SERRATİA ENFEKSİYONLARI

Enterobakter grubuna ait, Gram-negatif basillerdir. En az 15 türü vardır. Cins, fakültatif anaerob gram-negatif çubuklardan oluşmaktadır. Kırmızı boyanır. Hastaneden kazanılmış olan suşlar genelde beyaz-kremsi boyanırlar ve standart inkübatörlerde iyi çoğalırlar (35-37^◦C).

S.marcescens ve diğer Serratia türleri, çok fazla virülans faktörü salgılamazlar ve oportunistik olarak düşünülürler.  Hareketlidirler ve fimbriaları aracılığıyla hücrelere adhere olabilirler. S.marcescens, değişik hücre tiplerine toksik olan birkaç farklı hemolisin salgılayabilirler.

İnsandaki Serratia enfeksiyonları  daha ziyade ekzojen çevreden kaynaklanmaktadır. Hayvanlardan vs bulaşmaz. Genelde direkt olarak toprak, su vs ile temastan kazanılır. Serratia türleri sıklıkla hastane içi salgınlarla ilişkilendirilirler, hastane dışı salgınlar çok mutad değildir. Steril olması gereken hazır solüsyonlardan vs. fabrikasyon hatası olarak salgınlar tanımlanmıştır.

Bireysel hastane kökenli Serratia enfeksiyonu çok sık değildir. Hastada invazif bir cihaz varlığı hastaneden kazanılmış Serratia türleri için önemli bir risk faktörüdür. Ancak, surveyans verileri Serratia’nın cihaz ilişkili enfeksiyon patojeni olarak baskın karakterde olmadığını göstermektedir. Daha ziyade ortak kaynak salgınlarına yönelmek gerekir.

S.marcescens, üriner trakt enfeksiyonu, pnömoni ve kan akımı enfeksiyonu yapabildiği gösterilmiş bir insan patojenidir.  İntravenöz ilaç kullanılanlarda enfektif endokardit yapabilmektedir. Deri ve yumuşak doku enfeksiyonları, cerrahi alan enfeksiyonları hatta nekrotizan fasciit, osteomiyelit, septik artrit sık olmamakla birlikte tanımlanmıştır.

SSS enfeksiyonları genelde ventriküloperitoneal şant, lomber ponksiyon, veya spinal enjeksiyonlara bağlanmıştır. Yenidoğanlarda meningoensefalit bildirilmiştir.

Serratia türleri, gözü diğer bölgelere göre daha fazla tutar. P.aeruginosa’dan sonra hastane kaynaklı oküler enfeksiyonun en sık nedeni olarak bildiren çalışmalar vardır. Konjunktivit, keratokonjuktivit, korneal ülserler ve keratit şeklinde olabilir. Serratia kaynaklı endoftalmit seyrektir ama uzun dönem sonlanımı kötü olabilir.

Serratia türlerinde ampisilin, amoksisilin, ampisilin-sulbaktam, amoksisilin klavulanata doğal olarak direnç sahibidir. Aynı şekilde, dar spektrumlu sefalosporinlere (cefazolin gibi), cephamycin’e, makrolidlere, tetrasiklinlere ve nitrofurontain’e de dirençlidir. AmpC betalaktamaz üreterek geniş spektrumlu beta-laktam direnci de yapabilirler. ESBL üretimi ve karbapenemaz üretimi de tanımlanmıştır.

Serratia türleri florokinolonlar, aminoglikozidler, trimotoprim-sülfametaksazol, piperasilin-tazobaktam, tikarsilin-klavulanat, 3. Ve 4. Kuşak sefalosporinler, aztreonam ve karbapenemler gibi bir seri antibiyotiğe duyarlıdırlar.

TREATMENT OF HYPERCALCEMIA

Patients with mild hypercalcemia (<12 mg / dL) have no indications for immediate treatment. It may be advisable to increase fluid intake to reduce the risk of nephrolithiasis.

