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Understanding MRSA Symptoms

What Are the Symptoms of MRSA?

The symptoms of MRSA infection depend on where you’ve been infected.

MRSA most often appears as a skin infection, like a boil or abscess. It also might infect a surgical wound. In either case, the area would look:

  • Swollen
  • Red
  • Painful
  • Filled with pus

Many people who have a staph skin infection often mistake it for a spider bite.

If staph infects the lungs and causes pneumonia, you will have:

  • Shortness of breath
  • Fever
  • Cough
  • Chills

MRSA can cause many other symptoms, because once it gets into your bloodstream, MRSA can settle anywhere. It can cause abscess in your spleen, kidney, and spine. It can cause endocarditis (heart valve infections), osteomyelitis (bone infections),  joint infections, breast mastitis, and prosthetic device infections. Unlike most MRSA skin infections, which can be treated in the doctor’s office, these other more serious infections will land you in the hospital for intravenous antibiotic therapy.

Very rarely, staph can result in necrotizing fasciitis, or “flesh-eating” bacterial infections. These are serious skin infections that spread very quickly. While frightening, only a handful of necrotizing fasciitis cases has been reported.

Call Your Doctor About MRSA If:

You have signs of active infection, most likely of the skin with a spreading, painful, red rash or abscess; in most cases, MRSA is easily treated. However, MRSA infection can be serious, so seek medical care.

If you are already being treated for an infection, watch for signs that your medicine isn’t working. If you are taking an antibiotic, call your health care provider if:

  • The infection is no better after three or four days of antibiotic therapy.
  • The rash spreads.
  • You develop a fever, or your fever gets worse.

People who are ill or have a compromised immune system have a higher risk of getting serious MRSA infections. If you have a condition that lowers your immunity, call your doctor right away if you think that you might have an infection.

Optimal Treatment of MRSA Throat Carriers – Full Text View

The bacterium Staphylococcus aureus frequently colonizes the human skin and mucous membranes. Longitudinal studies usually divide S. aureus carriers into either persistent or intermittent carriers, but because the number of samplings, the follow-up periods and the study populations differ between studies, the designation of carrier state is inconsistent. It has been estimated that around 20 % of a population are persistent carriers, 60 % are intermittent carriers and 20 % are non-carriers. S. aureus is an opportunistic pathogen that can become invasive and cause a large spectrum of infections. S. aureus is frequently the cause of skin and soft tissue infections e.g. wounds, furuncles and abscesses, and can also cause urinary tract infections and pneumonia. If it enters the bloodstream, it can lead to metastatic infections e.g. endocarditis, arthritis, osteomyelitis and meningitis. Furthermore, S. aureus is a common pathogen in surgical site infections and in infections related to foreign bodies, such as catheters and prostheses.

Antibiotic resistance in bacteria is an increasing challenge worldwide and is also seen in S. aureus. The first methicillin resistant Staphylococcus aureus (MRSA) were seen in 1961 just one year after the antibiotic methicillin was introduced. For several decades MRSA was mainly a hospital-associated bacterium, but since the mid 1990’s it has become increasingly prevalent in the community where it often affects children and younger adults. MRSA can cause the same types of infections as the methicillin susceptible S. aureus, but often only colonizes the mucosa. When colonization is confirmed, the person is called a carrier of MRSA and there is a risk of both a wide spectrum of infections and spread of MRSA to others. The Danish Health Authority has published a National guideline on how to prevent the spread of MRSA and keep the prevalence of MRSA low in Denmark, especially in the health care setting. The finding of MRSA both in samples from clinical infections and in screening samples for MRSA carriage is notifiable and has to be reported to the Danish Patient Safety Authority and Statens Serum Institut, in order to monitor the number of MRSA positive persons in Denmark, potential outbreaks and risk factors for MRSA acquisition. Furthermore, the guideline recommends that MRSA carriers and their household members undergo a five day topical decolonization treatment consisting of nasal mupirocin ointment 2 % three times daily in the nostrils (mupirocin is an antibiotic usually active against MRSA) and chlorhexidine body wash 4 % once daily. Unfortunately, many patients are still MRSA carriers after completing the treatment and especially throat carriers are difficult to clear.

