Forum Kesehatan Medisiana

Hello,
GO bukan sesuatu yg hebat kayak GI Joe, Go adalah kuman yg didapat dari hasil perselingkuhan kelamin dg org yg bukan hak nya.

Nah bIla dlm pemeriksaan dikatakan GO nya dah baik, tetapi perselingkuhanya tetap berlangsung dg berbagai org maka Go nya akan datang lagi.
Bahayanya si Go kemudian di antibiotik sendiri sampai si GO kebal atau si anti biotik sdh ndak mempan lagi.

Inilah yg terjadi bahwa si adik kemudian mengikuti standard kembali dg anti biotik yg standard dg dosage berkala yg di naikan dg hasil nihil efeknya Walau sampai 1 tahun.

Jadi langkah yg mesti dilakukan adalah:

1. Berhentilah selingkuhan dg kelamin sembarangan.
2. Check atau test si Go yg perkasa tadi akan bisa di basmi dg anti biotik apa?
3. Basi si Go samapi ke akar2nya dg anti biotik yg perkasa n sanggub membasmi GO sampai ke akar2nya.
4. Akarnya bila si adik punya istri asli bukan selingkuhan, ya dia juga harus di basmi GO nya sampai ke akar2nya secara bersamaan dg si adik.
5. Setelah kedua nya adik n istri lengkap dlm pemeriksaan n hasil test tdk memiliki GO lagi, maka barulah keduanya boleh berhubungan secara resmi.
6. Buang semua selingkuhan si adik, n bertobat hanya berhubungan dg istri yg resmi saja, yg dlm hal ini sdh dinyatakan bebas GO tersebut

Sallam,.

enterococus faecalis
Membutuhkan specifics treatment dg specifics anti biotik combination.
Perbaikan tdk sekedar pergi n pulang ke dokter berganti macam2 dokter, tetapi harus dg penelitian terhadap si bacteria apa yg bisa membasminya termasuk bagaimana menata environtment pendukung pada tubuh tersebut.
Jadi bila test menyatakan postive demikian, seharusnya RS ybs akan memberikan penata laksanaan yg lebih lanjut dlm menyelesaikan hal dimaksud.
Juga tdk bisa atau tdk boleh mencoba2 sendiri antibiotik apa pun n melihat reda, baik atau tdk, karena justru akan menambah panjang daftar antibiotik yg di resist kan oleh sang bacteria.