Intermediate hypercalcemia (12-14 mg / dL) may not require immediate treatment. An acute rise in serum calcium can cause significant impairment in mental status and requires urgent treatment.

Severe hypercalcemia (> 14 mg / dL) should be treated;

The isotonic saline should be given at a rate of 200-300 mL / h and a rate of 100-150 mL / h urine output. If there is no heart / kidney failure, it is not necessary to give loop diuretics.

Calcitonin (4 IU / kg) should be given and serum calcium measured after hours. If hypocalcemic response is observed, this can be repeated every 6 to 12 hours (4-8 IU / kg).

Zolendronic acid (4 mg i.v., over a 15 minute period) should be started concurrently with treatment. The other alternative is pamidronate.

Administration of saline with calcitonin will cause a reduction in calcium in 12 to 48 hours. The bisphosphonate reduces serum calcium within 2 to 4 days.

Donesumab is an alternative drug in a patient with malignant, Zolendronic acid-resistant, severe hypercalcemia.

Hemodialysis.

The most common cause of hypercalcemia in non-hospitalized patients is HYPERPARATHYROIDISM.

Hydration with isotonic NaCl

Hypovolemia causes hypercalcemia by impairing renal clearance of calcium.

With saline treatment, hypercalcemia on a moderate level often does not become normal. Simultaneous bisphosphonates should also be initiated. If necessary calcitonin can be started.

Calcitonin

At pharmacological doses, calcitonin acts by increasing renal calcium excretion and, more importantly, by impairing osteoclast function and reducing bone resorption. Nasal form is not successful in hypercalcemia treatment.

Calcitonin is safe and does not have major toxicities. The effect is fast despite the weakness. It starts in six hours and reduces calcium up to 1-2 mg / dL maximum. Probably due to receptor down-regulation, tachyphylaxis develops within 48 hours.

Bisphosphonates

Bisphosphonates are nonhidrolizable analogs of inorganic phosphate adsorbing to the surface of bone hydroxyapatite. It disrupts osteoclast-mediated bone resorption and impairs calcium release.

Although zoledronic acid has the potential to cause osteonecrosis of the jaw, it is a side effect that is more commonly seen in chronic use.

The efficacy of zolendronic acid 4 mg and 8 mg doses were similar. 8 mg was associated with more renal toxicity.

Pamidronate is more effective than etidronate or clodronate.

Ibandronate 2mg / 4mg / 6mg is also effective in hypercalcemia. The efficacy is greater at 4 mg and 6 mg, but duration of action is dose independent.

Ibandronate appears to be as effective as pamidronate.

Clodronate and etidronate are relatively low-impact first-generation bisphosphonates. If the other bisphosphonates are not aviable, these two agents can be used.

Glucocorticoids

Where absorption of vitamin D-related dietary calcium is increased, glucocorticoids reduce the production of calcitriol within 2-5 days.

Denosumab

DenoSumab has a 60 mg injector and is used weekly.

It can also be used in chronic kidney failure. Optimal dosing is not clear in renal failure. The risk of hypocalcemia seems to be more in chronic kidney disease.

If the first dose is as low as 0.3 mg / kg, and if the target is not reached within 1 week, the second injection may be recommended as a prudent approach, considering the risk of hypocalcemia.

Measuring vitamin D levels prior to denosumab may also be warranted, because those with vitamin D deficiency are more susceptible to hypocalcemia. Even if the measurement of vitamin D levels is delayed, give vitamin D 50000 IU 1-2 days before donesumab; If the result is Vitamin D deficiency you will continue treatment; If there are no deficiencies, you will end up giving vitamin D. Some authors advocate this view.

Calcimimetics

Sinekalset

Dialysis

It is the approach to be considered in the last stage.