MRSA carriers have routinely been treated since 2009. Our current guideline recommends adding antibiotics to the standard regimen, clindamycin being our first line choice, on the second or third eradication attempt if the patient is a throat carrier and the isolate is clindamycin susceptible. To our knowledge, the only randomized, controlled trial including clindamycin for treatment of MRSA carriage, is a Swedish study that showed a significant effect of standard treatment plus the antibiotic rifampicin in combination with either clindamycin or sulfamethoxazole/trimethoprim compared to standard treatment alone in long-term MRSA carriers. As most of our patients are healthy individuals without infections, adding systemic antibiotics to the decolonization treatment must be considered thoroughly. There is a risk of side effects in the individual patient and prudent use of antibiotics in the era of a rising incidence of antimicrobial resistance is crucial to avoid selection of further resistance. Our group has recently published a retrospective study describing the MRSA treatment data of 164 patients treated in 2013. The study confirmed that throat carriers had a higher treatment failure rate but adding clindamycin to the first eradication attempt did not significantly increase the success rate. However, as there had been no randomization of patients the scientific evidence is low and the fact that there are no published studies using clindamycin as the only antibiotic for MRSA throat carriers, implies the need for a randomized trial on this subject.

Aim To investigate whether a significantly higher number of MRSA throat carriers become MRSA free when adding the oral antibiotic clindamycin to the standard regimen.

Primary endpoint: MRSA negative swabs at 1 month Secondary endpoint: MRSA negative swabs after 6 months

Methods The study is a randomized double blinded placebo-controlled study, including patients ≥18 years old that have tested MRSA positive in their throat after completing one standard topical decolonization treatment.

Recruitment of study subjects Patients are recruited from the Capital Region via MRSA KnowledgeCenter Hvidovre Hospital or MRSA team Herlev Hospital.

Patients have since their first positive MRSA result an active connection to the MRSA KnowledgeCenter Hvidovre Hospital / MRSA team Herlev Hospital either through the hygiene specialist nurses or doctors. Patients often call for support, guidance and treatment plans, and routine letters are often sent out to patients regarding their treatment, control swap results and more. When the department’s nurses or doctors have written or oral contact with a patient that could be a possible candidate for the trial, the possibility of participating in the trial will be mentioned and investigator’s contact details will be given.

The patient can contact the investigator by phone or email. After first contact with the investigator, and receiving information about the trial, the patient will have a minimum of 48 hours to decide whether he/she is interested in learning more about the project. Patients that respond positively will be invited to a personal meeting at either Hvidovre Hospital or Herlev Hospital, where oral information about the trial and possible side effects will be given to the patient. The meeting will occur in a private and undisturbed room with the door closed. The patient can bring a friend or relative at the meeting if desired. Patients will be offered 24 hours to provide oral and written informed consent in order to secure sufficient time for reflection on study participation. If a patient needs more time to consider entering the trial, more time will be given. Before signing the informed consent form, the investigator will secure that the patient has read and understood the written study information. Every possible study subject that has a personal meeting with the investigator, will be registered in REDcap, a secure web application for managing online databases.

When oral and written consent has been obtained, the subject will receive a randomized eradication package as described below, as well as a diary to fill out during the study from day 1 to 14, asking about compliance and adverse events.

Patient data Patient data will be pseudo-anonymized as each patient will receive a project number. The investigator will on another file in a locked drawer (investigator site file), as well as on a secured electronic file, only accessible for investigators, have access to the real identification of the patient (the CPR number).

Once included in the trial, one eCRF is created for each patient for collection of trial data. This will include the following data:

Project number, date of birth, age, sex, height, weight, relevant medical history/current medication, sites and dates of MRSA positive samples, prior MRSA decolonization treatments, household composition and household members MRSA carrier state, typing and resistance data of the MRSA strain, body mass index, laboratory and investigational results. For sexually active female subjects in the reproductive age, we also record the use of contraceptives.

The CRFs will be stored in the secure web application for managing online databases ‘REDCap’ which is designed for non-commercial clinical research. Obtained data will be transferred manually by investigators or appointed research nurses to the CRFs.

The eCRF does not contain information on the specific treatment the patient is randomized to as the randomization is done by the pharmacist.

The treatment The subject will receive a randomized eradication package, consisting of mupirocin nasal ointment 2 %, Chlorhexidine Bodywash 4 % and either placebo capsules 2 capsules three times daily for 10 days or clindamycin 300 mg capsules 2 capsules three times daily for 10 days. Placebo and clindamycin are manufactured to look exactly alike by Glostrup pharmacy, who is also in charge of the randomization/blinding of the packages.

