by Philip Darney, MD MSc
Professor and Chief
Department of Obstetrics, Gynecology and Reproductive Sciences, San Francisco General Hospital Division, UCSF
Reshared Knol
Introduction
Many women who want to avoid pregnancy prefer not to use hormones. Male and female sterilization operations (vasectomy in men and various methods of closing the tubes or oviducts in women), vaginal barriers (condoms, diaphragms and crèmes or foams), and the “natural” methods (ovulation timing, abstinence, and breast feeding) all provide contraception without the use of hormones. In fact, these are the most frequently used methods around the world, including the USA, where sterilization and condoms provide protection against unintended pregnancy to more people than all the other methods combined.
Depending on the method chosen and how it is used, non-hormonal methods have a much wider range of effectiveness than the hormonal contraceptives (pills, patches, rings and implantable methods), but they avoid the side effects of taking hormones. The most effective of these methods (male and female sterilization) are not reversible; the reversible non-hormonal methods are usually much less effective than hormonal contraceptives, but some people achieve much greater success than “typical” users. Our description of these methods will begin with the most effective and proceed to the less effective ones.
Sterilization
Female Sterilization Operations (Tubal Ligation or Tubal Occlusion)
Key points:
* Tubal sterilization remains a popular and highly effective method of contraception worldwide.
* The 12 year U.S. Collaborative Review of Sterilization (CREST) study reported a 10 year cumulative pregnancy rate of 1.8%, with the lowest failure rate in post-partum partial salpingectomy and highest among bipolar electrocautery.
* Other large series suggest 10 year failure rates for interval sterilization of 0.23% - 0.9%, with the Filshie clip having the lowest failure rate.
* Successful bilateral placement of Essure coils occurs in 92-95% of procedures.
* On the day of the procedure, current pregnancy should be excluded prior to tubal sterilization.
* While no pregnancies were reported in Essure clinical trials, five year data suggest a failure rate of 2.6 per 1000, with no reported ectopic pregnancies; most of these pregnancies were in women who did not follow-up after the procedure. Confirmation of tubal occlusion is crucial, and this method should be reserved for patients who are likely to follow up and to use an interval method of contraception.
More Visit Source Knol Non Hormonal Contraception
Reshared under Creative Commons Attribution 3.0 License
Showing posts with label Medical. Show all posts
Showing posts with label Medical. Show all posts
Tuesday, July 19, 2011
Tuesday, July 12, 2011
MRSA Methicillin Resistant Staphylococcus Aureus (MRSA) Infections of the Skin
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Source Knol: MRSA Methicillin Resistant Staphylococcus Aureus (MRSA) Infections of the Skin
by Bryan Cho MD, PhD, Board Certified Dermatologist
INTRODUCTION
Bacteria are microorganisms that are found almost everywhere. Most bacteria are harmless but some can cause infection. Methicillin-resistant Staphylococcus aureus (MRSA) is a bacterium that has emerged as a major cause of skin infections among otherwise healthy adults and children in the community. This bacterium is dangerous because it causes infections that cannot be treated with commonly used antibiotics that in the past would destroy the bacteria and cure the infection. Moreover, left untreated these infections can have serious complications. This knol will discuss the risk factors for MRSA infections, what MRSA skin infections look like, and how they can be treated and avoided.
HEALTHCARE ASSOCIATED-MRSA
MRSA was first diagnosed in 1961 as bacteria associated with serious infections that occurred in hospitalized patients or patients in healthcare facilities such as nursing homes or dialysis centers. MRSA infections that occurred in healthcare facilities were termed healthcare associated-MRSA (HA-MRSA). These infections were often serious and potentially life-threatening and included bloodstream infections, surgical site infections or pneumonia. Since being discovered, the number of MRSA infections has increased dramatically. In 1974, MRSA infections accounted for 2% of the total number of Staphylococcus infections; in 1995 it was 22%; in 2004 it was 63%[1]
HA-MRSA risk factors include:[2],[3]
1. Weakened immune system and severe illness
2. Previous exposure to antimicrobial agents
3. Surgery or open wounds
4. Residence in a long term healthcare facility (nursing home, skilled nursing facility)
5. Underlying disease or conditions, particularly:
1. Chronic renal disease
2. Insulin-dependent diabetes mellitus
3. Peripheral vascular disease
4. Dermatitis or skin lesions
6. Invasive devices (Urinary catheterization, intravenous lines (IV), Dialysis, tracheotomies, G tubes)
7. Patients in the intensive care unit (ICU)
8. Male, age older than 65
9. Repeated contact with the healthcare system
10. Previous colonization by a multidrug-resistant organism
COMMUNITY ACQUIRED-MRSA
In the past few years, a separate strain of MRSA bacteria has developed that affects healthy members of the community. This community acquired MRSA (CA-MRSA) has caused outbreaks of disease among professional athletes, high school athletic teams, and in day care settings. Developing a CA-MRSA infection does not imply any impairment in immune system function. The average age of patients with CA-MRSA infections is age 23 compared to age 68 for HA-MRSA.[4] Unlike HA-MRSA, CA-MRSA rarely causes life threatening infections. CA-MRSA most commonly causes skin infections such as boils or pimples. Because these infections can occur abruptly on otherwise normal skin, CA-MRSA infections are frequently mistaken for spider bites.
CA-MRSA may occur in the following populations:
1. The young and healthy, especially those who live in crowded conditions or have close physical contacts with others, including:
1. Athletes
2. Prisoners
3. Soldiers
2. Selected ethnic populations
3. IV drug users
Table 1. CA-MRSA versus HA-MRSA. (not shown in this post. Visit source knol)
SKIN INFECTIONS CAUSED BY MRSA:
Roughly 85% of CA-MRSA infections develop in the skin.[5] Each year there are an estimated 12 million outpatient (e.g., physician offices, emergency and outpatient departments) healthcare visits for skin and soft tissue infections in the United States[6]. In one study, three out of four patients seen in the emergency room for skin infections had Staphylococcal aureus infections and over 50% had MRSA infections.[7]
Most MRSA skin infections look like (Described below.):
o Impetigo
o Many small pimple-like bumps (folliculitis)
o Large painful boils (furuncle or carbuncle)
o Spider or insect bites
Less common and more serious skin and soft tissue infection caused by MRSA include:
o Cellulitis
o Infected wounds
Impetigo is a superficial skin infection that occurs on open, exposed areas of skin. This infection occurs most commonly in children but usually does not cause serious illness. The infection starts at sites of minor skin trauma such as insect bites or abrasions. The affected skin may develop small (less than 5mm) fluid filled bumps that develop golden honey-crusting when bumps burst. Usually, multiple skin lesions are present. Impetigo is easily spread within families and close contacts. Other risk factors for infection include warm, humid conditions and poor hygiene. Impetigo is most commonly caused by a bacterium called Streptococcus, but more and more frequently, impetigo is caused by MRSA; CA-MRSA now accounts for 7-20% of impetigo infections.[8] Impetigo caused by Streptococcus and CA-MRSA look identical.
Figure 1: Impetigo
Folliculitis is a superficial infection of the hair follicle. Folliculitis typically starts when hair follicles are damaged by trauma from scratching or shaving, from friction due to tight fitting clothing, or due to blockage. As a result, damaged follicles become infected with bacteria that cause red bumps or pimples centered on hair follicles. Buttocks, thighs, back and upper arms are commonly affected sites. The lesions of folliculitis are often clustered in groups and itch is the most common symptom. Folliculitis does not cause systemic symptoms such as fever or chills. About 3-25% of cases of folliculitis are due to CA-MRSA[9] other cases of folliculitis may be caused by non-MRSA strains of S. aureus, Pseudomonas aeruginosa, or fungi such as Candida or Pityrosporum
Figure 2: Folliculitis
Boils (Furuncle/Carbuncle):
Boils are caused by an infection, usually by Staph aureus that occurs deep within the hair follicle. These infections start as red, tender areas of skin that form large circular tender bumps filled with pus. A soft, white/yellow area will often form at the center of the boil where the pus may drain. Boils are typically larger than five millimeters. A single boil is called a furuncle; a network of interconnected boils is called a carbuncle. Boils can frequently be confused with spider or insect bites because they occur abruptly on skin without previous trauma. Symptoms like fevers and chills rarely occur and if present may be suggestive of a more serious infection. A 2004 study found that approximately 76% of purulent (pus containing) skin and soft tissue infection in adults seen in emergency rooms were caused by Staph aureus. Of these infections, 78% were cause by MRSA[10].
Figure 3: Boil
Cellulitis:
Cellulitis is a rapidly spreading infection of the deep fat and connective tissue under the skin. Bacteria usually enter through breaks in the skin caused by trauma (cuts, scrapes, blisters, burns, surgery or insect/animal bites), infection (athlete’s foot, boils) or external medical devices (catheter). Characteristic findings associated with cellulitis include:
1. Swelling
2. Bright red skin, pain (erythyma)
3. Local warmth of the infected skin.
4. Pain
Cellulitis can also cause fever, chills, red streaks along draining lymph vessels (lymphangitis), and enlarged lymph nodes. Skin on the lower legs is most commonly affected by this infection, though cellulitis can occur on any part of the body. Alcoholism, immunosuppression, diabetes mellitus, malignancy, intravenous drug abuse, and peripheral vascular disease are all risk factors for cellulitis. Cellulitis is rarely due to bacteria arriving from a distant source via the bloodstream (bacteremia).
Figure 4a: Cellulitis
Figure 4b: Lymphangitis
SERIOUS COMPLICATIONS
When MRSA infections are neglected or insufficiently treated, they may develop into serious infections that affect deeper underlying tissue (myositis, osteomyelitis), spread to the bloodstream (bacteremia, sepsis), or involve internal organs (pneumonia, endocarditis). Clinical presentations associated with invasive CA-MRSA include bacteremia (65.1%), pneumonia (14.0%), cellulitis (22.7%), osteomyelitis (8.1%), endocarditis (12.6%) and septic shock (3.8%).[11]
Patients with severe CA-MRSA infections requiring hospitalization and treatment include those who have fever, large abscesses, low blood pressure, blackened tissue (necrosis), severe bleeding and gas within infected tissue. In addition, other certain patient populations such as the immunocompromised, diabetic and infants younger than 6 months may require hospitalization. When serious systemic symptoms like fevers, chills or low blood pressure develop, you should be evaluated immediately by your physician.
TREATMENT
The treatment for MRSA skin infection depends on severity of the infection, the type of skin infection, and the patient’s risk factors for MRSA.
Impetigo:
For patients with a limited numbers of skin lesions, impetigo can be treated with the topical antibiotic mupirocin. When the disease is more severe, oral antibiotics should be used. The choice of antibiotic will depend on the resistance pattern of the infecting bacterium. For those cases of impetigo caused by CA-MRSA, sulfa drugs, tetracyclines, and clindamycin are usually effective. Once treatment is initiated, most cases of impetigo will resolve in 10-14days. Gentle washing of the affected skin to remove debris and crust is generally recommended. The American Academy of Pediatrics recommends that children with impetigo be with withheld from child care settings for the first 24-hours of antibiotic treatment. Precautionary measures that limit the spread of impetigo include hand washing, keeping the infected skin covered, and avoiding sharing common items (towels, clothing).
Folliculitis:
Treatment of CA-MRSA folliculitis varies but includes topical antibiotics, oral antibiotics and prophylactic use of antibacterial detergents. Many physicians start with topical antibiotics but may use oral antibiotics if topical antibiotics are ineffective, or the folliculitis is widespread. Most cases of folliculitis will respond to treatment and resolve in 10-14 days, however, a portion of patients may develop recurrent episodes. Recurrent folliculitis may suggest possible bacterial colonization (see below) and require decolonization treatment. Folliculitis can also evolve into deeper, larger lesions called furuncles (see below).
