. It can be life-threatening. However, another relatively new species, Plasmodium knowlesi, is also a dangerous species that is typically found only in long-tailed and pigtail macaque monkeys. Like P. falciparum, P. knowlesi may be deadly to anyone infected. The other three common species of malaria (P. vivax, P. malariae, and P. ovale) are generally less serious and are usually not life-threatening. It is possible to be infected with more than one species of Plasmodium at the same time.

Currently, about 2 million deaths per year worldwide are due to Plasmodium infections. The majority occur in children under 5 years of age in sub-Saharan African countries. There are about 400 million new cases per year worldwide. Most people diagnosed in the U.S. obtained their infection outside of the country, usually while living or traveling through an area where malaria is endemic.

What are malaria symptoms and signs?

The symptoms characteristic of malaria include flulike illness with fever, chills, muscle aches, and headache. Some patients develop nausea, vomiting, cough, and diarrhea. Cycles of chills, fever, and sweating that repeat every one, two, or three days are typical. There can sometimes be vomiting, diarrhea, coughing, and yellowing (jaundice) of the skin and whites of the eyes due to destruction of red blood cells and liver cells.

People with severe P. falciparum malaria can develop bleeding problems, shock, liver or kidney failure, central nervous system problems, coma, and can die from the infection or its complications. Cerebral malaria (coma, or altered mental status or seizures) can occur with severe P. falciparum infection. It is lethal if not treated quickly; even with treatment, about 15%-20% die.

How is malaria transmitted?

The life cycle of the malaria parasite (Plasmodium) is complicated and involves two hosts, humans and Anopheles mosquitoes. The disease is transmitted to humans when an infected Anopheles mosquito bites a person and injects the malaria parasites (sporozoites) into the blood. This is shown in Figure 1, where the illustration shows a mosquito taking a blood meal (circle label 1 in Figure 1).
Figure 1: CDC illustration of the life cycles of malaria parasites, Plasmodium spp.
Figure 1: CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC

Sporozoites travel through the bloodstream to the liver, mature, and eventually infect the human red blood cells. While in red blood cells, the parasites again develop until a mosquito takes a blood meal from an infected human and ingests human red blood cells containing the parasites. Then the parasites reach the Anopheles mosquito's stomach and eventually invade the mosquito salivary glands. When an Anopheles mosquito bites a human, these sporozoites complete and repeat the complex Plasmodium life cycle. P. ovale and P. vivax can further complicate the cycle by producing dormant stages (hypnozoites) that may not develop for weeks to years.
Malaria Treatment

Learn about the pill (drugs) used in the treatment of malaria.Three main factors determine treatments: the infecting species of Plasmodium parasite, the clinical situation of the patient (for example, adult, child, or pregnant female with either mild or severe malaria), and the drug susceptibility of the infecting parasites. Drug susceptibility is determined by the geographic area where the infection was acquired. Different areas of the world have malaria types that are resistant to certain medications. The correct drugs for each type of malaria must be prescribed by a doctor who is familiar with malaria treatment protocols. Since people infected with P. falciparum malaria can die (often because of delayed treatment), immediate treatment for P. falciparum malaria is necessary.

Learn more about malaria treatment »

Top Searched Malaria Terms:
yellow fever, cholera, tuberculosis, P. falciparum, travel, Plasmodium
Where is malaria a particular problem?

Malaria is a particular problem and a major one in areas of Asia, Africa, and Central and South America. Unless precautions are taken, anyone living in or traveling to a country where malaria is present can get the disease. Malaria occurs in about 100 countries; approximately 40% of the world population is at risk for contracting malaria. To get information on countries that have current malaria infection problems, the CDC (Centers for Disease Control) has a constantly updated web site (http://www.cdc.gov/malaria/travelers/
country_table/a.html) that lists the problem areas in detail.

HIV (AIDS) and malaria co-infection is a significant problem across Asia and sub-Saharan Africa. Research suggests that malaria and HIV co-infection can lead to worse clinical outcomes in patients. It seems that co-infections enhance the disease process of both pathogens.

What is the incubation period for malaria?