An emergency unblinding procedure will be established to allow investigators the option to withdraw the subject from the trial at any given time, in case of an emergency. This could be if a subject experiences serious adverse events, that could be caused by the active treatment. The pharmacist has created individual sealed and securely closed envelopes for each included subject ID available. The investigator can at any time, 24 hours a day, in case of an emergency unblind a subject, to reveal which treatment has been given. The sponsor will be notified within 24 hours.

Besides the oral treatment, the patient follows the standard treatment guidelines for MRSA decolonization.

After the treatment Thirty to sixty days after end of treatment, the subjects will routinely have MRSA control swabs taken by their GP according to the National MRSA guidelines. Subjects will be reminded about this screening test when entering the trial. If control swabs haven’t been received within 6 weeks after completing the treatment, an electronic reminder will be send. The swabs are routine samples that will be handled as regular MRSA control samples in the clinical microbiology laboratory at either Hvidovre hospital or Herlev hospital.

Swab results If the patient is MRSA positive one month after the treatment, no further screening samples will be needed for this project. The patient will leave the trial, and if additional treatment is considered by the doctors responsible for the treatment outside the trial, the randomization will be unblinded in order to plan the most optimal treatment, without revealing the investigator about the investigation medicine given prior to the drop out.

If MRSA negative at one month, no unblinding will take place as no new treatment will be planned. The subject will have new control swabs taken at the GP six to eight months after completing the treatment. If negative swabs at 6-8 months, the patient is declared MRSA free according to the National MRSA Guidelines.

Power calculation Anticipation is 30% better eradication success rate in the group receiving standard treatment plus clindamycin compared to the group treated with standard treatment and placebo. Power calculation shows that 31 patients are needed in each group, power being set at 80 %, and significance level at 0. 05 %. It is our goal to include 40 patients in each group, as 9 patients in each group is expected to either drop out or be non-compliant to the treatment.

The number of consumed tablets will be reported in the eCFR, to monitor consumption.

The returned capsules, if any, will be returned to the Glostrup pharmacy, for correct destruction.

The relevance of this trial is high. Hundreds of healthy MRSA carriers have been treated with clindamycin in the last decade without a strong scientific evidence of a better effect than standard treatment. It is very relevant to know, whether adding clindamycin to the treatment of throat carriers is superior to the standard treatment. The outcome of this trial will help us understand the most effective way to clear throat carriers of MRSA.

MRSA – NHS

MRSA is a type of bacteria that’s resistant to several widely used antibiotics. This means infections with MRSA can be harder to treat than other bacterial infections.

The full name of MRSA is methicillin-resistant Staphylococcus aureus. You might have heard it called a “superbug”.

MRSA infections mainly affect people who are staying in hospital. They can be serious, but can usually be treated with antibiotics that work against MRSA.

How you get MRSA

MRSA lives harmlessly on the skin of around 1 in 30 people, usually in the nose, armpits, groin or buttocks. This is known as “colonisation” or “carrying” MRSA.

You can get MRSA on your skin by:

  • touching someone who has it
  • sharing things like towels, sheets and clothes with someone who has MRSA on their skin
  • touching surfaces or objects that have MRSA on them

Getting MRSA on your skin will not make you ill, and it may go away in a few hours, days, weeks or months without you noticing. But it could cause an infection if it gets deeper into your body.

People staying in hospital are most at risk of this happening because:

  • they often have a way for the bacteria to get into their body, such as a wound, burn, feeding tube, drip into a vein, or urinary catheter
  • they may have other serious health problems that mean their body is less able to fight off the bacteria
  • they’re in close contact with a large number of people, so the bacteria can spread more easily

Healthy people, including children and pregnant women, are not usually at risk of MRSA infections.

Symptoms of MRSA

Having MRSA on your skin does not cause any symptoms and does not make you ill.

You will not usually know if you have it unless you have a screening test before going into hospital.

If MRSA gets deeper into your skin, it can cause:

  • swelling
  • warmth
  • pain
  • pus
  • redness, but this may be less visible on darker skin

If it gets further into your body, it can also cause:

Tell a member of staff if you get these symptoms while in hospital.

Call a GP or NHS 111 if you get these symptoms outside of hospital.

Screening and testing for MRSA

If you need to go into hospital and it’s likely you’ll be staying overnight, you may have a simple screening test to check your skin for MRSA before you’re admitted.