Boils (Furuncle/Carbuncle):
The most common presentation of CA-MRSA is as a boil, which is typically treated with incision and drainage. This treatment removes the source of infection and will cure most healthy people with no systemic signs of infection (e.g., fever, chills, elevated white blood cell count) when boils are less than five centimeters in diameter. In a recent randomized, placebo controlled trial in adult patients with deep skin abscesses, the majority of which were caused by MRSA, treatment success rates were over 90% for patients treated with incision and drainage alone.[12] Most recent Centers for Disease Control and Prevention (CDC) guidelines suggest that physicians should collect specimens for culture and antimicrobial susceptibility testing from all patients with abscesses or pus-containing skin lesions, particularly those with severe local infections, systemic signs of infection, or history suggesting connection to a cluster or outbreak of infections among epidemiologically linked individuals.
To perform an I&D, the skin is numbed with local anesthetic. A small incision is made on the skin overlying the boil and the pus is drained. Some abscesses have pockets of pus that must be broken up to release all of the pus. Packing material, such as gauze or gauze tape, may be placed in the drained abscess to keep the skin from closing and allow the wound to drain as it heals from the inside out. For patients with suspected MRSA, a sample of drained pus or of infected tissue will be sent for culture and susceptibility testing. If an I&D is not performed, your physician may remove fluid within a boil using a needle (aspiration) and send the fluid for culture. A culture can help confirm a case of suspected MRSA and guide the selection of an antibiotic when appropriate. In cases where a course of antibiotics was prescribed before culture results are available, the culture and sensitivity results help confirm or guide selection of the correct antibiotic.
Figure 5: Incision and Drainage
Patients with treated with I&D on an outpatient basis should contact their physician if they develop fevers/chills, worsening local symptoms or if their symptoms do not improve within 48 hours.
For some patients, an I&D may be the primary mode of therapy however, other patients may be treated with both an I&D and oral antibiotics. Factors which may influence a clinician to supplement I&D with antibiotics include:
* Severity and rapidity of progression of the skin infection or the presence of associated cellulitis
* An infected site more than five centimeters in diameter associated with failure of incision and drainage without effective antimicrobial therapy
* Signs and symptoms of systemic illness (fever, chills, elevated white blood cell count)
* Associated co-morbidities or immunosuppression (diabetes mellitus, neoplastic disease, HIV infection, transplantation, obesity, poor tissue oxygenation, nicotine use, poor nutritional status)
* Extremes of patient ages (very young or elderly)
* Location of abscess in area that may be difficult to drain completely
* Association with septic phlebitis or major vessels (central face)
* Lack of response to initial treatment with I&D alone
The choice of antibiotic therapy in treatment of CA-MRSA infections depends on the severity of the infection and the frequency of MRSA infections in the community. Local susceptibility data is often used to guide treatment.
Cellulitis:
Treatment of cellulitis consists of oral antibiotics and resting the affected limb or area. In severe cases, patients may require admission to a hospital for intravenous antibiotics and debridement of dead or infected tissue. Wounds or broken skin should be cleansed and bandaged. Wound dressings should be changed daily or when they become saturated or dirty.
With proper treatment most cases of cellulitis resolve in one to two weeks although more severe cases may take months to resolve. If untreated, cellulitis can result in severe debilitation or even death.
ANTIBIOTICS:
Both CA-MRSA and HA-MRSA are resistant to traditional anti-staphylococcal beta-lactam antibiotics, such as cephalexin. Sulfa drugs, tetracyclines, and clindamycin are usually effective at treating CA-MRSA; HA-MRSA is resistant even to these antibiotics. To treat HA-MRSA an intravenous administered antibiotic such as vancomycin or other newer oral medication such as linezolid are often required. A brief description of antibiotics that may be used to treat CA-MRSA or HA-MRSA is provided below.
Cephalosporins
Initial empiric antibiotic of choice in an uncomplicated skin infection in a community with higher rates of Methicillin sensitive Staph aureus than MRSA
Sulfa
Trimethoprim-sulfamethoxazole (Septra) remains the drug of choice for confirmed uncomplicated CA-MRSA especially when the rate of inducible clindamycin resistance is high. However, this class of medications does not provide coverage for beta-hemolytic streptococci which may also be the cause for erysipelas or cellulitis-like infections
These antibiotics are not recommended for women in third trimester of pregnancy or in infants less than two months of age.
Tetracyclines
Tetracyclines are effective on many strains of CA-MRSA. A small case series has demonstrated that doxycycline and minocycline were adequate for the treatment of MRSA soft tissue skin infections. This class of antibiotics is a good alternative treatment for confirmed CA-MRSA in cases where sulfa drugs are not tolerated or contraindicated.
However, they do not have activity against beta-hemolytic streptococcus and are contraindicated in children younger than age eight and during pregnancy
Clindamycin
Traditionally used for empiric therapy for uncomplicated skin infection alone or in combination with rifampin. A major advantage over trimethoprim-sulfamethoxazole (sulfa) is that when used empirically, clindamycin has better coverage for beta-hemolytic streptococci, another common cause of skin infections. Some strains of MRSA have developed inducible resistance to this class of antibiotics, therefore clindamycin not recommended in areas where inducible clindamycin resistant MRSA is present in greater than 10-15% of the local isolates. If clindamycin therapy is being considered, sensitivity testing for inducible clindamycin resistance should be performed using the D-zone disk-diffusion testing.
Rifampin
Because rifampin achieves high concentrations in mucosal surfaces, this antibiotic may promote eradication of MRSA colonization. However, because resistant strains of S. aureus develop rapidly when used as a single agent, rifampin should be used simultaneously with other antibiotics that target MRSA. Drug-drug interactions are common with rifampin and should be minimized prior to use. Women on contraception are recommended to use a second form of contraception as rifampin can decrease the effectiveness of oral contraceptives
Fluoroquinolones
Fluoroquinolones such as ciprofloxacin or levofloxacin are common first-line treatments for hospitalized patients with severe invasive S. aureus infection. Because of relatively high prevalence of resistance in the community and potential for rapid development of resistance, these antibiotics are not the optimal choice for the empiric treatment of CA-MRSA[13] Use of fluoroquinolones should be reserved for confirmed susceptible CA-MRSA infections when the use of other antibiotics is contraindicated. A major limitation of fluroquinolones for treatment of MRSA infections is that resistance can develop relatively quickly. Although many CA-MRSA strains remain sensitive to fluoroquinolones, resistance is emerging and overuse of these antibiotics favors the emergence of new CA-MRSA resistant strains
Macrolides/Azalides:
Erythromycin, clarithromycin and azithromycin are all FDA approved for the treatment o uncomplicated skin infections caused by S. aureus. Resistance to macrolides is common among CA-MRSA isolates which limits their usefulness as alternative agents for empiric treatment in areas with MRSA is high.
Vancomycin
Considered first line treatment for hospitalized patients with severe staphylococcal infections.
Linezolid
FDA approved for the treatment of complicated skin infections and hospital acquired pneumonia due to MRSA in adults. Has demonstrated superior tissue penetration in bone and muscle compared to vancomycin and has excellent penetration into skin and soft tissue. Available in a 100% bioavailable oral formulation, that can reduce hospital stays and duration of intravenous treatment. Due to the high bioavailability in oral form, linezolid can be used as an alternative treatment in patient with impaired renal function or poor venous access. This medication is expensive and has serious side effects that may include myelosuppression, peripheral and optic neuropathy and thrombocytopenia.
COLONIZATION
Rates of MRSA infection or recurrence are higher in people who are colonized with MRSA.
* Colonization means that the organism is present in or on the body but does not cause disease or symptoms.
* Infection means the organism is both present and causes disease.
The nostril and nasal passages (anterior nares) are the most common site of colonization by MRSA. Elimination of the bacteria at this site may prevent MRSA infections from recurring. However, MRSA colonization can also occur at sites other than the nose such as the throat, armpit, anus, and perineum. These sites may be important in development and transmission of the infection as well as in persistence or reappearance of colonization after use of nasal decolonization agents. Although having a MRSA infection raises the likelihood of having MRSA colonization, not all MRSA patients are colonized.[14] In a 2001-2002 US survey of non-institutionalized individuals, 0.8% of the U.S. population is colonized with MRSA.[15] Household or close contacts of MRSA colonized or infected patients are 7.5 times more likely to be colonized.[16]
Testing for Colonization
Testing for nasal colonization involves bacterial cultures of nasal swabs. Recent CDC guidelines suggest it is not necessary to routinely collect nasal cultures in all patients presenting with possible MRSA infection.
Decolonization Therapy
Decolonization is generally not recommended unless the patient has had recurrent infection; multiple infections recur within the same family or group of individuals; or if an individual is at higher risk for serious infection (e.g. diabetes, immunosuppressed). A number of different methods have been suggested with varying success. Most use a combination of oral antibiotics or an oral and topical antibiotic simultaneously. However, even the most intensive decolonization protocol results in eradication only about 66% of time. When attempting to eliminate MRSA colonization in a group, all members should receive the decolonization regimen simultaneously to decrease the risk of recolonization and to decrease the potential for emergence of resistance. Patients with indwelling lines, catheters, tracheostomies, G tubes, and other invasive devices are not good candidates for decolonization because such therapy is not likely to eradicate organisms from these surfaces.
Topical + Oral antibiotic
Mupirocin is the most effective among topical antibiotics for decolonization of the intranasal CA-MRSA. The antibiotic should be applied twice per day to both nostrils/nasal passages for five to10 days while on an appropriate oral antibiotic. For long term prevention, one study showed monthly use of mupirocin ointment applied intranasally twice per day for five days each month reduced nasal colonization and led to fewer cases of folliculitis or boils in 8/17 treated patients compared to 2/17 who received placebo.[17]
Rifampin + Other Oral Antibiotics
Rifampin is an oral antibiotic that achieves high concentrations in mucosal surfaces and is effective at reducing colonization by MRSA. However rifampin-resistant strains of MRSA develop rapidly when used as a single agent. Therefore, rifampin must be used in combination with another appropriate oral antibiotic that is active against MRSA for proper MRSA decolonization. Most courses of rifampin range from seven to 10 days with a daily dose of 600mg.
Rifampin should be used with caution because drug-drug interactions are common with rifampin. Women on oral contraception are recommended to use a second form of birth control because rifampin may decrease the effectiveness of oral contraceptives.
PREVENTION
The main mode of MRSA transmission is through direct physical contact, not through the air. Good hand cleansing is the single most important preventative measure to avoid for transmission of MRSA. Spread may also occur through contact with objects contaminated with MRSA infected skin or body fluids. Always clean hands immediately after touching infected skin or with any item that has come in direct contact with a draining wound. When washing hands, use an alcohol based hand gel or wash with an antibacterial soap for at least 15 seconds before rinsing with warm water. MRSA may survive on inanimate objects for up to 3 days. Clean equipment and other environmental surfaces than contact bare skin contact with an over the counter detergent/disinfectant that specifies Staphylococcus aureus on the product label and is suitable for the type of surface being cleaned
For caregivers of MRSA infected people, general recommendations are that caregivers should wash their hands with soap and water after physical contact with the infected or colonized person and before leaving the home.
· Towels used for drying hands after contact should be used once
· Disposable gloves should be worn if contact with body fluids is expected and hands should be washed after removing gloves
· Linens should be changed and washed routinely if they are soiled
· The infected person’s environment should be cleaned routinely
Controlling transmission
Infected or colonized patients should be able to participate in school/work or other social activities if draining wounds are covered, bodily fluids are contained, and the patients observe good hygienic practices.
Other MRSA prevention tips:[18]
§ Keep draining wounds covered with clean, dry, bandages.
§ Wash hands regularly with soap and water or alcohol-based hand gel (if hands are not visibly soiled). Always clean hands immediately after touching infected skin or any item that has come in direct contact with a draining wound.
§ Maintain good general hygiene with regular bathing.
§ Do not share items that may become contaminated with wound drainage, such as towels, clothing, bedding, bar soap, razors, and athletic equipment that touches the skin.
§ Launder clothing that has come in contact with wound drainage after each use and dry thoroughly.
§ If you are not able to keep your wound covered with a clean, dry bandage at all times, do not participate in activities where you have skin to skin contact with other persons (such as athletic activities) until your wound is healed.
§ Clean equipment and other environmental surfaces with which multiple individuals have bare skin contact. Use an over the counter detergent/disinfectant that specifies Staphylococcus aureus on the product label and is suitable for the type of surface being cleaned.