The period between the mosquito bite and the onset of the malarial illness is usually one to three weeks (seven to 21 days). This initial time period is highly variable as reports suggest that the range of incubation periods may range from four days to one year. The usual incubation period may be increased when a person has taken an inadequate course of malaria prevention medications. Certain types of malaria (P. vivax and P. ovale) parasites can also take much longer, as long as eight to 10 months, to cause symptoms. These parasites remain dormant (inactive or hibernating) in the liver cells during this time. Unfortunately, some of these dormant parasites can remain even after a patient recovers from malaria, so the patient can get sick again. This situation is termed relapsing malaria.

How is malaria diagnosed?

Clinical symptoms associated with travel to countries that have identified malarial risk (listed above) suggest malaria as a diagnosis. Malaria tests are not routinely ordered by most physicians so recognition of travel history is essential. Unfortunately, many diseases can mimic symptoms of malaria (for example, yellow fever, dengue fever, typhoid fever, cholera, filariasis, and even measles and tuberculosis). Consequently, physicians need to order the correct special tests to diagnose malaria, especially in industrialized countries where malaria is seldom seen. Without the travel history, it is likely that other tests will be ordered initially. In addition, the long incubation periods may tend to allow people to forget the initial exposure to infected mosquitoes.

The classic and most used diagnostic test for malaria is the blood smear on a microscope slide that is stained (Giemsa stain) to show the parasites inside red blood cells (see Figure 2).
Figure 2: CDC slide of a Giemsa stained smear of red blood cells showing Plasmodium malariae and Plasmodium falciparum parasites.
Figure 2: CDC slide of a Giemsa stained smear of red blood cells showing Plasmodium malariae and Plasmodium falciparum parasites. SOURCE: CDC/Steven Glenn, Laboratory & Consultation Division

Although this test is easily done, correct results are dependent on the technical skill of the lab technician who prepares and examines the slides with a microscope. Other tests based on immunologic principles exist; including RDTs (rapid diagnostic tests) approved for use in the U.S. in 2007 and polymerase chain reaction (PCR) tests. These are not yet widely available and are more expensive than the traditional Giemsa blood smear. Some investigators suggest such immunologic based tests be confirmed with a Giemsa blood smear.
What is the treatment for malaria?

Three main factors determine treatments: the infecting species of Plasmodium parasite, the clinical situation of the patient (for example, adult, child, or pregnant female with either mild or severe malaria), and the drug susceptibility of the infecting parasites. Drug susceptibility is determined by the geographic area where the infection was acquired. Different areas of the world have malaria types that are resistant to certain medications. The correct drugs for each type of malaria must be prescribed by a doctor who is familiar with malaria treatment protocols. Since people infected with P. falciparum malaria can die (often because of delayed treatment), immediate treatment for P. falciparum malaria is necessary.

Mild malaria can be treated with oral medication; severe malaria (one or more symptoms of either impaired consciousness/coma, severe anemia, renal failure, pulmonary edema, acute respiratory distress syndrome, shock, disseminated intravascular coagulation, spontaneous bleeding, acidosis, hemoglobinuria [hemoglobin in the urine], jaundice, repeated generalized convulsions, and/or parasitemia [parasites in the blood] of > 5%) requires intravenous (IV) drug treatment and fluids in the hospital.

Drug treatment of malaria is not always easy. Chloroquine phosphate (Aralen) is the drug of choice for all malarial parasites except for chloroquine-resistant Plasmodium strains. Although almost all strains of P. malariae are susceptible to chloroquine, P. falciparum, P. vivax, and even some P. ovale strains have been reported as resistant to chloroquine. Unfortunately, resistance is usually noted by drug-treatment failure in the individual patient. There are, however, multiple drug-treatment protocols for treatment of drug-resistant Plasmodium strains (for example, quinine sulfate plus doxycycline [Vibramycin, Oracea, Adoxa, Atridox] or tetracycline [Achromycin], or clindamycin [Cleocin], or atovaquone-proguanil [Malarone]). There are specialized labs that can test the patient's parasites for resistance, but this is not done frequently. Consequently, treatment is usually based on the majority of Plasmodium species diagnosed and its general drug-resistance pattern for the country or world region where the patient became infested. For example, P. falciparum acquired in the Middle East countries is usually susceptible to chloroquine, but if it's acquired in sub-Sahara African countries, it's usually resistant to chloroquine. The WHO's treatment policy, recently established in 2006, is to treat all cases of uncomplicated P. falciparum malaria with artemisinin-derived combination therapy (ACTs). ACTs are drug combinations (for example, artesunate-amodiaquine, artesunate-mefloquine, artesunate-pyronaridine, dihydroartemisinin-piperaquine, and chlorproguanil-dapsoneartesunate) used to treat drug-resistant P. falciparum. Unfortunately, as of 2009, a number of P. falciparum-infected individuals have parasites resistant to ACT drugs.