CATETER RELATED BLOODSTREAM INFECTIONS-diagnosis

LCBI (Laboratory confirmed Bloodstream infection) must have at least one of the following conditions;

• The patient must have a pathogen defined in at least 1 blood culture and this pathogen should not be responsible for infection on the other side of the body.
• The patient must have at least one of the following symptoms; Tremor or hypotension; And the pathogen should not be associated with infection in another area, or if the pathogen is a common commensal, it should be shown at least ≥ 2 blood cultures and cultures should be obtained from different parts of the body.

MBI-LCBI denilen bir kavram da, LCBI’nin bir alt grubu olarak ortaya atılmıştır

(MBI: Mukozal bariyer injuri).

This concept is the presence of enteric organisms in at least one blood culture from patients with neutropenia or diarrhea, who are advanced haemopoietic stem cell transplant patients with advanced Graft Versus Host disease.

Although the most sensitive finding in catheter-related bloodstream infection (CRBI) is fever, the specificity is low.

Inflammation and purulence in the catheter entry site have better specificity, but lower sensitivity.

Other clinical findings; Hemodynamic instability, altered mental status, catheter dysfunction, septicemia findings starting with catheter infusion.

Complications due to bloodstream infections can also be seen; Suppurative thrombophlebitis, endocarditis, osteomyelitis, metastatic infection etc.

Conditions where no other source of infection is present, if the S. aureus, coagulase (-) Staphylococci and Candida species are obtained in blood cultures, the CRBI is mentioned.

Cultures from peripheral venules have lower false positives than cultures from the catheter. In blood cultures from both routes, the (-) predictive value is very good.

If there is no possibility of obtaining peripheral vascular blood culture; It is necessary to take ≥ 2 blood cultures from 2 separate lumens of the multi-lumen catheter.

Diagnostic criteria for CRBI;

The production of the same microorganism from two catheter tips and at least 1 peripheral venous culture,

Production of the same microorganism from at least 2 blood cultures (one from the central lumen of the catheter, the other from the peripheral vein or the second lumen of the catheter). This should meet the criteria of quantitative blood cultures or the criteria of Differential time to Positivity.

If the quantitative culture from the catheter hub shows a colony count of ≥ 3 folds compared to the cultures provided from the peripheral veins or the cultures obtained from the second lumen, CRBI is considered to be in favor.

In semi- quantitative culture; If both the catheter entry site, the catheter nipple and the peripheral culture produce> 15 cfu of the same microorganism, this is in favor of CRBI.

Diferential time to positivity; If the cultures taken from the catheter start> 120 minutes before the culture from the peripheral veins, CRBI can be shown with 85% sensitivity and 91% specificity.

TÜRKÇE

PAN -Diagnosis

Türkçe

Significant reduction of hepatitis B virus infection has also reduced the frequency of PAN in the world in parallel. In addition, some patients, previously classified as PAN, are now classified as separate diagnoses (such as MPA).

The diagnosis is mostly made at middle and advanced ages and the incidence increases with age. It makes its peak in the 6th decade of life.

It's a little more in men (1,5: 1).

Many cases are idiopathic, the pathogenesis of some patients is associated with HBV, HCV and hairy cell leukemia.

HBV-associated PAN usually develops within 4 months after HBV.

Regardless of the underlying cause, PAN is characterized by segmental transmural inflammation of musculature arteries.

PAN does not hold venues.

The cellular infiltrate consists of polymorphonuclear leukocytes and mononuclear cells.

It may be leukocytoclastosis  (fragmentation of white blood cells).

Necrosis of the arterial wall leads to a homogeneous eosinophilic appearance known as fibrinoid necrosis.

Damage to the internal and external elastic lamina may cause aneurysmal dilatation.

In the same sample, lesions at various stages can be found.

Granulomatous inflammation leads to another diagnosis. Not on the PAN.

PAN’lı hastalar tipik olarak sistemik semptom ve bulgularla gelirler.

On the skin; Purpura, tender erythematous nodules, ulcers, and bullous or vesicular eruptions may be present.

Skin lesions are more frequent in lower extremity and extremity edema is frequent. Skin lesions can be serious enough to go to gangrene.