[1] Klevens RM, Edwards JR, Tenover FC, McDonald LC, Horan T, Gaynes R; National Nosocomial Infections Surveillance System. Changes in the epidemiology of methicillin-resistant Staphylococcus aureus inintensive care units in US hospitals, 1992-2003. Clin Infect Dis. 2006 Feb 1;42(3):389-91.
[2] Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, Harrison LH,Lynfield R, Dumyati G, Townes JM, Craig AS, Zell ER, Fosheim GE, McDougal LK,Carey RB, Fridkin SK; Active Bacterial Core surveillance (ABCs) MRSA Investigators.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
[3] Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, Harrison LH,Lynfield R, Dumyati G, Townes JM, Craig AS, Zell ER, Fosheim GE, McDougal LK,Carey RB, Fridkin SK; Active Bacterial Core surveillance (ABCs) MRSA Investigators.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
[4] Naimi TS, LeDell KH, Como-Sabetti K, Borchardt SM, Boxrud DJ, Etienne J,Johnson SK, Vandenesch F, Fridkin S, O'Boyle C, Danila RN, Lynfield R. Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection.JAMA. 2003 Dec 10;290(22):2976-84.
[5] Naimi TS, LeDell KH, Como-Sabetti K, Borchardt SM, Boxrud DJ, Etienne J,Johnson SK, Vandenesch F, Fridkin S, O'Boyle C, Danila RN, Lynfield R. Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection.JAMA. 2003 Dec 10;290(22):2976-84.
[6] McCaig LF, McDonald LC, Mandal S, Jernigan DB. Staphylococcus aureus-associated skin and soft tissue infections in ambulatory care. Emerg Infect Dis. 2006 Nov;12(11):1715-23.
[7] Abrahamian FM, Moran GJ. Methicillin-resistant Staphylococcus aureus infections.N Engl J Med. 2007 Nov 15;357(20):2090;
[8] Cohen PR . Community-acquired methicillin resistant Staphylococcus aureus skin infections: a review of epidemiology, clinical fetures, management and prevention. Int. J. Dermatol. 2007 Jan;46(1):1-11
[9] Cohen PR . Community-acquired methicillin resistant Staphylococcus aureus skin infections: a review of epidemiology, clinical fetures, management and prevention. Int. J. Dermatol. 2007 Jan;46(1):1-11
[10] Abrahamian FM, Moran GJ. Methicillin-resistant Staphylococcus aureus infections.N Engl J Med. 2007 Nov 15;3(20):2090;
[11] Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, Harrison LH,Lynfield R, Dumyati G, Townes JM, Craig AS, Zell ER, Fosheim GE, McDougal LK,Carey RB, Fridkin SK; Active Bacterial Core surveillance (ABCs) MRSA Investigators.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
[12] Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P, Harris H. randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection. Antimicrob Agents Chemother. 2007 Nov;51(11):4044-8
[13] Gorwitz RJ, Jernigan, DB, Powers JH, Jernigan JA and Parcipants of the Centers for Disease Control and Prevention-Convened Experts Meeting on Management of MRSA in the Community. Strategies for Clinical Management of MRSA in the Community: Summary of Experts’ Meeting Convened by the Centers of Disease Control and Prevention, March 2006
[14] Frazee BW, Lynn J, Charlebois ED, Lambert L, Lowery D, Perdreau-Remington F. High prevalence of methicillin-resistant Staphylococcus aureus in emergency department skin and soft tissue infections.Ann Emerg Med. 2005 Mar;45(3):311-20.
[15] Kuehnert MJ, Kruszon-Moran D, Hill HA, McQuillan G, McAllister SK, Fosheim G, McDougal LK, Chaitram J, Jensen B, Fridkin SK, Killgore G, Tenover FC. Prevalence of Staphylococcus aureus nasal colonization in the United States, 2001-2002. J Infect Dis. 2006 Jan 15;193(2):172-9.
[16] Calfee DP, Durbin LJ, Germanson TP, Toney DM, Smith EB, Farr BM. Spread of methicillin-resistant Staphylococcus aureus (MRSA) among household contacts of individuals with nosocomially acquired MRSA.Infect Control Hosp Epidemiol. 2003 Jun;24(6):422-6.
[17] Raz R, Miron D, Colodner R, Staler Z, Samara Z, Keness Y. A 1-year trial of nasal mupirocin in the prevention of recurrent staphylococcal nasal colonization and skin infection.Arch Intern Med. 1996 May 27;156(10):1109-12.
[18] Gorwitz RJ, Jernigan, DB, Powers JH, Jernigan JA and Parcipants of the Centers for Disease Control and Prevention-Convened Experts Meeting on Management of MRSA in the Community. Strategies for Clinical Management of MRSA in the Community: Summary of Experts’ Meeting Convened by the Centers of Disease Control and Prevention, March 2006
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Source Knol: MRSA Methicillin Resistant Staphylococcus Aureus (MRSA) Infections of the Skin
Source Knol: MRSA Methicillin Resistant Staphylococcus Aureus (MRSA) Infections of the Skin
by Bryan Cho MD, PhD, Board Certified Dermatologist
INTRODUCTION
Bacteria are microorganisms that are found almost everywhere. Most bacteria are harmless but some can cause infection. Methicillin-resistant Staphylococcus aureus (MRSA) is a bacterium that has emerged as a major cause of skin infections among otherwise healthy adults and children in the community. This bacterium is dangerous because it causes infections that cannot be treated with commonly used antibiotics that in the past would destroy the bacteria and cure the infection. Moreover, left untreated these infections can have serious complications. This knol will discuss the risk factors for MRSA infections, what MRSA skin infections look like, and how they can be treated and avoided.
HEALTHCARE ASSOCIATED-MRSA
MRSA was first diagnosed in 1961 as bacteria associated with serious infections that occurred in hospitalized patients or patients in healthcare facilities such as nursing homes or dialysis centers. MRSA infections that occurred in healthcare facilities were termed healthcare associated-MRSA (HA-MRSA). These infections were often serious and potentially life-threatening and included bloodstream infections, surgical site infections or pneumonia. Since being discovered, the number of MRSA infections has increased dramatically. In 1974, MRSA infections accounted for 2% of the total number of Staphylococcus infections; in 1995 it was 22%; in 2004 it was 63%[1]
HA-MRSA risk factors include:[2],[3]
1. Weakened immune system and severe illness
2. Previous exposure to antimicrobial agents
3. Surgery or open wounds
4. Residence in a long term healthcare facility (nursing home, skilled nursing facility)
5. Underlying disease or conditions, particularly:
1. Chronic renal disease
2. Insulin-dependent diabetes mellitus
3. Peripheral vascular disease
4. Dermatitis or skin lesions
6. Invasive devices (Urinary catheterization, intravenous lines (IV), Dialysis, tracheotomies, G tubes)
7. Patients in the intensive care unit (ICU)
8. Male, age older than 65
9. Repeated contact with the healthcare system
10. Previous colonization by a multidrug-resistant organism
COMMUNITY ACQUIRED-MRSA
In the past few years, a separate strain of MRSA bacteria has developed that affects healthy members of the community. This community acquired MRSA (CA-MRSA) has caused outbreaks of disease among professional athletes, high school athletic teams, and in day care settings. Developing a CA-MRSA infection does not imply any impairment in immune system function. The average age of patients with CA-MRSA infections is age 23 compared to age 68 for HA-MRSA.[4] Unlike HA-MRSA, CA-MRSA rarely causes life threatening infections. CA-MRSA most commonly causes skin infections such as boils or pimples. Because these infections can occur abruptly on otherwise normal skin, CA-MRSA infections are frequently mistaken for spider bites.
CA-MRSA may occur in the following populations:
1. The young and healthy, especially those who live in crowded conditions or have close physical contacts with others, including:
1. Athletes
2. Prisoners
3. Soldiers
2. Selected ethnic populations
3. IV drug users
Table 1. CA-MRSA versus HA-MRSA. (not shown in this post. Visit source knol)
SKIN INFECTIONS CAUSED BY MRSA:
Roughly 85% of CA-MRSA infections develop in the skin.[5] Each year there are an estimated 12 million outpatient (e.g., physician offices, emergency and outpatient departments) healthcare visits for skin and soft tissue infections in the United States[6]. In one study, three out of four patients seen in the emergency room for skin infections had Staphylococcal aureus infections and over 50% had MRSA infections.[7]
Most MRSA skin infections look like (Described below.):
o Impetigo
o Many small pimple-like bumps (folliculitis)
o Large painful boils (furuncle or carbuncle)
o Spider or insect bites
Less common and more serious skin and soft tissue infection caused by MRSA include:
o Cellulitis
o Infected wounds
Impetigo is a superficial skin infection that occurs on open, exposed areas of skin. This infection occurs most commonly in children but usually does not cause serious illness. The infection starts at sites of minor skin trauma such as insect bites or abrasions. The affected skin may develop small (less than 5mm) fluid filled bumps that develop golden honey-crusting when bumps burst. Usually, multiple skin lesions are present. Impetigo is easily spread within families and close contacts. Other risk factors for infection include warm, humid conditions and poor hygiene. Impetigo is most commonly caused by a bacterium called Streptococcus, but more and more frequently, impetigo is caused by MRSA; CA-MRSA now accounts for 7-20% of impetigo infections.[8] Impetigo caused by Streptococcus and CA-MRSA look identical.
Figure 1: Impetigo
Folliculitis is a superficial infection of the hair follicle. Folliculitis typically starts when hair follicles are damaged by trauma from scratching or shaving, from friction due to tight fitting clothing, or due to blockage. As a result, damaged follicles become infected with bacteria that cause red bumps or pimples centered on hair follicles. Buttocks, thighs, back and upper arms are commonly affected sites. The lesions of folliculitis are often clustered in groups and itch is the most common symptom. Folliculitis does not cause systemic symptoms such as fever or chills. About 3-25% of cases of folliculitis are due to CA-MRSA[9] other cases of folliculitis may be caused by non-MRSA strains of S. aureus, Pseudomonas aeruginosa, or fungi such as Candida or Pityrosporum
Figure 2: Folliculitis
Boils (Furuncle/Carbuncle):
Boils are caused by an infection, usually by Staph aureus that occurs deep within the hair follicle. These infections start as red, tender areas of skin that form large circular tender bumps filled with pus. A soft, white/yellow area will often form at the center of the boil where the pus may drain. Boils are typically larger than five millimeters. A single boil is called a furuncle; a network of interconnected boils is called a carbuncle. Boils can frequently be confused with spider or insect bites because they occur abruptly on skin without previous trauma. Symptoms like fevers and chills rarely occur and if present may be suggestive of a more serious infection. A 2004 study found that approximately 76% of purulent (pus containing) skin and soft tissue infection in adults seen in emergency rooms were caused by Staph aureus. Of these infections, 78% were cause by MRSA[10].
Figure 3: Boil
Cellulitis:
Cellulitis is a rapidly spreading infection of the deep fat and connective tissue under the skin. Bacteria usually enter through breaks in the skin caused by trauma (cuts, scrapes, blisters, burns, surgery or insect/animal bites), infection (athlete’s foot, boils) or external medical devices (catheter). Characteristic findings associated with cellulitis include:
1. Swelling
2. Bright red skin, pain (erythyma)
3. Local warmth of the infected skin.
4. Pain
Cellulitis can also cause fever, chills, red streaks along draining lymph vessels (lymphangitis), and enlarged lymph nodes. Skin on the lower legs is most commonly affected by this infection, though cellulitis can occur on any part of the body. Alcoholism, immunosuppression, diabetes mellitus, malignancy, intravenous drug abuse, and peripheral vascular disease are all risk factors for cellulitis. Cellulitis is rarely due to bacteria arriving from a distant source via the bloodstream (bacteremia).