New drug treatments of malaria are currently under study because Plasmodium species continue to produce resistant strains that frequently spread to other areas. One promising drug class under investigation is the spiroindolones, which have been effective in stopping P. falciparum experimental infections.
Is malaria a particular problem during pregnancy?

Yes. Malaria may pose a serious threat to a pregnant woman and her fetus. Malaria infection in pregnant women may be more severe than in women who are not pregnant. Malaria may also increase the risk of problems with the pregnancy, including prematurity, abortion, and stillbirth. Statistics indicate that in sub-Saharan Africa, between 75,000-200,000 infants die from malaria per year; worldwide estimates indicate about 2 million children die from malaria each year. Therefore, all pregnant women who are living in or traveling to a malaria risk area should consult a doctor and take prescription drugs (for example, sulfadoxine-pyrimethamine) to avoid contracting malaria. Treatment of malaria in the pregnant female is similar to the usual treatment described above; however, drugs such as primaquine (Primaquine), tetracycline (Achromycin, Sumycin), doxycycline, and halofantrine (Halfan) are not recommended as they may harm the fetus. In addition to monitoring the patient for anemia, an OB/GYN specialist often is consulted for further management.

Is malaria a particular problem for children?

Yes. All children, including young infants, living in or traveling to malaria risk areas should take antimalarial drugs (for example, chloroquine and mefloquine [Lariam]). Although the recommendations for most antimalarial drugs are the same as for adults, it is crucial to use the correct dosage for the child. The dosage of drug depends on the age and weight of the child. A specialist in pediatric infectious diseases is recommended for consultation in prophylaxis (prevention) and treatment of children. Since an overdose of an antimalarial drug can be fatal, all antimalarial (and all other) drugs should be stored in childproof containers well out of the child's reach.

How do people avoid getting malaria?

If people must travel to an area known to have malaria, they need to find out which medications to take, and take them as prescribed. Current CDC recommendations suggest individuals begin taking antimalarial drugs about one to two weeks before traveling to a malaria infested area and for four weeks after leaving the area (prophylactic or preventative therapy). Doctors, travel clinics, or the health department can advise individuals as to what medicines to take to keep from getting malaria. Currently, there is no vaccine available for malaria, but researchers are trying to develop one.

Avoid travel to or through countries where malaria occurs if possible. If people must go to areas where malaria occurs, they should take all of the prescribed preventive medicine. In addition, the 2010 CDC international travel recommendations suggest the following precautions be taken in malaria and other disease-infested areas of the world; the following CDC recommendations are not unique for malaria but are posted by the CDC in their malarial prevention publication.

Avoid outbreaks: To the extent possible, travelers should avoid traveling in areas of known malaria outbreaks. The CDC Travelers' Health web page provides alerts and information on regional disease transmission patterns and outbreak alerts (http://www.cdc.gov/travel).


Be aware of peak exposure times and places: Exposure to arthropod bites may be reduced if travelers modify their patterns of activity or behavior. Although mosquitoes may bite at any time of day, peak biting activity for vectors of some diseases (for example, dengue, chikungunya) is during daylight hours. Vectors of other diseases (for example, malaria) are most active in twilight periods (for example, dawn and dusk) or in the evening after dark. Avoiding the outdoors or focusing preventive actions during peak hours may reduce risk.


Wear appropriate clothing: Travelers can minimize areas of exposed skin by wearing long-sleeved shirts, long pants, boots, and hats. Tucking in shirts and wearing socks and closed shoes instead of sandals may reduce risk. Repellents or insecticides such as permethrin can be applied to clothing and gear for added protection; this measure is discussed in detail below.


Check for ticks: Travelers should be advised to inspect themselves and their clothing for ticks during outdoor activity and at the end of the day. Prompt removal of attached ticks can prevent some infections.


Bed nets: When accommodations are not adequately screened or air conditioned, bed nets are essential to provide protection and to reduce discomfort caused by biting insects. If bed nets do not reach the floor, they should be tucked under mattresses. Bed nets are most effective when they are treated with an insecticide or repellent such as permethrin. Pretreated, long-lasting bed nets can be purchased prior to traveling, or nets can be treated after purchase. The permethrin will be effective for several months if the bed net is not washed. (Long-lasting pretreated nets may be effective for much longer.)