Kidney; The most commonly affected organ in autopsy series. Renal insufficiency, hypertension, perirenal hematomas (rupture of renal artery aneurysms), multiple renal infarcts may also be present.

Incomplete narrowing of the inflamed arteries does not cause inflammation or necrosis, although it causes glomerular ischaemia. Therefore, urine examination shows sub-nephrotic proteinuria, often with minimal proteinuria and possibly moderate hematuria. However, erythrocytic eruptions, which are representative of glomerular inflammation, are not usually seen. SLE or ANCA (+) vasculitis should be considered if seen. As a result of renal ischemia, RAAS activation is considered as the cause of hypertension.

Neurological; 70% of patients have a mononeuritis multiplex. Over time, the number of affected nerves increases, so the first asymmetric involvement may return to distal symmetric polyneuropathy.

SSS involvement occurs in 5-10% patients.

GIS; The involvement of the mesenteric artery may be recognized early by abdominal pain. Because the patient is afraid of eating or because of malabsorption, weight loss may occur.

Nausea-vomiting, melena, bloody / bloodless diarrhea and GI bleeding can also be seen.

Intestinal infarction and perforation may also develop.

Splenic infarct

Patients with PAN have increased risk of perforation during colonoscopy.

Although AMI is not a very common occurrence, PAN can cause coronary ischemia.

Rarely, cholecystitis, appendicitis, segmental pancreatic infarction can occur.

Myalgia and muscle weakness are frequently observed.

Orchitis (10%)

Eye findings; Ischemic retinopathy, retinal detachment, optic neuropathy

Breast and uterine involvement

Bronchial artery involvement has been described in PAN, but other diseases should be considered if there are other parenchymal involvements due to capilleritis or vasculitis.

Diagnosis

PAN diagnosis is considered by the patient's clinic and radiological imaging, but is confirmed with biopsies from the affected organs.

The renal biopsy to be performed in the PAN can give us the pathognomonic inflammation in the middle-sized arteries. Because of the multiplicity of microaneurysms, there may sometimes be an increased risk of bleeding. Some advocate renal biopsy only if arteriography is negative.

Conventional mesenteric or renal arteriography is an alternative to biopsy.

Less invasive techniques such as CT and MRI can be used.

The PAN classification of ACR in 1990 can determine the disease with 82% sensitivity and 87% specificity.

≥ 4kg weight loss without any other explanation

Livedo reticularis

Testicular pain or tenderness

Miyaji (except shoulder and hip zone), muscle weakness, limb tenderness or polyneuropathy

Mononeuropathy or polyneuropathy

Diastolic blood pressure greater than 90 mmHg (new onset)

Elevation of serum BUN (> 40 mg / dL) or creatinine (> 1,5 mg / dL) levels.

Evidence of HBV infection

Characteristic angiographic abnormalities (other than those resulting in noninflammatory disease processes)

HİPERKALSEMİ-TEDAVİ

Hafif hiperkalsemili (<12 mg/dL) hastaların acil tedavi endikasyonu yoktur. Nefrolitiyazis riskini azaltmak için sıvı alımını arttırmaları önerilebilir.

Orta düzeyde hiperkalsemide (12-14 mg/dL) de acil tedavi gerekmeyebilir. Akut bir yükselme, bilinçte belirgin bozulmalar yapabilir ki, acil tedavi gerektirir.

Ağır hiperkalsemi (>14 mg/dL) tedavi edilmelidir;

• İzotonik salin 200-300 mL/h hızında ve 100-150 mL/h idrar çıkımı sağlayacak şekilde verilmelidir. Kalp/böbrek yetersizliği yoksa loop diüretikleri vermek gerekli değilidir.

• Kalsitonin (4 IU/kg) verip saatler sonra serum kalsiyumunu ölçmek gerekir. Eğer hipokalsemik yanıt izlenirse bu işlem 6-12 saatte bir tekrarlanabilir (4-8 IU/kg).
• Zolendronik asiti (4 mg i.v., 15 dakikanın üzerinde bir sürede) de tedavilerle birlikte başlamak gerekir. Diğer alternatif pamidronattır.