Figure 4a: Cellulitis
Figure 4b: Lymphangitis
SERIOUS COMPLICATIONS
When MRSA infections are neglected or insufficiently treated, they may develop into serious infections that affect deeper underlying tissue (myositis, osteomyelitis), spread to the bloodstream (bacteremia, sepsis), or involve internal organs (pneumonia, endocarditis). Clinical presentations associated with invasive CA-MRSA include bacteremia (65.1%), pneumonia (14.0%), cellulitis (22.7%), osteomyelitis (8.1%), endocarditis (12.6%) and septic shock (3.8%).[11]
Patients with severe CA-MRSA infections requiring hospitalization and treatment include those who have fever, large abscesses, low blood pressure, blackened tissue (necrosis), severe bleeding and gas within infected tissue. In addition, other certain patient populations such as the immunocompromised, diabetic and infants younger than 6 months may require hospitalization. When serious systemic symptoms like fevers, chills or low blood pressure develop, you should be evaluated immediately by your physician.
TREATMENT
The treatment for MRSA skin infection depends on severity of the infection, the type of skin infection, and the patient’s risk factors for MRSA.
Impetigo:
For patients with a limited numbers of skin lesions, impetigo can be treated with the topical antibiotic mupirocin. When the disease is more severe, oral antibiotics should be used. The choice of antibiotic will depend on the resistance pattern of the infecting bacterium. For those cases of impetigo caused by CA-MRSA, sulfa drugs, tetracyclines, and clindamycin are usually effective. Once treatment is initiated, most cases of impetigo will resolve in 10-14days. Gentle washing of the affected skin to remove debris and crust is generally recommended. The American Academy of Pediatrics recommends that children with impetigo be with withheld from child care settings for the first 24-hours of antibiotic treatment. Precautionary measures that limit the spread of impetigo include hand washing, keeping the infected skin covered, and avoiding sharing common items (towels, clothing).
Folliculitis:
Treatment of CA-MRSA folliculitis varies but includes topical antibiotics, oral antibiotics and prophylactic use of antibacterial detergents. Many physicians start with topical antibiotics but may use oral antibiotics if topical antibiotics are ineffective, or the folliculitis is widespread. Most cases of folliculitis will respond to treatment and resolve in 10-14 days, however, a portion of patients may develop recurrent episodes. Recurrent folliculitis may suggest possible bacterial colonization (see below) and require decolonization treatment. Folliculitis can also evolve into deeper, larger lesions called furuncles (see below).
Boils (Furuncle/Carbuncle):
The most common presentation of CA-MRSA is as a boil, which is typically treated with incision and drainage. This treatment removes the source of infection and will cure most healthy people with no systemic signs of infection (e.g., fever, chills, elevated white blood cell count) when boils are less than five centimeters in diameter. In a recent randomized, placebo controlled trial in adult patients with deep skin abscesses, the majority of which were caused by MRSA, treatment success rates were over 90% for patients treated with incision and drainage alone.[12] Most recent Centers for Disease Control and Prevention (CDC) guidelines suggest that physicians should collect specimens for culture and antimicrobial susceptibility testing from all patients with abscesses or pus-containing skin lesions, particularly those with severe local infections, systemic signs of infection, or history suggesting connection to a cluster or outbreak of infections among epidemiologically linked individuals.
To perform an I&D, the skin is numbed with local anesthetic. A small incision is made on the skin overlying the boil and the pus is drained. Some abscesses have pockets of pus that must be broken up to release all of the pus. Packing material, such as gauze or gauze tape, may be placed in the drained abscess to keep the skin from closing and allow the wound to drain as it heals from the inside out. For patients with suspected MRSA, a sample of drained pus or of infected tissue will be sent for culture and susceptibility testing. If an I&D is not performed, your physician may remove fluid within a boil using a needle (aspiration) and send the fluid for culture. A culture can help confirm a case of suspected MRSA and guide the selection of an antibiotic when appropriate. In cases where a course of antibiotics was prescribed before culture results are available, the culture and sensitivity results help confirm or guide selection of the correct antibiotic.
Figure 5: Incision and Drainage
Patients with treated with I&D on an outpatient basis should contact their physician if they develop fevers/chills, worsening local symptoms or if their symptoms do not improve within 48 hours.
For some patients, an I&D may be the primary mode of therapy however, other patients may be treated with both an I&D and oral antibiotics. Factors which may influence a clinician to supplement I&D with antibiotics include:
* Severity and rapidity of progression of the skin infection or the presence of associated cellulitis
* An infected site more than five centimeters in diameter associated with failure of incision and drainage without effective antimicrobial therapy
* Signs and symptoms of systemic illness (fever, chills, elevated white blood cell count)
* Associated co-morbidities or immunosuppression (diabetes mellitus, neoplastic disease, HIV infection, transplantation, obesity, poor tissue oxygenation, nicotine use, poor nutritional status)
* Extremes of patient ages (very young or elderly)
* Location of abscess in area that may be difficult to drain completely
* Association with septic phlebitis or major vessels (central face)
* Lack of response to initial treatment with I&D alone
The choice of antibiotic therapy in treatment of CA-MRSA infections depends on the severity of the infection and the frequency of MRSA infections in the community. Local susceptibility data is often used to guide treatment.
Cellulitis:
Treatment of cellulitis consists of oral antibiotics and resting the affected limb or area. In severe cases, patients may require admission to a hospital for intravenous antibiotics and debridement of dead or infected tissue. Wounds or broken skin should be cleansed and bandaged. Wound dressings should be changed daily or when they become saturated or dirty.
With proper treatment most cases of cellulitis resolve in one to two weeks although more severe cases may take months to resolve. If untreated, cellulitis can result in severe debilitation or even death.
ANTIBIOTICS:
Both CA-MRSA and HA-MRSA are resistant to traditional anti-staphylococcal beta-lactam antibiotics, such as cephalexin. Sulfa drugs, tetracyclines, and clindamycin are usually effective at treating CA-MRSA; HA-MRSA is resistant even to these antibiotics. To treat HA-MRSA an intravenous administered antibiotic such as vancomycin or other newer oral medication such as linezolid are often required. A brief description of antibiotics that may be used to treat CA-MRSA or HA-MRSA is provided below.
Cephalosporins
Initial empiric antibiotic of choice in an uncomplicated skin infection in a community with higher rates of Methicillin sensitive Staph aureus than MRSA
Sulfa
Trimethoprim-sulfamethoxazole (Septra) remains the drug of choice for confirmed uncomplicated CA-MRSA especially when the rate of inducible clindamycin resistance is high. However, this class of medications does not provide coverage for beta-hemolytic streptococci which may also be the cause for erysipelas or cellulitis-like infections
These antibiotics are not recommended for women in third trimester of pregnancy or in infants less than two months of age.
Tetracyclines
Tetracyclines are effective on many strains of CA-MRSA. A small case series has demonstrated that doxycycline and minocycline were adequate for the treatment of MRSA soft tissue skin infections. This class of antibiotics is a good alternative treatment for confirmed CA-MRSA in cases where sulfa drugs are not tolerated or contraindicated.
However, they do not have activity against beta-hemolytic streptococcus and are contraindicated in children younger than age eight and during pregnancy
Clindamycin
Traditionally used for empiric therapy for uncomplicated skin infection alone or in combination with rifampin. A major advantage over trimethoprim-sulfamethoxazole (sulfa) is that when used empirically, clindamycin has better coverage for beta-hemolytic streptococci, another common cause of skin infections. Some strains of MRSA have developed inducible resistance to this class of antibiotics, therefore clindamycin not recommended in areas where inducible clindamycin resistant MRSA is present in greater than 10-15% of the local isolates. If clindamycin therapy is being considered, sensitivity testing for inducible clindamycin resistance should be performed using the D-zone disk-diffusion testing.
Rifampin
Because rifampin achieves high concentrations in mucosal surfaces, this antibiotic may promote eradication of MRSA colonization. However, because resistant strains of S. aureus develop rapidly when used as a single agent, rifampin should be used simultaneously with other antibiotics that target MRSA. Drug-drug interactions are common with rifampin and should be minimized prior to use. Women on contraception are recommended to use a second form of contraception as rifampin can decrease the effectiveness of oral contraceptives
Fluoroquinolones
Fluoroquinolones such as ciprofloxacin or levofloxacin are common first-line treatments for hospitalized patients with severe invasive S. aureus infection. Because of relatively high prevalence of resistance in the community and potential for rapid development of resistance, these antibiotics are not the optimal choice for the empiric treatment of CA-MRSA[13] Use of fluoroquinolones should be reserved for confirmed susceptible CA-MRSA infections when the use of other antibiotics is contraindicated. A major limitation of fluroquinolones for treatment of MRSA infections is that resistance can develop relatively quickly. Although many CA-MRSA strains remain sensitive to fluoroquinolones, resistance is emerging and overuse of these antibiotics favors the emergence of new CA-MRSA resistant strains
Macrolides/Azalides:
Erythromycin, clarithromycin and azithromycin are all FDA approved for the treatment o uncomplicated skin infections caused by S. aureus. Resistance to macrolides is common among CA-MRSA isolates which limits their usefulness as alternative agents for empiric treatment in areas with MRSA is high.
Vancomycin
Considered first line treatment for hospitalized patients with severe staphylococcal infections.
Linezolid
FDA approved for the treatment of complicated skin infections and hospital acquired pneumonia due to MRSA in adults. Has demonstrated superior tissue penetration in bone and muscle compared to vancomycin and has excellent penetration into skin and soft tissue. Available in a 100% bioavailable oral formulation, that can reduce hospital stays and duration of intravenous treatment. Due to the high bioavailability in oral form, linezolid can be used as an alternative treatment in patient with impaired renal function or poor venous access. This medication is expensive and has serious side effects that may include myelosuppression, peripheral and optic neuropathy and thrombocytopenia.
COLONIZATION
Rates of MRSA infection or recurrence are higher in people who are colonized with MRSA.
* Colonization means that the organism is present in or on the body but does not cause disease or symptoms.
* Infection means the organism is both present and causes disease.
The nostril and nasal passages (anterior nares) are the most common site of colonization by MRSA. Elimination of the bacteria at this site may prevent MRSA infections from recurring. However, MRSA colonization can also occur at sites other than the nose such as the throat, armpit, anus, and perineum. These sites may be important in development and transmission of the infection as well as in persistence or reappearance of colonization after use of nasal decolonization agents. Although having a MRSA infection raises the likelihood of having MRSA colonization, not all MRSA patients are colonized.[14] In a 2001-2002 US survey of non-institutionalized individuals, 0.8% of the U.S. population is colonized with MRSA.[15] Household or close contacts of MRSA colonized or infected patients are 7.5 times more likely to be colonized.[16]
Testing for Colonization
Testing for nasal colonization involves bacterial cultures of nasal swabs. Recent CDC guidelines suggest it is not necessary to routinely collect nasal cultures in all patients presenting with possible MRSA infection.
Decolonization Therapy
Decolonization is generally not recommended unless the patient has had recurrent infection; multiple infections recur within the same family or group of individuals; or if an individual is at higher risk for serious infection (e.g. diabetes, immunosuppressed). A number of different methods have been suggested with varying success. Most use a combination of oral antibiotics or an oral and topical antibiotic simultaneously. However, even the most intensive decolonization protocol results in eradication only about 66% of time. When attempting to eliminate MRSA colonization in a group, all members should receive the decolonization regimen simultaneously to decrease the risk of recolonization and to decrease the potential for emergence of resistance. Patients with indwelling lines, catheters, tracheostomies, G tubes, and other invasive devices are not good candidates for decolonization because such therapy is not likely to eradicate organisms from these surfaces.
Topical + Oral antibiotic
Mupirocin is the most effective among topical antibiotics for decolonization of the intranasal CA-MRSA. The antibiotic should be applied twice per day to both nostrils/nasal passages for five to10 days while on an appropriate oral antibiotic. For long term prevention, one study showed monthly use of mupirocin ointment applied intranasally twice per day for five days each month reduced nasal colonization and led to fewer cases of folliculitis or boils in 8/17 treated patients compared to 2/17 who received placebo.[17]
Rifampin + Other Oral Antibiotics
Rifampin is an oral antibiotic that achieves high concentrations in mucosal surfaces and is effective at reducing colonization by MRSA. However rifampin-resistant strains of MRSA develop rapidly when used as a single agent. Therefore, rifampin must be used in combination with another appropriate oral antibiotic that is active against MRSA for proper MRSA decolonization. Most courses of rifampin range from seven to 10 days with a daily dose of 600mg.