Insecticides: Aerosol insecticides, vaporizing mats, and mosquito coils can help to clear rooms or areas of mosquitoes; however, some products available internationally may contain pesticides that are not registered in the United States. Insecticides should always be used with caution, avoiding direct inhalation of spray or smoke.


Optimum protection can be provided by applying repellents. The CDC recommended insect repellent should contain up to 50% DEET (N,N-diethyl-m-toluamide), which is the most effective mosquito repellent for adults and children over 2 months of age.
What is the prognosis (outcome) for people with malaria?

The majority of people who become infected with P. malariae, vivax, or ovale do well and the fevers abate after about 96 hours. However, in endemic areas, reinfection is common. Malaria caused by P. falciparum or P. knowlesi, even when treated, have outcomes ranging from fair to poor, depending on how the parasites react to treatment. Untreated people often die from these infections. In general, patients who are infants, children under the age of 5 (especially in sub-Saharan countries), and those with depressed immune systems (for example, AIDS or cancer patients) have a more guarded prognosis.

Where can people get more information about malaria?

"The History of Malaria, an Ancient Disease," Centers for Disease Control and Prevention

"About Malaria," Centers for Disease Control and Prevention

Traveler's Health - Yellow Book, Centers for Disease Control and Prevention

"Malaria," eMedicine.com
Malaria At A Glance

Malaria is a disease caused by Plasmodium spp. parasites that infects about 400 million people per year with about 2 million deaths.
Symptoms include recurrent cycles (every one to three days) of fever, chills, muscle aches, headaches; nausea, vomiting, and jaundice also may occur.
Anopheles mosquitoes transmit the parasites to humans when they bite. The parasites undergo a complicated life cycle in both mosquitoes and humans; the cycle begins again when the mosquitoes take a blood meal from a human that is contaminated with mature parasites.
Africa, Asia, and Central and South America are the areas with high numbers of malarial infections.
The incubation period for malaria symptoms is about one to three weeks but may be extended to eight to 10 months after the initial infected mosquito bites occur. Some people may have dormant parasites that may get reactivated years after the initial infection.
Malaria is diagnosed by the patient's history of recurrent symptoms and the identification of the parasites in the patient's blood, usually by a Giemsa blood smear.
Malaria is usually treated by using combinations of two or more anti-parasite drugs incorporated into pills that are taken before exposure (prophylactic or preventative therapy) or during infection. More serious infections are treated by IV anti-parasitic drugs in the hospital.
Infants, children, and pregnant females, along with immunodepressed patients are at higher risk for worse outcomes when infected with malaria parasites.
To reduce the chance of getting malaria, people should avoid malaria-endemic areas of the world, use mosquito repellents, cover exposed skin, and use mosquito netting covered areas when sleeping.
The prognosis for the majority of malaria patients is good; most recover with no problems, unless infected with P. falciparum or P. knowlesi, which may have fair to poor outcomes unless treated immediately. Infants, children under 5 years of age, pregnant females, and those with depressed immune systems frequently have a fair to poor prognosis unless effectively treated early in the infection.

REFERENCES:

D'Acremont, V., C. Lengeler, and B. Genton. "Reduction in the Proportion of Fevers Associated With Plasmodium falciparum Parasitaemia in Africa: A Systematic Review." Malaria Journal 9.240 Aug. 22, 2010 doi:10.1186/1475-2875-9-240.

Rottmann, M., C. McNamara, B. Yeung, et al. "Spiroindolones, a Potent Compound Class for the Treatment of Malaria." Science 329 (2010): 1175-1180.

Typhoid Fever

What is typhoid fever?

Typhoid fever is an acute illness associated with fever that is most often caused by the Salmonella typhi bacteria. It can also be caused by Salmonella paratyphi, a related bacterium that usually leads to a less severe illness. The bacteria are deposited in water or food by a human carrier and are then spread to other people in the area.