This is normally done at a pre-admission clinic or a GP surgery. A nurse will run a cotton bud (swab) over your skin so it can be checked for MRSA.

Swabs may be taken from several places, such as your nose, throat, armpits, groin or any damaged skin. This is painless and only takes a few seconds.

The results will be available within a few days.

If you’re not carrying MRSA, it’s unlikely you’ll be contacted about the result and you should follow the instructions from the hospital.

If you’re carrying MRSA, you’ll be told by the hospital or a GP.

You may need treatment to remove the bacteria to reduce your risk of getting an infection or spreading the bacteria.

Treatments for MRSA

Removing MRSA from your skin

If screening finds MRSA on your skin, you may need treatment to remove it. This is known as decolonisation.

This usually involves:

  • applying antibacterial cream inside your nose 3 times a day for 5 days
  • washing with an antibacterial shampoo every day for 5 days
  • changing your towel, clothes and bedding every day during treatment – the laundry should be washed separately from other people’s and at a high temperature

Treatment is normally done at home, but may be started after going into hospital if you need to be admitted quickly.

Treatment for an MRSA infection

If you get an MRSA infection, you’ll usually be treated with antibiotics that work against MRSA.

These may be taken as tablets or given as injections. Treatment can last a few days to a few weeks.

During treatment, you may need to stay in your own room or in a ward with other people who have an MRSA infection to help stop it spreading.

You can normally still have visitors, but it’s important they take precautions to prevent MRSA spreading.

Preventing MRSA

If you’re staying in hospital, there are some simple things you can do to reduce your risk of getting or spreading MRSA.

You should:

  • wash your hands often (hand wipes and alcohol hand gel are also effective) – especially before and after eating and after going to the toilet
  • follow the advice you’re given about wound care and looking after devices that could lead to infection (such as urinary catheters or drips)
  • report any unclean facilities to staff – do not be afraid to talk to staff if you’re concerned about hygiene

If you’re visiting someone in hospital, clean your hands before and after entering the ward and before touching the person.  Gel or wipes are often placed by patients’ beds and at the entrance to wards.

It’s also a good idea to put a dressing over any breaks in your skin, such as sores or cuts, to stop MRSA getting into your body.

Get more advice about visiting someone in hospital

Video: MRSA

This video explains how MRSA is caught, what happens when you have it and how to prevent infection.

Media last reviewed: 12 January 2021
Media review due: 12 January 2024

Page last reviewed: 24 March 2020
Next review due: 24 March 2023

Staph Infection In Throat – Causes, Symptoms, And Prevention

Staph infection of the throat is one of the commonly occurring illnesses of the upper respiratory tract affecting several people worldwide. This article will help you understand more about staph infection in the throat and mouth or staph throat, its causes, signs, and symptoms along with treatment for the same.

What Is Staph Infection?

As the name suggests, staph infection or staph throat occurs due to a bacteria called Staphylococcus aureus which is a commonly found human pathogen.

This bacteria is the leading cause of bacterial infections among humans such as;

  • Infective endocarditis
  • Device-related infections
  • Infections of the skin
  • Soft tissues, and
  • The respiratory tract.

The most common sites for colonization of this bacteria in the human body are the groin, armpits, nose, and throat.

Can You Get Staph Infection In Your Throat?

The bacteria staphylococcus aureus releases toxins that cause inflammation, swelling, and infection of the throat. Studies have found out that the throat is the most common site for methicillin-resistant staphylococcus aureus (MRSA).

Higher rates of staphylococcal infections are documented at extremes of life, with peaks during the first few years of life and gradual decline during young adulthood and then increased rates with advancing age.

Staph infection shows an increased incidence among males as compared to females. Also, persons with HIV are very likely to have a staph infection.

Symptoms Of Staph Infection In The Throat

Staph infection of the throat generally presents with signs and symptoms corresponding to the exact site infected. Also, the duration of signs and symptoms indicate whether the infection is acute, sub-acute, or chronic.

Some commonly observed signs and symptoms of staph infection in the throat are;

  1. The scraped sensation of rawness in the throat
  2. Pain in throat while swallowing solid food or liquids
  3. Voice may be altered due to thick mucus secretion in the throat and impeded movements of the vocal cords due to inflammation and swelling
  4. Tonsils may be inflamed and swollen causing throat pain and difficulty in swallowing
  5. Lymph nodes of the neck may become enlarged and painful as they attempt to drain out the bacteria
  6. Excess mucus secretion from the nose and throat may be present. In case of involvement of the sinuses, post-nasal dripping of mucus may be experienced by the patient
  7. Nasal obstruction and post-nasal irritation may be present especially in infants
  8. Constitutional symptoms like fever, loss of appetite, headache and body ache may be present.