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Author: Susan L Fraser, MD; Chief Editor: Burke A Cunha, MD more...
Updated: Sep 19, 2011
Background
Enterococci are part of the normal intestinal flora of humans and animals but are also important pathogens responsible for serious infections. The genus Enterococcus includes more than 17 species, but only a few cause clinical
infections in humans. With increasing antibiotic resistance, enterococci are recognized as feared nosocomial pathogens that can be challenging to treat.
Enterococcus species are hardy, facultative anaerobic organisms that can survive and grow in many environments. In the laboratory, enterococci are distinguished by their morphologic appearance on Gram stain and culture (grampositive
cocci that grow in chains) and their ability to (1) hydrolyze esculin in the presence of bile, (2) grow in 6.5% sodium chloride, (3) demonstrate pyrrolidonyl arylamidase and leucine aminopeptidase, and (4) react with group D antiserum. Before they were assigned their own genus, they were known as group D streptococci.
Enterococcus faecalis and Enterococcus faecium are the most prevalent species cultured from humans, accounting for more than 90% of clinical isolates. Other enterococcal species known to cause human infection include Enterococcus avium, Enterococcus gallinarum, Enterococcus casseliflavus, Enterococcus durans, Enterococcus raffinosus and Enterococcus mundtii.[1] E faecium represents most vancomycin-resistant enterococci (VRE).
Isolation of enterococci resistant to multiple antibiotics has become increasingly common in the hospital setting.[2]
According to National Nosocomial Infections Surveillance (NNIS) data from January 2003 through December 2003, more than 28% of enterococcal isolates in ICUs of the more than 300 participating hospitals were vancomycinresistant.
Clonal spread is the dominant factor in the dissemination of multidrug-resistant enterococci in North America and Europe.[3] Virulence and pathogenicity factors have been described using molecular techniques. Several genes isolated from resistant enterococci (agg, gelE, ace, cylLLS, esp, cpd, fsrB) encode virulence factors such as the production of gelatinase and hemolysin, adherence to caco-2 and hep-2 cells, and capacity for biofilm formation.[4, 3]
Enterococci have both an intrinsic and acquired resistance to antibiotics, making them important nosocomial pathogens. Intrinsically, enterococci tolerate or resist beta-lactam antibiotics because they contain penicillin-binding proteins (PBPs); therefore, they are still able to synthesize some cell-wall components. They are intrinsically resistant to penicillinase-susceptible penicillin (low level), penicillinase-resistant penicillins, cephalosporins, nalidixic acid, aztreonam, macrolides, and low levels of clindamycin and aminoglycosides.
They use already-formed folic acid, which allows them to bypass the inhibition of folate synthesis, resulting in resistance to trimethoprim-sulfamethoxazole.
Enterococci also have acquired resistance, which includes resistance to penicillin by beta-lactamases, chloramphenicol, tetracyclines, rifampin, fluoroquinolones, aminoglycosides (high levels), and vancomycin.
The genes that encode intrinsic or acquired vancomycin resistance result in a peptide to which vancomycin cannot bind; therefore, cell-wall synthesis is still possible.
Unlike streptococcal species, enterococci are relatively resistant to penicillin, with minimum inhibitory concentrations (MICs) that generally range from 1-8 mcg/mL for E faecalis and 16-64 mcg/mL for E faecium. Therefore, exposure to these antibiotic agents inhibits but does not kill these species. Combining a cell wall–active agent such as ampicillin or vancomycin with an aminoglycoside may result in synergistic bactericidal activity against enterococci.
The acquisition of vancomycin resistance by enterococci has seriously affected the treatment and infection control of these organisms. VRE, particularly E faecium strains, are frequently resistant to all antibiotics that are effective treatment for vancomycin-susceptible enterococci, which leaves clinicians treating VRE infections with limited therapeutic options.
Newer antibiotics (eg, quinupristin-dalfopristin, linezolid, daptomycin, tigecycline) with activity against many VRE strains View updated Privacy Policy, effective January 16, 2012 have improved this situation, but resistance to these agents has already been described. A mutation (G2576U) in the domain V of the 23S rRNA is responsible for linezolid resistance,[3] whereas resistance to quinupristin-dalfopristin may be the result of several mechanisms: modification of enzymes, active efflux, and target modification. Resistance of E faecalis and E faecium to daptomycin, a newer cyclic lipopeptide antibiotic that acts on the bacterial cell membrane, has also been reported.[5]
Six phenotypes of vancomycin resistance, termed VanA, VanB, VanC, VanD, VanE, and VanG, have been described.
The VanA and VanB phenotypes are clinically significant and mediated by 1-2 acquired transferable operons that consist of 7 genes in 2 clusters termed VANA and VANB operons. In 1988, these gene clusters first were reported in
enterococcal strains. VanA is carried on a transposon Tn1546 that is almost always plasmid-mediated.
In the United States and Europe, the 3 major phenotypes include VanA, VanB, and VanD. VanA is the most common, and enterococcal isolates exhibit high-level resistance to both vancomycin and teicoplanin, while VanB isolates have
variable resistance to vancomycin and remain susceptible to teicoplanin. The VanC phenotype is mediated by the chromosomal VANC1 and VANC2 genes, which are constitutively present in E gallinarum (VANC1) and E casseliflavus (VANC2). These genes confer relatively low resistance levels to vancomycin and are not transferable.
To date, the VanD, VanE, and VanG phenotypes have been described in only a few strains of enterococci.
Three patients infected with vancomycin-resistant Staphylococcus aureus (VRSA) have been reported in the United States.[6, 7] The in vivo conjugative transfer potential of the vanA resistance gene from vancomycin-resistant E faecalis to methicillin-resistant S aureus (MRSA) was confirmed in the first of these cases. This poses an emerging threat to patient safety. E faecium isolates with a complex-17 lineage have also emerged in hospital and community settings in 5 continents over just the past 2 decades. This continued global spread of resistant organisms and the creation of new, highly virulent pathogens from transfer of resistance genes underscore.

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Jadi jelas tdk boleh sembarangan.
Masuk ke RS yg benar, check all the possibility, repair with possible high cure antibiotik arrangement, while increased body performance.

Sallam,
 

Hello,
Selama ini a sign atau pola pemikiranya berbasis pada kuman tersebut, pada hal some of kuman need by body, bagaimana kalau treatment nya berbasis pada the whole body, jadi bukan hanya pada kumanya mati dg apa, tapi kenapa si kuman bisa subur n berkembang pesat.
Singapore n malaysia, saya pikir akan sama saja kalau basis tretmentnya menuju ke si kuman n bukan keseluruh tubuh dlm rantai aksi reaksi.
persoalanya ybs n anda sabar tdk dg menjalankan protokol yg diharuskan nantinya; kalau maunya instant ya susah.
Fyi, ada patient yg dikendarai memilki kelainan hormonal thyeroid, ke Singapore n Malaysia, hasilnya ya sama juga, ternyata hasil nya bukan demikian n membaik dlm bulan ke 3 berbanding target hormonal therapy 9-12 bulan.
jadi menurut saya sangat tergantung banyak faktor.