The incidence of typhoid fever in the United States has markedly decreased since the early 1900s. Today, approximately 400 cases are reported annually in the United States, mostly in people who recently have traveled to endemic areas. This is in comparison to the 1920s, when over 35,000 cases were reported in the U.S. This improvement is the result of improved environmental sanitation. Mexico and South America are the most common areas for U.S. citizens to contract typhoid fever. India, Pakistan, and Egypt are also known high-risk areas for developing this disease. Worldwide, typhoid fever affects more than 13 million people annually, with over 500,000 patients dying of the disease.

If traveling to endemic areas, you should consult with your health-care professional and discuss if you should receive vaccination for typhoid fever.
How do patients get typhoid fever?

Typhoid fever is contracted by the ingestion of the bacteria in contaminated food or water. Patients with acute illness can contaminate the surrounding water supply through stool, which contains a high concentration of the bacteria. Contamination of the water supply can, in turn, taint the food supply. About 3%-5% of patients become carriers of the bacteria after the acute illness. Some patients suffer a very mild illness that goes unrecognized. These patients can become long-term carriers of the bacteria. The bacteria multiplies in the gallbladder, bile ducts, or liver and passes into the bowel. The bacteria can survive for weeks in water or dried sewage. These chronic carriers may have no symptoms and can be the source of new outbreaks of typhoid fever for many years.

How does the bacteria cause disease, and how is it diagnosed?

After the ingestion of contaminated food or water, the Salmonella bacteria invade the small intestine and enter the bloodstream temporarily. The bacteria are carried by white blood cells in the liver, spleen, and bone marrow. The bacteria then multiply in the cells of these organs and reenter the bloodstream. Patients develop symptoms, including fever, when the organism reenters the bloodstream. Bacteria invade the gallbladder, biliary system, and the lymphatic tissue of the bowel. Here, they multiply in high numbers. The bacteria pass into the intestinal tract and can be identified for diagnosis in cultures from the stool tested in the laboratory. Stool cultures are sensitive in the early and late stages of the disease but often must be supplemented with blood cultures to make the definite diagnosis.

What are the symptoms of typhoid fever?

The incubation period is usually one to two weeks, and the duration of the illness is about four to six weeks. The patient experiences

poor appetite,


headaches,


generalized aches and pains,


fever,


lethargy,


diarrhea.

People with typhoid fever usually have a sustained fever as high as 103 F-104 F (39 C-40 C).

Chest congestion develops in many patients, and abdominal pain and discomfort are common. The fever becomes constant. Improvement occurs in the third and fourth week in those without complications. About 10% of patients have recurrent symptoms (relapse) after feeling better for one to two weeks. Relapses are actually more common in individuals treated with antibiotics.
How is typhoid fever treated, and what is the prognosis?

Typhoid fever is treated with antibiotics that kill the Salmonella bacteria. Prior to the use of antibiotics, the fatality rate was 20%. Death occurred from overwhelming infection, pneumonia, intestinal bleeding, or intestinal perforation. With antibiotics and supportive care, mortality has been reduced to 1%-2%. With appropriate antibiotic therapy, there is usually improvement within one to two days and recovery within seven to 10 days.

Several antibiotics are effective for the treatment of typhoid fever. Chloramphenicol was the original drug of choice for many years. Because of rare serious side effects, chloramphenicol has been replaced by other effective antibiotics. The choice of antibiotics needs to be guided by identifying the geographic region where the organism was acquired and the results of cultures once available. (Certain strains from South America show a significant resistance to some antibiotics.) Ciprofloxacin (Cipro), ampicillin (Omnipen, Polycillin, Principen), and trimethoprim-sulfamethoxazole (Bactrim, Septra) are frequently prescribed antibiotics. If relapses occur, patients are retreated with antibiotics.

The carrier state, which occurs in 3%-5% of those infected, can be treated with prolonged antibiotics. Often, removal of the gallbladder, the site of chronic infection, will cure the carrier state.

For those traveling to high-risk areas, vaccines are now available.
Typhoid Fever At A Glance

Typhoid fever usually is caused by Salmonellae typhi bacteria.
Typhoid fever is contracted by the ingestion of contaminated food or water.
Diagnosis of typhoid fever is made when the Salmonella bacteria is detected with a stool culture.
Typhoid fever is treated with antibiotics.
Typhoid fever symptoms are poor appetite, headaches, generalized aches and pains, fever, and lethargy.
Approximately 3%-5% of patients become carriers of the bacteria after the acute illness.

REFERENCE:

United States. Centers for Disease Control and Prevention. "Typhoid Fever." Oct. 24, 2005. .