Throat examination of a patient with a staph infection in the throat may show the following signs which may tell about the type of infection;

  • Catarrhal – Congestion and swelling of the throat with redness
  • Purulent – The wall of the throat may be coated with pus-like mucus discharge
  • Ulcerative – In some cases, ulcerations may form on the wall of the throat

Causes Of Staph Infection In Throat

Approximately 10-15% of cases of throat infection occur due to two major bacteria, Staphylococcus and Streptococcus. Most of the staph infections and strep infections of the throat are either hospital-associated or acquired through community spread. Frequently, a common viral cold may get converted to a superadded bacterial infection.

How Do You Get Staph Infection In Your Throat?

Some risk factors associated with a staph infection in the throat are;

  1. Pre-existing upper respiratory tract infection
  2. Prolonged hospitalization
  3. Prolonged use of antibiotics
  4. Compromised immune status as in HIV
  5. Gastro-intestinal tract illnesses
  6. Environmental causes;
  • Cold foods or cold drinks lower the resistance by causing vasoconstriction
  • Spread from one infected person to another
  • Pollution
  • Crowded or poorly ventilated environment
  • Foreign body stuck in the throat

How To Treat Staph Infection In Throat?

A sore throat is generally self-limiting and recovers within a week. Staph infection of the throat on the other hand requires proper medical management to prevent its potential complications. Also, the management of antibiotic-resistant staph infection of the throat remains to be a major challenge for clinicians worldwide.

Conservative management of staph infection of the throat includes the following;

  1. Adequate bed rest and sleep
  2. Plenty of water to prevent dehydration
  3. Antibiotics, as advised by your doctor, will be required to control the infection
  4. Analgesics or anti-inflammatory medicines are prescribed to manage fever, pain, and inflammation or swelling of the upper respiratory tract
  5. Decongestants may be advised in case the patient complains of shortness of breath
  6. Lozenges may be advised to soothe the throat
  7. Warm saline gargles several times a day are advised
  8. Steam inhalation 3-4 times a day is advised to soothe the throat and reduce symptoms of throat swelling and congestion, mucus production, and cough

How To Prevent Staph Infection?

Some tips which help to prevent staph infection are;

  1. Avoid close contact with a person with a throat infection. Also avoid sharing utensils, food, or water with an infected person
  2. Maintain distance if you notice a person coughing or sneezing
  3. Drink plenty of water
  4. Wash your hands with soap and water frequently
  5. Avoid touching your nose and mouth with unclean hands
  6. Eat a nutritious diet rich in nuts, grains, and seeds. A well-balanced diet with adequate proteins, fats, and carbohydrates are necessary to prevent infections and maintain immunity
  7. Adequate sleep and regular exercise are necessary for optimal health
  8. Maintain general hygiene like taking a bath, wearing clean clothes, cleaning bedding and other surroundings

When To See A Doctor?

Staph infection of the throat is in itself a serious condition of the throat which has to be diagnosed and treated timely. Patients must see a doctor under the following conditions;

  1. Throat pain severe enough to cause pain on swallowing
  2. High-grade fever not responding to medicines
  3. Bloodstained mucous secretion from the throat
  4. Difficulty in breathing
  5. Inability to eat or drink
  6. Persistence of symptoms in spite of being on medications

A sore throat can range anything from a plain viral infection to a staph infection or a strep throat. If you are noticing any of the symptoms mentioned above, you must visit a doctor immediately and seek proper treatment for the same.

Tonsillectomy for persistent MRSA carriage in the throat—Description of three cases

Highlights

In several countries a search and destroy policy is part of the standard of care.

The eradication of methicillin-resistant Staphylococcus aureus (MRSA) carriage yields two objectives: prevention of infection and prevention of transmission.

MRSA carriage can be divided into uncomplicated and complicated carriage, both with their own treatment guidelines.

In a minority of cases, eradication treatment fails despite repeated treatments following guidelines, and throat carriage is associated with treatment failure.