Sallam,

Hello,
pengajaran dokter secara umum memang berorientasi pada penyakit, makanya saya batasi bahwa penyakit hanya karena 2 sebab, karena virus n karena bacteria,
Nah bila ada gangguan n dokter melihat itu sebagai disease jadi ketika ketemu bacterianya lalu itu yg diubak2.
Perlu disadari bahwa keunikan bacteria ini, adalah:
1. resist terhadap berbagai antibiotik
2. Ada dlm jumlah sedikit berguna bagi tubuh, tetapi dlm jumlah yg banyak merugikan tubuh karena tdk bisa dibasmi dg cara atau sop biasa dg antibiotik.

jadi bila waktu pemberian antibiotik ternyata sdh semua tanpa hasil, perlu dipkirkan bahwa kesaktian si bacteria itu karena apa? apa yg membuat di begitu sakti?
bagaimana mengeliminir kesaktiannya?
Apa yg terjadi sebenarnya pada tubuh itu, ini yg saya sebut the whole body.
jadi kita tdk melihat pada bacteria itu saja yg dlm jumlah sedikit dibutuhkan tetapi dlm jumlah banyak menjadikanya infeksi saluran tersebut.

nah bagaimana saya bisa tau kalau kita tdk pernah menginvestigasi tubuh ybs secara sepenuhnya (tdk hanya pada cause n bacteria saja), dg demikian bagaimana saya bisa menganjurkan protokol apa yg harus dijalankan?

sejak semula kita hanya berbicara ttg hasil antibiotik, hasil kondisi, hasil pemeriksaan sekilas, tanpa tau kenapa, n bagaimananya?

Sallam,

Hello,
Wah kalau tanya SOP dokter, mestinya tanyanya ke dokter ybs, karena protokol pelaksanaan atau SOP yg di canangkan kan harus sesuai dg hasil analisa diagnosanya si pengambil keputusan tersebut; sementara saya kan tdk tau hasilnya n hanya membaca cerita yg anda sampaikan anda disini, tanpa sedikit pun sempat mendalami yg sering saya sebut sebagai "investigasi" tubuh tersebut

Protokol atau Etics yg dicanangkan bagi kami:

First, do no harm. dg demikian, Naturopathic physicians selalu harus yakin bahwa apa yg dilakukan tdk akan merusak tatanan tubuh ybs

Oleh karena itu, tdk sembarangan biarpun hanya juice atau apapun, saya perlu dg yakin bahwa itu akan membantu bukan malah merusak; apalagi melihat case anda sdh menjalani proses selama 1 tahunan.
1 Tahun, bisa sangat berubah apa pun itu.

Sallam,

Hello,
Saya mo tanya.
Selama ini apa yg terjadi?
Ada luka right sampai infeksi right, diobati dg antibiotik n tdk sembuh, malah ada dibebrapa tempat right?
Artinya ada luka n luka tadi tdk bisa sembuh.

Nah sekarang saya tanya lagi:
Dikikis, artinya apa? luka yg ada tadi di perdalam n diperlebar.
Bisa sembuhkah?

jadi apakah protokol yg hendak dijalankan akan bermanfaatkah?

Sallam,

Hello,
Sepertinya sdh saya jawab apa yg akan saya lakukan di:
http://www.medisiana.com/klinik-penyakit-dalam/penyakit-kelamin/msg4008/#msg4008
Bacteria itu tdk ngumpul disatu tempat, tapi menyebar diseluruh rangkaian saluran kemih, oleh karena itu utk bagaian2 yg lemah n dia bisa menyerang, maka terjadilah luka n bernanah disana (kira2 demikian gampangnya) n hasilnya si nanah ikut keluar ke ujung saluran (ujung p*nis) sebagai cairan kental putih tersebut.
Jadi bila memBom dg antibiotik tdk bisa membasmi si bacteria, maka perlu dicari kenapa si bacteria sakti bisa begitu banyak populasinya n kemudian merusak jaringan pada system tubuh itu?
Ini tdk mudah, tdk juga instant, karena terbentukanya juga tdk instant.
Sallam,