Rifampin should be used with caution because drug-drug interactions are common with rifampin. Women on oral contraception are recommended to use a second form of birth control because rifampin may decrease the effectiveness of oral contraceptives.
PREVENTION
The main mode of MRSA transmission is through direct physical contact, not through the air. Good hand cleansing is the single most important preventative measure to avoid for transmission of MRSA. Spread may also occur through contact with objects contaminated with MRSA infected skin or body fluids. Always clean hands immediately after touching infected skin or with any item that has come in direct contact with a draining wound. When washing hands, use an alcohol based hand gel or wash with an antibacterial soap for at least 15 seconds before rinsing with warm water. MRSA may survive on inanimate objects for up to 3 days. Clean equipment and other environmental surfaces than contact bare skin contact with an over the counter detergent/disinfectant that specifies Staphylococcus aureus on the product label and is suitable for the type of surface being cleaned
For caregivers of MRSA infected people, general recommendations are that caregivers should wash their hands with soap and water after physical contact with the infected or colonized person and before leaving the home.
· Towels used for drying hands after contact should be used once
· Disposable gloves should be worn if contact with body fluids is expected and hands should be washed after removing gloves
· Linens should be changed and washed routinely if they are soiled
· The infected person’s environment should be cleaned routinely
Controlling transmission
Infected or colonized patients should be able to participate in school/work or other social activities if draining wounds are covered, bodily fluids are contained, and the patients observe good hygienic practices.
Other MRSA prevention tips:[18]
§ Keep draining wounds covered with clean, dry, bandages.
§ Wash hands regularly with soap and water or alcohol-based hand gel (if hands are not visibly soiled). Always clean hands immediately after touching infected skin or any item that has come in direct contact with a draining wound.
§ Maintain good general hygiene with regular bathing.
§ Do not share items that may become contaminated with wound drainage, such as towels, clothing, bedding, bar soap, razors, and athletic equipment that touches the skin.
§ Launder clothing that has come in contact with wound drainage after each use and dry thoroughly.
§ If you are not able to keep your wound covered with a clean, dry bandage at all times, do not participate in activities where you have skin to skin contact with other persons (such as athletic activities) until your wound is healed.
§ Clean equipment and other environmental surfaces with which multiple individuals have bare skin contact. Use an over the counter detergent/disinfectant that specifies Staphylococcus aureus on the product label and is suitable for the type of surface being cleaned.
[1] Klevens RM, Edwards JR, Tenover FC, McDonald LC, Horan T, Gaynes R; National Nosocomial Infections Surveillance System. Changes in the epidemiology of methicillin-resistant Staphylococcus aureus inintensive care units in US hospitals, 1992-2003. Clin Infect Dis. 2006 Feb 1;42(3):389-91.
[2] Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, Harrison LH,Lynfield R, Dumyati G, Townes JM, Craig AS, Zell ER, Fosheim GE, McDougal LK,Carey RB, Fridkin SK; Active Bacterial Core surveillance (ABCs) MRSA Investigators.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
[3] Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, Harrison LH,Lynfield R, Dumyati G, Townes JM, Craig AS, Zell ER, Fosheim GE, McDougal LK,Carey RB, Fridkin SK; Active Bacterial Core surveillance (ABCs) MRSA Investigators.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
[4] Naimi TS, LeDell KH, Como-Sabetti K, Borchardt SM, Boxrud DJ, Etienne J,Johnson SK, Vandenesch F, Fridkin S, O'Boyle C, Danila RN, Lynfield R. Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection.JAMA. 2003 Dec 10;290(22):2976-84.
[5] Naimi TS, LeDell KH, Como-Sabetti K, Borchardt SM, Boxrud DJ, Etienne J,Johnson SK, Vandenesch F, Fridkin S, O'Boyle C, Danila RN, Lynfield R. Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection.JAMA. 2003 Dec 10;290(22):2976-84.
[6] McCaig LF, McDonald LC, Mandal S, Jernigan DB. Staphylococcus aureus-associated skin and soft tissue infections in ambulatory care. Emerg Infect Dis. 2006 Nov;12(11):1715-23.
[7] Abrahamian FM, Moran GJ. Methicillin-resistant Staphylococcus aureus infections.N Engl J Med. 2007 Nov 15;357(20):2090;
[8] Cohen PR . Community-acquired methicillin resistant Staphylococcus aureus skin infections: a review of epidemiology, clinical fetures, management and prevention. Int. J. Dermatol. 2007 Jan;46(1):1-11
[9] Cohen PR . Community-acquired methicillin resistant Staphylococcus aureus skin infections: a review of epidemiology, clinical fetures, management and prevention. Int. J. Dermatol. 2007 Jan;46(1):1-11
[10] Abrahamian FM, Moran GJ. Methicillin-resistant Staphylococcus aureus infections.N Engl J Med. 2007 Nov 15;3(20):2090;
[11] Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, Harrison LH,Lynfield R, Dumyati G, Townes JM, Craig AS, Zell ER, Fosheim GE, McDougal LK,Carey RB, Fridkin SK; Active Bacterial Core surveillance (ABCs) MRSA Investigators.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
[12] Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P, Harris H. randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection. Antimicrob Agents Chemother. 2007 Nov;51(11):4044-8
[13] Gorwitz RJ, Jernigan, DB, Powers JH, Jernigan JA and Parcipants of the Centers for Disease Control and Prevention-Convened Experts Meeting on Management of MRSA in the Community. Strategies for Clinical Management of MRSA in the Community: Summary of Experts’ Meeting Convened by the Centers of Disease Control and Prevention, March 2006
[14] Frazee BW, Lynn J, Charlebois ED, Lambert L, Lowery D, Perdreau-Remington F. High prevalence of methicillin-resistant Staphylococcus aureus in emergency department skin and soft tissue infections.Ann Emerg Med. 2005 Mar;45(3):311-20.
[15] Kuehnert MJ, Kruszon-Moran D, Hill HA, McQuillan G, McAllister SK, Fosheim G, McDougal LK, Chaitram J, Jensen B, Fridkin SK, Killgore G, Tenover FC. Prevalence of Staphylococcus aureus nasal colonization in the United States, 2001-2002. J Infect Dis. 2006 Jan 15;193(2):172-9.
[16] Calfee DP, Durbin LJ, Germanson TP, Toney DM, Smith EB, Farr BM. Spread of methicillin-resistant Staphylococcus aureus (MRSA) among household contacts of individuals with nosocomially acquired MRSA.Infect Control Hosp Epidemiol. 2003 Jun;24(6):422-6.
[17] Raz R, Miron D, Colodner R, Staler Z, Samara Z, Keness Y. A 1-year trial of nasal mupirocin in the prevention of recurrent staphylococcal nasal colonization and skin infection.Arch Intern Med. 1996 May 27;156(10):1109-12.
[18] Gorwitz RJ, Jernigan, DB, Powers JH, Jernigan JA and Parcipants of the Centers for Disease Control and Prevention-Convened Experts Meeting on Management of MRSA in the Community. Strategies for Clinical Management of MRSA in the Community: Summary of Experts’ Meeting Convened by the Centers of Disease Control and Prevention, March 2006
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Source Knol: MRSA Methicillin Resistant Staphylococcus Aureus (MRSA) Infections of the Skin
Monday, July 11, 2011
How to Identify Symptoms of a Stomach Virus - Knol Reblogged
Source Knol: How to Identify Symptoms of a Stomach Virus
by eHowKnol, The eHow database is the world's most popular place to find clear instructions on how to do just about everything. at Demand Media
A stomach virus is also known as the stomach flu (viral gastroenteritis) and can affect people of all ages. It is a temporary health condition caused by an infection; the virus typically causes severe cramping and pain, but is commonly mistaken for the regular flu (influenza). A stomach virus is commonly caused by parasites such as cryptosporidium and giardia, as well as bacteria such as E.coli, Shigella and Salmonella.
The most common symptoms of a stomach virus include:
* Watery diarrhea
* Extreme abdominal discomfort
* Vomiting
* Headache
* Ongoing fever
* Chills
* Excessive thirst
* Severe weakness
* Lethargy and fatigue
* Dizziness
The symptoms of a stomach flu typically occur within 4 to 48 hours of eating the contaminated food or being exposed to the bacteria. The symptoms can last for 2 – 4 days, but typically do not extend for longer than 10 days.
Any type of infection that enters the gastrointestinal tract can trigger the spread of a stomach virus, and cause irritation or inflammation in the stomach or intestines. The virus may be caused by:
* Eating spoiled food
* Drinking contaminated water
* Inhaling or ingesting bacteria
* Having an allergic reaction to certain types of food
* Lactose intolerance
* Gluten intolerance
The most common types of viruses that cause stomach flu include:
* Caliciviruses – a virus that typically occurs between October and April, and results in diarrhea, vomiting and fatigue. The symptoms typically appear within 1-3 days of exposure to the contaminated foods or fluids, but most people can recover within 7 days.
* Adenovirus – a common ‘infant’ stomach virus that causes vomiting and diarrhea. This type of virus can occur any time of year and can be especially dangerous for infants with weak immune systems.
* Rotavirus – a virus that typically occurs in children who are 3 – 15 months old; this virus causes fever, diarrhea and abdominal pain and typically occurs between November and April.
* Astrovirus – a common type of stomach virus that occurs during the winter months. This one typically triggers vomiting, diarrhea, fatigue and abdominal discomfort.
Is It a Stomach Virus or the Flu?
Since many of the symptoms of a stomach virus are similar to those of influenza, it can be difficult to diagnose the problem. The average flu is a viral infection that begins with a high fever and congestion, and is often accompanied by fatigue. However, the flu cannot be treated with an antibiotic that is necessary to treat the stomach virus because it is not a bacterial infection.
In most cases, people suffering from the stomach flu will experience extreme dehydration, headaches and diarrhea. Overall, they will experience many of the common symptoms of the flu but also a number of digestive problems and gastrointestinal pain.
There is no specific treatment for recovering from a stomach virus. Sufferers must eat bland food, drink plenty of water and get enough rest to allow the body to recover naturally. Antibiotics are not very effective in treating viruses, because once the bacteria has reached the intestinal tract, it can be difficult for the body to absorb any type of medication.
The best strategy for recovering from the virus involves drinking clear liquids and eating easily-digestible foods. Oral rehydration solutions that contain minerals and salts such as potassium may be especially beneficial for young children and the elderly.
Individuals who are taking prescription medications may need to stop taking certain types of drugs until the symptoms disappear. Frequent episodes of vomiting and diarrhea can lead to malabsorption, making most medications ineffective and increasing the chances of toxicity.
Making an appointment with the doctor is recommended at the onset of a stomach virus, or if the symptoms do not disappear within 7-10 days. Extreme cases can become difficult to manage without oral rehydration solutions and supplements, and a doctor may be able to recommend certain foods and supplements for those who are not recovering from the stomach virus in an appropriate period of time.
Since the stomach will become especially sensitive to certain types of food and fluids after the initial stages of symptoms have settled down, the sufferer will need to drink extra fluids and eat a simple, easily-digestible diet. A bland diet comprised of simple carbohydrates can help the person with the stomach flu get the energy they need to recover and restore their body to good health. Foods that will not irritate the stomach lining or trigger a gastrointestinal reaction include:
* Dry toast
* Bananas
* Applesauce
* Cooked rice
* Puffed rice with lactose-free milk
* Soda crackers
* Boiled and mashed fruit
* Boiled and mashed vegetables
It’s also important to reduce the risk of extreme dehydration; drinking fresh water and flat, caffeine-free soda can help replenish the body with lost fluids and increase the chances of recovery.
Eating properly-cooked food and making sure that hands are washed and cleaned thoroughly before handling fresh food are essential for preventing food borne illnesses. People who have a sensitive stomach should also avoid uncooked fish products and undercooked meats, as these may contain a significant amount of bacteria that can trigger the stomach virus.
Water-borne parasites are often found in third world countries, so anyone traveling to these areas should avoid drinking tap water and plan ahead to have a bottled water supply.
Any allergic reactions to seafood, shellfish, peanuts or even wheat products should be addressed by a doctor so that a healthy meal plan that does not contain these foods, or derivatives of these foods, can be arranged.