Three cases in which tonsillectomy was performed after recurrent treatment failure are described. In all cases, one course of antibiotic treatment after tonsillectomy was successful in eradicating MRSA from the throat.

Abstract

In several countries, including the Netherlands, a search and destroy policy is part of the standard of care. Due to this policy and the restrictive use of antibiotics, the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in the Netherlands – carrier state and infections – is among the lowest in the world. In the Netherlands, healthcare workers who are MRSA carriers are not allowed to perform work involving direct patient care. This means that treatment failure can have major implications for their working career. Despite repeated treatments according to guidelines, the eradication of MRSA fails in a minority of cases. It appears that performing a tonsillectomy can be part of the solution to this problem. As yet, tonsillectomy is not recommended as supplementary treatment for persistent MRSA carriage in the throat. There are a few expert opinions suggesting that tonsillectomy could possibly be helpful in decolonization. This article reports three recent cases in which MRSA eradication was successful only after tonsillectomy. It is believed that if eradication is necessary, tonsillectomy, if applicable, should be considered.

Keywords

MRSA

Tonsillectomy

Carrier

Staphylococcus aureus

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View Abstract

© 2017 The Author(s). Published by Elsevier Ltd on behalf of International Society for Infectious Diseases.

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What It Is, Symptoms & Treatment



Overview

What is MRSA?

MRSA stands for Methicillin-resistant Staphylococcus aureus. It is a type of Staphylococcus aureus bacterium. These bacteria are resistant to common antibiotics, including methicillin. You may have read about MRSA being a superbug.

What is

Staphylococcus aureus (staph)?

Staphylococcus aureus (staph) bacteria live in the nose or on skin. You can harbor staph bacteria, including MRSA, and not know it. A healthcare expert might refer to this as bacterial colonization.

Colonized people (carriers) may one day develop an MRSA infection, or they might stay healthy.

Staph, including MRSA, bacteria live in these body parts:

  • Armpits.
  • Buttocks (your butt).
  • Groin.
  • Nose.

How common is MRSA?

Approximately 1 in 3 Americans are carriers of staph bacteria at any time. Up to half of these could be MRSA. It’s important to emphasize that Staph aureus or MRSA carriage is not a disease.

What are the types of MRSA infections?

Two categories of MRSA are:

  • Hospital-associated (HA): HA-MRSA refers to MRSA infections that are associated with healthcare settings, such as hospitals and nursing homes.
  • Community-associated (CA): CA-MRSA infections are those that occur in people who have not had a recent hospitalization or other contact with the healthcare system.

Who is at risk for MRSA infection?

MRSA infection affects all ages and genders. Animals can carry MRSA, although they often get it from people. Intravenous drug users who share needles are 16 times more likely to get MRSA infection.

Certain workers and members of the community are more at risk for MRSA infection. These include:

  • Athletes.
  • Healthcare professionals.
  • Members of the military.
  • Prison inmates.
  • Students and employees at schools and child care centers.
  • Veterinarians, farm workers and livestock workers.



Symptoms and Causes

What is the relationship between MRSA colonization and infection?

Many people who carry MRSA never get sick. The bacterium remains within the skin or mucosa where it has established colonization. Problems arise when MRSA on the skin surface in a colonized person enters the skin through a wound or other opening and invades deeper structures.

How does MRSA spread?

You can get colonized with MRSA through direct contact with an infected person or animal. MRSA can survive on surfaces for hours, sometimes weeks. You can pick up the bacteria by touching or sharing contaminated items, such as:

  • Bedsheets.
  • Clothes.
  • Medical equipment.
  • Sports equipment.
  • Towels.
  • Utensils.

What are the symptoms of MRSA infection?

MRSA can cause a skin rash or infection that looks like a spider bite or pimples. The red, swollen bumps may feel warm and be tender to touch. The rash may ooze.

MRSA can also cause deeper infections in different parts of the body. In severe infections the bacterium may invade the bloodstream, a situation which would be called a bloodstream infection. Symptoms of bloodstream infection include fever and chills.



Diagnosis and Tests

How is MRSA infection diagnosed?

To diagnose an MRSA infection, your healthcare provider will take a small sample of skin or discharge from an open wound. Your provider may order a blood test called a blood culture. A lab checks for MRSA in these samples.



Management and Treatment

What are different forms of MRSA infection?

MRSA infections can occur at various sites and may be serious, even life-threatening. Important MRSA infections include:

How is MRSA infection managed or treated?