Salinle kalsitoninin verilmesi 12-48 saatte kalsiyumda düşüşe neden olacaktır. Bifosfonat verilince de 2.-4. gün etkisi başlar.

Zolendronik aside dirençli, maligniteden kaynaklanan ağır hiperkalsemili hastad Donesumab alternatiftir.

Hemodiyaliz.

Ayaktan hastaların en sık hiperkalsemi nedeni HİPERPARATİROİDİZM’dir.

İzotonik NaCl ile hidrasyon

Hipovolemi kalsiyumun renal klirensini bozarak hiperkalsemi yapar.

Salin tedavisiyle orta düzey üzeri hiperkalsemi sıklıkla normal hale gelmez. Eş zamanlı bifosfonat da başlanmalıdır. Duruma göre kalsitonin de başlanabilir.

Kalsitonin

Farmakolojik dozlarda kalsitonin, renal kalsiyum atılımını arttırmak suretiyle ve daha önemli olarak da, osteoklast fonksiyonlarını bozarak kemik rezorbsiyonunu azaltarak etki etmektedir. Nazal form hiperkalsemi tedavisinde başarılı değildir.

Kalsitonin güvenlidir ve major toksisiteleri yoktur. Etkisi zayıf olmasına rağmen hızlıdır. Altı saat içerisinde başlar ve kalsiyumu maximum 1-2 mg/dL kadar düşürür.  Muhtemelen reseptör down-reülasyonuna bağlı olarak 48 saat içerisinde taşiflaksi gelişir.

Bifosfonatlar

Bifosfonatlar, kemik hidroksiapatitinin yüzeyine adsorbe olan inorganik fosfatın, nonhidrolizable analoglarıdır. Osteoklast aracılı kemik rezorbsiyonunu bozarak kalsiyum serbestleşmesini bozarlar.

Zolendronik asitin çene osteonekrozu yapma potansiyeli olsa da; bu daha ziyade kronik kullanımlarda görülen bir yan etkidir.

Zolendronik asidin 4 mg ve 8 mg’lık dozlarının etkinliği benzer bulunmuştur. 8 mg daha fazla renal toksisiteyle ilşkili bulunmuştur.

Pamidronat , etidronat veya clodronata göre daha etkindir.

İbandronat 2mg/4mg/6mg ; da hiperkalsemide etkindir. Etkinlik 4 ve 6 mg’da daha fazladır ancak etki süresi dozdan bağımsızdır.

İbandronat, pamidronat kadar etkin gibi görünmektedir.

Clodronat ve etidronat nispeten düşük etkili ilk jenerasyon bifosfonatlardır. Diğer bifosfonatlar yoksa gündeme gelebilirler.

Glukokortikoidler

Vitamin D ilişkili diyet kalsiyumunun emiliminin arttığı durumlarda glukokortikoidler 2-5 gün içerisinde kalsitiriol yapımını azaltırlar.

Denosumab

kullanıma hazır 60 mg enjektörü vardır ve haftada bir kullanılır.

Kronik böbrek yetmezliğinde kullanılabilir. Böbrek yetmezliğinde optimal dozu net değildir. Hipokalsemi riski KBY’lilerde daha fazla gibi görünmektedir.

İlk dozun 0.3 mg/kg gibi düşük bir doz olması ve 1 hafta içerisinde hedefe ulaşılamadığı takdirde ikinci enjeksiyonun yapılması, hipokalsemi riski düşünüldüğünde, ihtiyatlı bir yaklaşım tarzı olarak önerilebilir.

Donesumab öncesi vitamin D düzeylerinin ölçülmesi de ihtiyaten gerekebilir, çünkü D vitamini eksikliği olanlar hipokalsemiye daha yatkındırlar. Hatta sonuç çıkması sürecekse donesumab öncesi Vitamin D 50000 IU 1-2 verin; sonuç Vit D eksiliği gelirse devam edersiniz, eksiklik yoksa kesersiniz diyenler bile varmış.