Exercising good hygiene is another way to protect yourself from a stomach virus. Washing hands thoroughly after going to the bathroom, keeping the nails clean and trim, and maintaining clean silverware and serving plates are simple ways to reduce the risk of contracting or spreading a stomach virus.
by eHowKnol, The eHow database is the world's most popular place to find clear instructions on how to do just about everything. at Demand Media
A stomach virus is also known as the stomach flu (viral gastroenteritis) and can affect people of all ages. It is a temporary health condition caused by an infection; the virus typically causes severe cramping and pain, but is commonly mistaken for the regular flu (influenza). A stomach virus is commonly caused by parasites such as cryptosporidium and giardia, as well as bacteria such as E.coli, Shigella and Salmonella.
Common Symptoms of a Stomach Virus
The most common symptoms of a stomach virus include:
* Watery diarrhea
* Extreme abdominal discomfort
* Vomiting
* Headache
* Ongoing fever
* Chills
* Excessive thirst
* Severe weakness
* Lethargy and fatigue
* Dizziness
The symptoms of a stomach flu typically occur within 4 to 48 hours of eating the contaminated food or being exposed to the bacteria. The symptoms can last for 2 – 4 days, but typically do not extend for longer than 10 days.
Common Causes of a Stomach Virus
Any type of infection that enters the gastrointestinal tract can trigger the spread of a stomach virus, and cause irritation or inflammation in the stomach or intestines. The virus may be caused by:
* Eating spoiled food
* Drinking contaminated water
* Inhaling or ingesting bacteria
* Having an allergic reaction to certain types of food
* Lactose intolerance
* Gluten intolerance
The most common types of viruses that cause stomach flu include:
* Caliciviruses – a virus that typically occurs between October and April, and results in diarrhea, vomiting and fatigue. The symptoms typically appear within 1-3 days of exposure to the contaminated foods or fluids, but most people can recover within 7 days.
* Adenovirus – a common ‘infant’ stomach virus that causes vomiting and diarrhea. This type of virus can occur any time of year and can be especially dangerous for infants with weak immune systems.
* Rotavirus – a virus that typically occurs in children who are 3 – 15 months old; this virus causes fever, diarrhea and abdominal pain and typically occurs between November and April.
* Astrovirus – a common type of stomach virus that occurs during the winter months. This one typically triggers vomiting, diarrhea, fatigue and abdominal discomfort.
Is It a Stomach Virus or the Flu?
Since many of the symptoms of a stomach virus are similar to those of influenza, it can be difficult to diagnose the problem. The average flu is a viral infection that begins with a high fever and congestion, and is often accompanied by fatigue. However, the flu cannot be treated with an antibiotic that is necessary to treat the stomach virus because it is not a bacterial infection.
In most cases, people suffering from the stomach flu will experience extreme dehydration, headaches and diarrhea. Overall, they will experience many of the common symptoms of the flu but also a number of digestive problems and gastrointestinal pain.
Recovering from a Stomach Virus
There is no specific treatment for recovering from a stomach virus. Sufferers must eat bland food, drink plenty of water and get enough rest to allow the body to recover naturally. Antibiotics are not very effective in treating viruses, because once the bacteria has reached the intestinal tract, it can be difficult for the body to absorb any type of medication.
The best strategy for recovering from the virus involves drinking clear liquids and eating easily-digestible foods. Oral rehydration solutions that contain minerals and salts such as potassium may be especially beneficial for young children and the elderly.
Individuals who are taking prescription medications may need to stop taking certain types of drugs until the symptoms disappear. Frequent episodes of vomiting and diarrhea can lead to malabsorption, making most medications ineffective and increasing the chances of toxicity.
Making an appointment with the doctor is recommended at the onset of a stomach virus, or if the symptoms do not disappear within 7-10 days. Extreme cases can become difficult to manage without oral rehydration solutions and supplements, and a doctor may be able to recommend certain foods and supplements for those who are not recovering from the stomach virus in an appropriate period of time.
Foods to Eat If You Have a Stomach Virus
Since the stomach will become especially sensitive to certain types of food and fluids after the initial stages of symptoms have settled down, the sufferer will need to drink extra fluids and eat a simple, easily-digestible diet. A bland diet comprised of simple carbohydrates can help the person with the stomach flu get the energy they need to recover and restore their body to good health. Foods that will not irritate the stomach lining or trigger a gastrointestinal reaction include:
* Dry toast
* Bananas
* Applesauce
* Cooked rice
* Puffed rice with lactose-free milk
* Soda crackers
* Boiled and mashed fruit
* Boiled and mashed vegetables
It’s also important to reduce the risk of extreme dehydration; drinking fresh water and flat, caffeine-free soda can help replenish the body with lost fluids and increase the chances of recovery.
Ways to Prevent a Stomach Virus
Eating properly-cooked food and making sure that hands are washed and cleaned thoroughly before handling fresh food are essential for preventing food borne illnesses. People who have a sensitive stomach should also avoid uncooked fish products and undercooked meats, as these may contain a significant amount of bacteria that can trigger the stomach virus.
Water-borne parasites are often found in third world countries, so anyone traveling to these areas should avoid drinking tap water and plan ahead to have a bottled water supply.
Any allergic reactions to seafood, shellfish, peanuts or even wheat products should be addressed by a doctor so that a healthy meal plan that does not contain these foods, or derivatives of these foods, can be arranged.
Exercising good hygiene is another way to protect yourself from a stomach virus. Washing hands thoroughly after going to the bathroom, keeping the nails clean and trim, and maintaining clean silverware and serving plates are simple ways to reduce the risk of contracting or spreading a stomach virus.
Female Sexual Function and Dysfunction - Knol
Source Knol: Female Sexual Function and Dysfunction
by Tom F. Lue, Professor and Vice Chair of Urology University of California, San Francisco
Alan Shindel, Assistant Professor of Urology, University of California, Davis, University of California Davis Medical Center
Irwin Goldstein, Director of Sexual Medicine, Alvarado Hospital; Clincial Professor of Surgery, UCSD, San Diego, California
Introduction
In 1893, the physician and sexual medicine specialist Edward Martin stated, “In the case of a woman, performance of the sexual act, at least insofar as her partner is concerned, requires only the presence of a sufficiently long and patulous (open) mucous canal.”[1] While this statement may seem shockingly misogynistic (hating or dismissive of women), when it was written it was fairly progressive to openly address women’s sexuality. Although our understanding of women’s sexual function and dysfunction has not progressed as rapidly as our understanding of men’s sexuality has, we have certainly made progress since Martin’s day.
Female Sexual Function
What are the phases of sexual response in women?
The famed sex researchers William Masters and Virginia Johnson derived a basic scheme for sexual response in men and women consisting of four distinct phases called excitement, plateau, orgasm, and resolution.[2] In the vast majority of men studied by Masters and Johnson these steps occurred in a fairly predictable pattern. In contrast, these researchers found much more variation among women with respect to sexual experience. In some women the sequence of events was similar to what was observed in men (blue line in graphic below). In other women a discrete orgasm phase did not occur (violet line in graphic below) and in some women there were multiple orgasms during a single sexual encounter (yellow line in graphic below). Helen Singer Kaplan, another prominent sex researcher, later elaborated on the Masters and Johnson schema by incorporating the concept of desire, defined as an interest in sexual activity that precedes actual sexual arousal.[3]
The paradigm created by Masters, Johnson, and Kaplan has been accepted for many years as representative of sexual response in both men and women. Recently, a leading expert in women’s sexual health (Rosemary Basson) has advocated a new model of female sexual function that stresses the interdependence of relationship factors and sexual function in women. In this new model, sexuality and sexual function in women follow a circular path in which emotional cues and relationship issues play a fundamental role and intrinsic sexual desire plays a much smaller role.[4]
No one model can adequately encompass the sexual experience for all individuals. In a recent study of 129 women, about 2/3 of respondents endorsed the Masters & Johnson model as most representative of their sexual response, while approximately 1/3 selected the Basson model. Interestingly, women who endorsed the Basson model were more likely to have sexual health concerns, particularly low sexual desire.[5]
What physical changes occur during the sexual response cycle in women?
During sexual arousal in women, numerous changes occur throughout the body. For the purposes of this review, we will focus on genital changes only. The attached diagrams demonstrate the anatomy of the female pelvis with a focus on the genital organs.
Vaginal lubrication
Prior to the 1960s, it was thought that the vaginal lubrication produced during sexual arousal was derived from glandular tissue. However, in a series of elegant experiments Masters and Johnson demonstrated that there were no discrete glands within the vagina and therefore vaginal lubrication could not be derived from glands.[2] It was subsequently discovered that vaginal lubrication is caused by the production of a transudate (a watery fluid with very low protein content) from the blood vessels supplying the vagina. Normally, the walls of blood vessels do not permit fluid to leak through. However, during sexual excitement, increased blood flow to the pelvic region causes pressure to build up in the small blood vessels around the vagina. This process is driven by nerves from the sacral portion of the spinal cord, which is part of the parasympathetic nervous system. This increased pressure forces fluid out of the blood vessels and into the vaginal canal, thus producing a slippery lubricant fluid. This fluid is the lubrication that a woman feels when she gets wet from sexual arousal.[6]
The clitoris is composed of inner-tube like cylinders of spongy tissue called corpora cavernosa. The internal portion (crura) of the clitoris attaches to the pelvic bones. During sexual excitement, blood flow to the corpora cavernosa increases, causing them to swell. Because the veins that drain blood from the clitoris are located to the side of the corpora cavernosa, compression from the swelling corpora will tend to obstruct these veins, causing blood to become trapped inside the clitoris. The overall process leads to engorgement (enlargement) and increased sensitivity of the clitoris.[7]
What about female ejaculation and the G spot?
During sexual climax, some women experience a spurting of fluid from the urethra; this is commonly referred to as female ejaculation. This is an atypical but not abnormal occurrence and should not be interpreted as a problem.
The G spot (or Grafenberg Spot, for the physician who first described it) is an anatomical area that can be a source of great pleasure during sexual stimulation for some women. It is most commonly located on the front wall of the vagina near the base of the bladder although the exact location may vary. The G Spot has been a source of great controversy in the medical community as some investigators contend that there is not enough evidence to prove its existence.[8] Other experts and many women very strongly maintain that the G spot does exist and can play an important role in sexual pleasure.[9]
The existence and importance of the “G spot” for a particular woman’s enjoyment of sex varies from woman to woman, like most aspects of sexuality. Interestingly, women who ejaculate at climax report sensitivity in the expected location of the G spot more frequently than women who do not ejaculate. [9] The G-spot has often been referred to as a “female prostate,” and recent evidence has supported the notion that the “G-spot” may indeed be a gland that surrounds the urethra and produces the fluid ejaculated at orgasm. The physical characteristics of female ejaculate have been not been well studied but there is good evidence that it is similar in some respects to semen, which is ejaculated by men at climax.[10] Further research is needed before definitive statements about the G spot and female ejaculation can be made. For the time being, G spot sensitivity and ejaculation can be considered normal variants of female sexual response.
It is a fairly long article and there is a lot of content on Female Sexual Disorders. There are images explaining anatomy of various organs. Visit source knol for more detailed content.
Source Knol: Female Sexual Function and Dysfunction
by Tom F. Lue, Professor and Vice Chair of Urology University of California, San Francisco
Alan Shindel, Assistant Professor of Urology, University of California, Davis, University of California Davis Medical Center
Irwin Goldstein, Director of Sexual Medicine, Alvarado Hospital; Clincial Professor of Surgery, UCSD, San Diego, California
Introduction
In 1893, the physician and sexual medicine specialist Edward Martin stated, “In the case of a woman, performance of the sexual act, at least insofar as her partner is concerned, requires only the presence of a sufficiently long and patulous (open) mucous canal.”[1] While this statement may seem shockingly misogynistic (hating or dismissive of women), when it was written it was fairly progressive to openly address women’s sexuality. Although our understanding of women’s sexual function and dysfunction has not progressed as rapidly as our understanding of men’s sexuality has, we have certainly made progress since Martin’s day.
Female Sexual Function
What are the phases of sexual response in women?
The famed sex researchers William Masters and Virginia Johnson derived a basic scheme for sexual response in men and women consisting of four distinct phases called excitement, plateau, orgasm, and resolution.[2] In the vast majority of men studied by Masters and Johnson these steps occurred in a fairly predictable pattern. In contrast, these researchers found much more variation among women with respect to sexual experience. In some women the sequence of events was similar to what was observed in men (blue line in graphic below). In other women a discrete orgasm phase did not occur (violet line in graphic below) and in some women there were multiple orgasms during a single sexual encounter (yellow line in graphic below). Helen Singer Kaplan, another prominent sex researcher, later elaborated on the Masters and Johnson schema by incorporating the concept of desire, defined as an interest in sexual activity that precedes actual sexual arousal.[3]
The paradigm created by Masters, Johnson, and Kaplan has been accepted for many years as representative of sexual response in both men and women. Recently, a leading expert in women’s sexual health (Rosemary Basson) has advocated a new model of female sexual function that stresses the interdependence of relationship factors and sexual function in women. In this new model, sexuality and sexual function in women follow a circular path in which emotional cues and relationship issues play a fundamental role and intrinsic sexual desire plays a much smaller role.[4]
No one model can adequately encompass the sexual experience for all individuals. In a recent study of 129 women, about 2/3 of respondents endorsed the Masters & Johnson model as most representative of their sexual response, while approximately 1/3 selected the Basson model. Interestingly, women who endorsed the Basson model were more likely to have sexual health concerns, particularly low sexual desire.[5]
What physical changes occur during the sexual response cycle in women?
During sexual arousal in women, numerous changes occur throughout the body. For the purposes of this review, we will focus on genital changes only. The attached diagrams demonstrate the anatomy of the female pelvis with a focus on the genital organs.
Vaginal lubrication
Prior to the 1960s, it was thought that the vaginal lubrication produced during sexual arousal was derived from glandular tissue. However, in a series of elegant experiments Masters and Johnson demonstrated that there were no discrete glands within the vagina and therefore vaginal lubrication could not be derived from glands.[2] It was subsequently discovered that vaginal lubrication is caused by the production of a transudate (a watery fluid with very low protein content) from the blood vessels supplying the vagina. Normally, the walls of blood vessels do not permit fluid to leak through. However, during sexual excitement, increased blood flow to the pelvic region causes pressure to build up in the small blood vessels around the vagina. This process is driven by nerves from the sacral portion of the spinal cord, which is part of the parasympathetic nervous system. This increased pressure forces fluid out of the blood vessels and into the vaginal canal, thus producing a slippery lubricant fluid. This fluid is the lubrication that a woman feels when she gets wet from sexual arousal.[6]
The clitoris is composed of inner-tube like cylinders of spongy tissue called corpora cavernosa. The internal portion (crura) of the clitoris attaches to the pelvic bones. During sexual excitement, blood flow to the corpora cavernosa increases, causing them to swell. Because the veins that drain blood from the clitoris are located to the side of the corpora cavernosa, compression from the swelling corpora will tend to obstruct these veins, causing blood to become trapped inside the clitoris. The overall process leads to engorgement (enlargement) and increased sensitivity of the clitoris.[7]
What about female ejaculation and the G spot?
During sexual climax, some women experience a spurting of fluid from the urethra; this is commonly referred to as female ejaculation. This is an atypical but not abnormal occurrence and should not be interpreted as a problem.
The G spot (or Grafenberg Spot, for the physician who first described it) is an anatomical area that can be a source of great pleasure during sexual stimulation for some women. It is most commonly located on the front wall of the vagina near the base of the bladder although the exact location may vary. The G Spot has been a source of great controversy in the medical community as some investigators contend that there is not enough evidence to prove its existence.[8] Other experts and many women very strongly maintain that the G spot does exist and can play an important role in sexual pleasure.[9]
The existence and importance of the “G spot” for a particular woman’s enjoyment of sex varies from woman to woman, like most aspects of sexuality. Interestingly, women who ejaculate at climax report sensitivity in the expected location of the G spot more frequently than women who do not ejaculate. [9] The G-spot has often been referred to as a “female prostate,” and recent evidence has supported the notion that the “G-spot” may indeed be a gland that surrounds the urethra and produces the fluid ejaculated at orgasm. The physical characteristics of female ejaculate have been not been well studied but there is good evidence that it is similar in some respects to semen, which is ejaculated by men at climax.[10] Further research is needed before definitive statements about the G spot and female ejaculation can be made. For the time being, G spot sensitivity and ejaculation can be considered normal variants of female sexual response.
It is a fairly long article and there is a lot of content on Female Sexual Disorders. There are images explaining anatomy of various organs. Visit source knol for more detailed content.
Source Knol: Female Sexual Function and Dysfunction
Sunday, July 10, 2011
BRAIN: CT, MRI - Noninvasive imaging of the central nervous system - Reshared Knol
Source Knol: BRAIN: CT, MRI
by Christopher Hess, Assistant Professor, Neuroradiology, University of California San Francisco, San Francisco, CA
Derk D Purcell, Radiologist at CPMC Radiology
Introduction
The complexity of the organ that determines how a person thinks, moves, feels and remembers is overshadowed only by its unique vulnerability. The brain is hidden from direct view by the protective bony covering of the skull, which not only shields it from injury but also hinders the study of its function in both health and disease. The cells in the arteries that supply the brain are so tightly bound that even most normal cells in the bloodstream are prevented from crossing the so-called “blood-brain barrier,” thereby rendering the normal chemistry of the brain invisible to the routine laboratory blood tests that are often used to evaluate the heart, liver or kidneys.
Computed tomography (CT) and magnetic resonance imaging (MRI) have revolutionized the study of the brain by allowing doctors and researchers to look at the brain noninvasively. Like other organs in the human body, the structure of the brain is highly organized according to its function. Different parts of the brain play specific roles that govern different activities, such as movement, cognition, and vision. These imaging techniques have allowed for the first time the noninvasive evaluation of brain structure, allowing doctors to infer causes of abnormal function due to different diseases.
How are brain images made with CT?
Computed tomography is based on the measurement of the amount of energy that the head absorbs as a beam of radiation passes through it from a source to a detector. Within a CT scanner, the radiation source and detector are mounted opposite one another along a circular track, or gantry, allowing them to rotate rapidly and synchronously around the table on which the patient lies. As the x-ray source and detector move around the patient’s head, measurements consisting of many projections through the head are obtained at prescribed angles and stored on a computer. The table moves horizontally in and out of the scanner in order to cover the entire head [1, 2].
The “tome” in tomography is the Greek word for “slice.” At the core of the scanner is a computer that not only controls the radiation source, the rotation of the x-ray tube and detector, and the movement of the table, but also generates anatomical slices, or tomograms, from the measured projections. The mathematical technique that allows an image of the head to be recovered from its projections is referred to as the backprojection algorithm [3]. Because the patient is positioned horizontally on the table, the backprojection algorithm yields slices that are transaxial, which means the slices are oriented at right angles to the long axis of the body.
The primary physical quantity that is captured with CT is density, or mass per unit volume. Prior to display and storage of CT images, pixel intensities are mapped to a standard numerical scale to allow reliable discrimination between different densities of tissue such as air, water, fat, bone, and various brain constituents. When the images are reviewed on a computer, the intensities are further modified by a process referred to as windowing in order to optimally depict the density of different tissues for visual display. Extremely dense material, such as metal or bone, appears bright on CT images, whereas tissue that is less dense, like fat or water, appears dark.
Magnetic resonance imaging relies upon signals derived from water molecules, which comprise between 70% and 80% of the average human brain. This ubiquitous biological molecule has two protons, which by virtue of their positive charge act as small magnets on a subatomic scale. Positioned within the large magnetic field of an MR scanner, typically 30 to 60 thousand times stronger than the magnetic field of the earth, these microscopic magnets collectively produce a tiny net magnetization that can be measured outside of the body and used to generate very high-resolution images that reveal information about water molecules in the brain and their local environment.
Protons placed in a magnetic field have the interesting property that they will absorb energy at specific frequencies, and then re-emit the energy at the same frequency. To measure the net magnetization, a coil placed around the head is used to both to generate electromagnetic waves and measure the electromagnetic waves that are emitted from the head in response. Unlike CT, which uses x-rays with very high frequency energy, MRI uses electromagnetic waves in the same portion of the electromagnetic spectrum as broadcast FM radio.
MRI is also a tomographic imaging modality, in that it produces two-dimensional images that consist of individual slices of the brain. Images in MRI need not be acquired transaxially, and the table or scanner does not move to cover different slices in the brain. Rather, images can be obtained in any plane through the head by electronically “steering” the plane of the scan. Precise spatial localization is achieved through a process termed gradient encoding [4]. The switching on and off of these magnetic field gradients are the source of the loud clicking and whirring noises that are heard during an MRI scan. While this process requires more time than CT scanning, imaging can be performed relatively rapidly using modern gradient systems [5].
Image intensity in MRI depends upon several parameters. These are proton density, which is determined by the relative concentration of water molecules, and T1, T2, and T2* relaxation, which reflect different features of the local environment of individual protons. The degree to which these parameters contribute to overall image intensity is controlled by the application and timing of radiofrequency energy through different pulse sequences. The most commonly used pulse sequences in brain imaging preferentially emphasize T1 relaxation, T2 relaxation, T2* relaxation or proton density. Specialized pulse sequences can sensitize images to flowing blood, minute changes in local brain oxygen content, or even to the microscopic movement of water molecules within the brain. Each pulse sequence confers a different contrast weighting to the image, such that when combined, the aggregate intensities from the different pulse sequences allow inference about the properties and local environment of the brain tissue being studied. For example, using MRI, one can infer the phase (solid or liquid), content (fat, water, air, blood) or movement (static or pulsatile) of a given structure in the brain
What is a contrast agent?
Contrast media, or “dyes” are used both in brain CT and MRI to provide another mechanism for modulating image intensity beyond what is possible using intrinsic tissue contrast. These are externally administered pharmaceutical agents given during an imaging examination to highlight normal or diseased brain structures. The additional information provided by a contrast agent may or may not be necessary to make an accurate diagnosis.
Contrast agents are most often administered by intravenous injection, but may in certain cases require intrathecal (spinal) injection using a lumbar puncture (spinal tap) procedure. Because they are water soluble they are normally removed from the body by the kidneys, though when the kidneys are diseased the liver may also contribute to their elimination. CT contrast agents are typically iodine-containing compounds that transiently increase the density of structures that they pass through. MRI contrast agents contain the heavy metal gadolinium, which changes the inherent T1 and T2 relaxation parameters of tissues.
The normal path of intravenously-injected contrast agents is through the heart, lungs and arteries of the chest and neck before entering the head. Once in the head, contrast passes first into the arterial system of the brain and its coverings, then through the cerebral microcirculation to supply the brain itself, ultimately passing into the intracranial venous system. Once it has passed into the large veins in the head, contrast is transmitted into the veins of the neck. From there, the contrast enters the heart for the second time, beginning the process of recirculation. The relative timing of the scan with respect to the location of the contrast agent within the blood pool allows detailed imaging of the arteries, brain, or veins.
Contrast agents in neuroimaging are usually given to evaluate blood vessels or to assess the integrity of the blood-brain barrier. In the former case, CT or MR angiography can diagnose cerebral aneurysms, vascular malformations, and narrowed or occluded arteries. In the latter, enhancement of the brain itself is used for the diagnosis of disease. The cells that line the capillaries of the normal brain are tightly bound together to form the “blood-brain barrier,” which allows the passage of oxygen and nutrients into the brain but prevents the transit of disease-causing organisms and large molecules, including contrast agents. Brain tumors, infections and inflammatory processes often disrupt the blood-brain barrier, giving rise to abnormal enhancement within the brain.
What do brain CT and MRI images show?