Kalsimimetikler

Sinekalset  

Diyaliz

En son aşamada düşünülür.

GIANT CELL ARTERITIS: CLINICAL FEATURES

                                                                                           Türkçe
Giant cell arteritis (GCA) is the most common systemic vasculitis.

The greatest risk factor for GCA is aging. The disease, which is almost never seen under the age of 50, peaks at ages 70-79.

The disease is a little more common in females. GCA can also be found in patients' families.

Patients with GCA are not associated with increased mortality if there is no significant aortic disease. Approximately 40-60% of GCA patients have polymyalgia rheumatica (PMR), but only 15% of patients with PMR have GCA.

The onset of the disease is mostly subacute, but may also be acute.

Fever is present near the half of the patients and is usually at low levels. However, fever can reach 39° C in 15% of patients, It may also be due to a skipped infection.

Fatigue, weight loss (usually low level) are common.

Headache is present in 2/3 of the patients.

Jaw claudication is an experience where almost half of the patients live. In one analysis, jaw claudication was reported to be the most associated symptom with temporal artery biopsy results.

Amorozis fugax, temporary loss of vision, mostly affecting one eye. It may be an early manifestation. It is valuable in terms of prior notice of permanent blindness.

Persistent vision loss is painless and sudden. It can be partial or complete. It may be unilateral or bilateral. Persistent visual loss in patients with GCA has been reported to be 15-20%, even with appropriate treatment. Once it develops; Rarely returns. Moreover, other eyes of untreated patients may experience visual loss within 1 week (25-50% risk).

If visual loss returns quickly after the appropriate dose of glucocorticoid therapy, the risk of vision loss is virtually eliminated.

If vision loss is already present, this treatment will significantly reduce the risk of further deterioration.

Causes of vision loss;

Arterial ischemic optic neuropathy (AION),

Central or branchial occlusion of the retinal artery (CRAO / BRAO),

Posterior ischemic optic neuropathy (PION,

Cerebral ischemia (rare).

AION accounts for at least 80%. AION typically develops as a consequence of the occlusion of the posterior silier artery, a branch of the ophthalmic artery (the main feeder vessel in the eye) originating from the internal carotid artery .

CRAO is responsible for 10% of permanent blindness due to GCA.

Diplopi % 5

Charles Bonnet Syndrome; Visual hallucinations in the person with vision loss. It may also be associated with glucocorticoid. It's actually a psychiatric syndrome.

Peripheral symmetric synovitis with pit edema occurs in a small proportion of patients.

INVOLVEMENT OF GREAT BLOOD VESSELS İN GCA

Aortic aneurysms occur in 10-20% of GCA patients. The thoracic aorta, especially the descending aorta, is frequently involved compared to the abdominal aorta.

A small proportion of patients may have aortic rupture and dissection, with or without aneurysms.

GCA may also affect the subclavian artery from distal to the vertebral artery dissection site, to axillary and proximal brachial arteries.

The upper extremity disease associated with GCA is not symmetrical, but is characteristically bilateral.

Stroke is rare. Ataxia, vertigo, dysarthria, etc. are rare.

Intracranial vessel involvement is very rareApproximately 10% of GCA patients have upper respiratory symptoms. A nonproductive cough is the most common symptom.

Macroglossia, lingual infarct, and scalp necrosis are rarely reported.

Pulses may be felt weakly and may be inconsistent blood pressure arterial measurements.

A murmur of aortic regurgitation should not be skipped because it may be a finding of a descending aortic aneurysm and its associated aortic valve dilatation.

Anemia can sometimes be profound and reactive thrombocytosis may also be present. Leukocytosis tends not to increase even in active disease.

Serum albumin can be slightly lowered and responds quickly to glucocorticoid therapy.

Liver enzymes, especially ALP, have increased slightly in 25-30% of patients. It returns to normal with glucocorticoid therapy.

ESR is typically elevated, and GCA is a disease that can exceed the ESR of 100. The CRP also generally increases proportionally. Neither is specific for GCA.

Increased concentrations of IL-6 appear to be closely related to the clinical activity of GCA. However, the clinical significance is unknown and is not present in routine practice.

Vancomycin Resistant Enterococcus: a current overview of diagnosis, prevention and treatment

Although many enterococcus species can be held responsible for VRE, Enterococcus faecum and Enterococcus faecalis constitute 95% of VRE infections.

We can add vancomycin resistant strains such as E. gallinarus and E.casselflavius ​​to these, but these two organisms are more or less related to colonization. Their pathogens are low and they can live in nature for years.

Vancomycin inhibits enterococci by binding to the D-alanyl-D-alanine (D-Ala-D-Ala) terminal of cell wall precursors.

In the case of residence, the D-Ala-D-Ala terminus is replaced by the D-Ala-D-lactate termination. Vancomycin binds to this end with low affinity. As a result, the MIC value for vancomycin is almost 1000 fold.

The accepted MIC value for vancomycin susceptibility is ≤4 mcg / mL, while the value that is resistant is considered to be ≥32 mcg / mL. Values ​​between 8-16 mcg / mL Vancomycin is considered to be intermediate, at which Vancomycin is not preferred.

Pulse-field gel electrophoresis (PFGE) is used in the analysis of both endemic and epidemic clusters of VRE infection and colonization.

The vast majority of VREs are Enterococcus faecum.

Risk factors

• Previous antibiotic therapy history is the most common risk factor for VRE. Vancomycin and cephaloporins are prominent antibiotics. Ceftazidime has been found one of the most prominent in a study.
• Administration of antibiotics for anaerobic treatment is known to increase the intensity of the fecal colonization of VRE, which decreases after the antibiotic is discontinued.

Patient characteristics

• More than 72 hours of hospital stay, important underlying medical conditions, need for ICU and invasive devices.
• Colonization pressure
• Exposure to contaminating surfaces
• Patient from care centers

The patient known to be colonized with VRE is estimated to have been colonized for at least 1 year.

The percentage of VRE infection development in patients who are contaminating with VRE is about 8%. This rate is higher in severely ill patients and those with immunodeficiencies.

Routine surveillance cultures are not recommended to detect colonized patients with VRE in non-epidemic centers. Active surveillance cultures are recommended for high-risk patients and are recommended for centers with increased frequency of VRE.

The most important method of protection is hand washing. In particular, it should be ensured that health personnel take into account contact measures.

VRE hasta odasındaki yüzeylerde saatlerce-günlerce kalabilmektedir.

VRE description: Vancomycin resistance is defined as ≤ 16 mm by disc diffusion method or 8 μg / ml by agar dilution method (MIC) or automated methods.

To say that there is an epidemic; We need to show that in the healthcare facility, 3 or more infections with clinical significance have been acquired within 7 days.

Optimal antibiotic treatment in infected patients with VRE has not been definitively identified. Linezolid is FDA approved. While quinopristin-dalfopristin has been FDA approved in the past, this approval has been lifted due to ineffectiveness.

aminoglycosides.

E.faecalis, like E. gallinarus and E.casselflavius, are generally susceptible to beta-lactams.

Linezolid, daptomycin and tigecycline have activity against both E. faecium and E. faecalis.

The effect of quinopristin-dalfopristin is only against E. faecum, not against E. faecalis.
Türkçe 

1. Treatment of hypercalcemia,
2. Metformin and renal impirment, 
3. PBC - Primary biliary cirrhosis, 
4. Giant cell arteridis:Clinical features,  
5. PAN -Diagnosis, 
6. Cateter Releated Bloodstream Infections-diagnosis,
7. Exercise-induced hematuria
8. Serratia Infections-Brief