Interpretation of brain images requires a detailed knowledge of anatomy and a comprehensive understanding of how different diseases affect the brain and its supporting structures. Radiologists are medical doctors who specialize in acquiring and interpreting images; neuroradiologists focus specifically on imaging of the nervous system. These specialists work together with neurologists, neurosurgeons and primary care physicians to use CT and MRI to diagnose disorders of the brain and understand their significance for patients. Several different anatomical structures are routinely visualized with neuroimaging:
THE BRAIN. The gray matter of the brain consists of the cortex that lines the external surface of the brain and the gray nuclei deep inside of the brain, including the thalami and basal ganglia. Within the gray matter lie the cell bodies of the roughly 85 billion neurons that constitute the processing engine for the brain. White matter is comprised of the neuronal axons that interconnect different regions of the brain and serve as the interface between the brain and the rest of the body. Different diseases affect the gray and white matter in distinct patterns.
BLOOD VESSELS. The arterial supply to the brain arises from paired carotid and vertebral arteries in the neck. These four vessels continue into the head and divide into separate anterior, middle and posterior cerebral arteries that provide oxygen and nutrients to different regions of the brain. These vessels are interconnected at the base of the brain through a network of arteries called the circle of Willis. The principal veins within the head, the dural venous sinuses, collect blood that has passed through the brain. Blood vessels may cause symptoms by becoming enlarged or narrowed, occluded, or by supplying vascular malformations in or around the brain.
BRAIN COVERINGS. The brain is not rigidly adherent to the skull. It is surrounded by three layers of covering: the innermost pia mater, the middle arachnoid mater, and the outermost dura mater. Cerebrospinal fluid (CSF), a translucent liquid derived from blood and contained within the space between the pia and arachnoid mater, serves as a chemical and physical cushion for the brain. Blood from ruptured aneurysms, trauma or pus from infections such as meningitis may collect within the spaces between meningeal layers or within the CSF.
THE SKULL. The bones that surround the brain, including the calvarium, facial skeleton and skull base, are collectively referred to as the skull. These structures provide protection for the brain and a rigid frame to support the functions of the face. Because cortical bones contain very little water, they are evaluated reliably only with CT. The marrow within these bones, however, can be seen on MRI images. Bones can be the primary source of disease, or they can be secondarily involved by different infections and tumors, for example.
SURROUNDING TISSUES. The skull is surrounded not only by the scalp, but also fat, muscles, blood vessels, and various special glands. Importantly, the front of the head contains an array of muscles, salivary glands, and lymph nodes that may be primarily or secondarily affected by various disorders. The physical location of abnormalities in these regions often gives clues as to the source of disease.
Still there is lot more material in this long article and there are excellent images. There are references. For further reading visit:
Source Knol: BRAIN: CT, MRI
by Christopher Hess, Assistant Professor, Neuroradiology, University of California San Francisco, San Francisco, CA
Derk D Purcell, Radiologist at CPMC Radiology
Introduction
The complexity of the organ that determines how a person thinks, moves, feels and remembers is overshadowed only by its unique vulnerability. The brain is hidden from direct view by the protective bony covering of the skull, which not only shields it from injury but also hinders the study of its function in both health and disease. The cells in the arteries that supply the brain are so tightly bound that even most normal cells in the bloodstream are prevented from crossing the so-called “blood-brain barrier,” thereby rendering the normal chemistry of the brain invisible to the routine laboratory blood tests that are often used to evaluate the heart, liver or kidneys.
Computed tomography (CT) and magnetic resonance imaging (MRI) have revolutionized the study of the brain by allowing doctors and researchers to look at the brain noninvasively. Like other organs in the human body, the structure of the brain is highly organized according to its function. Different parts of the brain play specific roles that govern different activities, such as movement, cognition, and vision. These imaging techniques have allowed for the first time the noninvasive evaluation of brain structure, allowing doctors to infer causes of abnormal function due to different diseases.
How are brain images made with CT?
Computed tomography is based on the measurement of the amount of energy that the head absorbs as a beam of radiation passes through it from a source to a detector. Within a CT scanner, the radiation source and detector are mounted opposite one another along a circular track, or gantry, allowing them to rotate rapidly and synchronously around the table on which the patient lies. As the x-ray source and detector move around the patient’s head, measurements consisting of many projections through the head are obtained at prescribed angles and stored on a computer. The table moves horizontally in and out of the scanner in order to cover the entire head [1, 2].
The “tome” in tomography is the Greek word for “slice.” At the core of the scanner is a computer that not only controls the radiation source, the rotation of the x-ray tube and detector, and the movement of the table, but also generates anatomical slices, or tomograms, from the measured projections. The mathematical technique that allows an image of the head to be recovered from its projections is referred to as the backprojection algorithm [3]. Because the patient is positioned horizontally on the table, the backprojection algorithm yields slices that are transaxial, which means the slices are oriented at right angles to the long axis of the body.
The primary physical quantity that is captured with CT is density, or mass per unit volume. Prior to display and storage of CT images, pixel intensities are mapped to a standard numerical scale to allow reliable discrimination between different densities of tissue such as air, water, fat, bone, and various brain constituents. When the images are reviewed on a computer, the intensities are further modified by a process referred to as windowing in order to optimally depict the density of different tissues for visual display. Extremely dense material, such as metal or bone, appears bright on CT images, whereas tissue that is less dense, like fat or water, appears dark.
Magnetic resonance imaging relies upon signals derived from water molecules, which comprise between 70% and 80% of the average human brain. This ubiquitous biological molecule has two protons, which by virtue of their positive charge act as small magnets on a subatomic scale. Positioned within the large magnetic field of an MR scanner, typically 30 to 60 thousand times stronger than the magnetic field of the earth, these microscopic magnets collectively produce a tiny net magnetization that can be measured outside of the body and used to generate very high-resolution images that reveal information about water molecules in the brain and their local environment.
Protons placed in a magnetic field have the interesting property that they will absorb energy at specific frequencies, and then re-emit the energy at the same frequency. To measure the net magnetization, a coil placed around the head is used to both to generate electromagnetic waves and measure the electromagnetic waves that are emitted from the head in response. Unlike CT, which uses x-rays with very high frequency energy, MRI uses electromagnetic waves in the same portion of the electromagnetic spectrum as broadcast FM radio.
MRI is also a tomographic imaging modality, in that it produces two-dimensional images that consist of individual slices of the brain. Images in MRI need not be acquired transaxially, and the table or scanner does not move to cover different slices in the brain. Rather, images can be obtained in any plane through the head by electronically “steering” the plane of the scan. Precise spatial localization is achieved through a process termed gradient encoding [4]. The switching on and off of these magnetic field gradients are the source of the loud clicking and whirring noises that are heard during an MRI scan. While this process requires more time than CT scanning, imaging can be performed relatively rapidly using modern gradient systems [5].
Image intensity in MRI depends upon several parameters. These are proton density, which is determined by the relative concentration of water molecules, and T1, T2, and T2* relaxation, which reflect different features of the local environment of individual protons. The degree to which these parameters contribute to overall image intensity is controlled by the application and timing of radiofrequency energy through different pulse sequences. The most commonly used pulse sequences in brain imaging preferentially emphasize T1 relaxation, T2 relaxation, T2* relaxation or proton density. Specialized pulse sequences can sensitize images to flowing blood, minute changes in local brain oxygen content, or even to the microscopic movement of water molecules within the brain. Each pulse sequence confers a different contrast weighting to the image, such that when combined, the aggregate intensities from the different pulse sequences allow inference about the properties and local environment of the brain tissue being studied. For example, using MRI, one can infer the phase (solid or liquid), content (fat, water, air, blood) or movement (static or pulsatile) of a given structure in the brain
What is a contrast agent?
Contrast media, or “dyes” are used both in brain CT and MRI to provide another mechanism for modulating image intensity beyond what is possible using intrinsic tissue contrast. These are externally administered pharmaceutical agents given during an imaging examination to highlight normal or diseased brain structures. The additional information provided by a contrast agent may or may not be necessary to make an accurate diagnosis.
Contrast agents are most often administered by intravenous injection, but may in certain cases require intrathecal (spinal) injection using a lumbar puncture (spinal tap) procedure. Because they are water soluble they are normally removed from the body by the kidneys, though when the kidneys are diseased the liver may also contribute to their elimination. CT contrast agents are typically iodine-containing compounds that transiently increase the density of structures that they pass through. MRI contrast agents contain the heavy metal gadolinium, which changes the inherent T1 and T2 relaxation parameters of tissues.
The normal path of intravenously-injected contrast agents is through the heart, lungs and arteries of the chest and neck before entering the head. Once in the head, contrast passes first into the arterial system of the brain and its coverings, then through the cerebral microcirculation to supply the brain itself, ultimately passing into the intracranial venous system. Once it has passed into the large veins in the head, contrast is transmitted into the veins of the neck. From there, the contrast enters the heart for the second time, beginning the process of recirculation. The relative timing of the scan with respect to the location of the contrast agent within the blood pool allows detailed imaging of the arteries, brain, or veins.
Contrast agents in neuroimaging are usually given to evaluate blood vessels or to assess the integrity of the blood-brain barrier. In the former case, CT or MR angiography can diagnose cerebral aneurysms, vascular malformations, and narrowed or occluded arteries. In the latter, enhancement of the brain itself is used for the diagnosis of disease. The cells that line the capillaries of the normal brain are tightly bound together to form the “blood-brain barrier,” which allows the passage of oxygen and nutrients into the brain but prevents the transit of disease-causing organisms and large molecules, including contrast agents. Brain tumors, infections and inflammatory processes often disrupt the blood-brain barrier, giving rise to abnormal enhancement within the brain.
What do brain CT and MRI images show?
Interpretation of brain images requires a detailed knowledge of anatomy and a comprehensive understanding of how different diseases affect the brain and its supporting structures. Radiologists are medical doctors who specialize in acquiring and interpreting images; neuroradiologists focus specifically on imaging of the nervous system. These specialists work together with neurologists, neurosurgeons and primary care physicians to use CT and MRI to diagnose disorders of the brain and understand their significance for patients. Several different anatomical structures are routinely visualized with neuroimaging:
THE BRAIN. The gray matter of the brain consists of the cortex that lines the external surface of the brain and the gray nuclei deep inside of the brain, including the thalami and basal ganglia. Within the gray matter lie the cell bodies of the roughly 85 billion neurons that constitute the processing engine for the brain. White matter is comprised of the neuronal axons that interconnect different regions of the brain and serve as the interface between the brain and the rest of the body. Different diseases affect the gray and white matter in distinct patterns.
BLOOD VESSELS. The arterial supply to the brain arises from paired carotid and vertebral arteries in the neck. These four vessels continue into the head and divide into separate anterior, middle and posterior cerebral arteries that provide oxygen and nutrients to different regions of the brain. These vessels are interconnected at the base of the brain through a network of arteries called the circle of Willis. The principal veins within the head, the dural venous sinuses, collect blood that has passed through the brain. Blood vessels may cause symptoms by becoming enlarged or narrowed, occluded, or by supplying vascular malformations in or around the brain.
BRAIN COVERINGS. The brain is not rigidly adherent to the skull. It is surrounded by three layers of covering: the innermost pia mater, the middle arachnoid mater, and the outermost dura mater. Cerebrospinal fluid (CSF), a translucent liquid derived from blood and contained within the space between the pia and arachnoid mater, serves as a chemical and physical cushion for the brain. Blood from ruptured aneurysms, trauma or pus from infections such as meningitis may collect within the spaces between meningeal layers or within the CSF.
THE SKULL. The bones that surround the brain, including the calvarium, facial skeleton and skull base, are collectively referred to as the skull. These structures provide protection for the brain and a rigid frame to support the functions of the face. Because cortical bones contain very little water, they are evaluated reliably only with CT. The marrow within these bones, however, can be seen on MRI images. Bones can be the primary source of disease, or they can be secondarily involved by different infections and tumors, for example.
SURROUNDING TISSUES. The skull is surrounded not only by the scalp, but also fat, muscles, blood vessels, and various special glands. Importantly, the front of the head contains an array of muscles, salivary glands, and lymph nodes that may be primarily or secondarily affected by various disorders. The physical location of abnormalities in these regions often gives clues as to the source of disease.
Still there is lot more material in this long article and there are excellent images. There are references. For further reading visit:
Source Knol: BRAIN: CT, MRI
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