The two principles of treating Staph aureus infections, including MRSA infections, are source control and antibiotic therapy:

  • Source control: This refers to reducing the numbers of bacteria at the site of infection. In the case of skin infections, your provider may drain boils or abscesses. Other deeper infections may require more complicated surgery.
  • Antibiotic treatment: The antibiotic used to treat the infection depends on whether the Staph aureus infection is or is not an MRSA infection.

What should I know about MRSA treatments?

Milder infections can be treated with oral antibiotics (antibiotic pills). More severe infections may require intravenous antibiotic treatment. It is very important to take all of the antibiotics exactly as your healthcare provider prescribes.

You should also call your provider if an infection doesn’t start to clear up within a few days of taking a prescribed antibiotic. You may need to go to the hospital for stronger intravenous antibiotics.



Prevention

How can I prevent MRSA infections?

You can lower your risk of getting MRSA by taking these steps:

  • Keep wounds clean and bandaged.
  • Don’t share personal items like towels and razors.
  • Place a towel on a locker room bench before sitting on it naked.
  • Regularly wash sheets, towels and workout clothes in the recommended water temperature. (Hot water isn’t necessary.) Dry everything in a dryer. You don’t need to use bleach or wash potentially contaminated items separately.
  • Shower immediately after working out or participating in activities that increase your risk of MRSA exposure.
  • Use disinfecting sprays that kill germs to wipe down high-touch areas like light switches, remote controls and athletic equipment. Check labels to find disinfectants that kill staph bacteria.
  • Wash hands with hot water and soap for at least 20 seconds. Use alcohol-based hand sanitizer when hand-washing isn’t possible.



Outlook / Prognosis

What is the prognosis (outlook) for people who have a MRSA infection?

Most MRSA skin infections clear up with treatment. MRSA is most dangerous if it enters the bloodstream. MRSA bloodstream infections can be serious. A bloodstream infection requires immediate medical attention.



Living With

When should I call the doctor?

You should call your healthcare provider if you experience:

  • Fever and chills.
  • Infection that doesn’t improve after a few days of antibiotics.
  • Rash.
  • Signs of skin infection (abscesses or boils).

What questions should I ask my doctor?

You may want to ask your healthcare provider:

  • What is the best treatment?
  • What are treatment side effects?
  • What should I do if I forget to take the medicine?
  • What are signs of complications of the infection?

A note from Cleveland Clinic

Many people carry Staph aureus or MRSA bacteria in their skin or noses for varying periods of time and never know it. This is not a problem. In some people, MRSA bacteria cause painful skin infections or more serious invasive infections. People in hospitals or nursing homes are at increased risk for MRSA infections. But you can pick up the bacteria in community settings, too. Contact your healthcare provider if you develop a skin infection or show signs of MRSA.

Staphylococcus aureus Throat Colonization Is More Frequent than Colonization in the Anterior Nares

J Clin Microbiol. 2006 Sep; 44(9): 3334–3339.

Peter Nilsson

Department of Clinical Microbiology and Infection Control, The County Hospital of Halmstad, Halmstad, Sweden

Torvald Ripa

Department of Clinical Microbiology and Infection Control, The County Hospital of Halmstad, Halmstad, Sweden

Department of Clinical Microbiology and Infection Control, The County Hospital of Halmstad, Halmstad, Sweden

*Corresponding author. Mailing address: Department of Clinical Microbiology and Infection Control, The County Hospital of Halmstad, S-30185 Halmstad, Sweden. Phone: 46 35 136549. Fax: 46 35 131869. E-mail: [email protected]

Received 2006 Apr 26; Revised 2006 Jun 10; Accepted 2006 Jun 24.

Copyright © 2006, American Society for MicrobiologyThis article has been cited by other articles in PMC.

Abstract

The aim of this study was to determine the frequency and persistence of Staphylococcus aureus carriage in the throat in relation to anterior naris carriage. By use of a sensitive enrichment broth, S. aureus was cultured from the two sites from 259 patients upon admission to an orthopedic ward and from 87 staff members of the same ward. The throat was the most common carriage site in both groups. Forty percent of the patients and 54% of the staff were positive for S. aureus in the throat, compared to 31% and 36%, respectively, in the anterior nares. To determine the persistence of carriage, 67 individuals were repeatedly sampled from the anterior nares and the throat over 2 years (5 to 10 sampling occasions; mean, 7.8). The majority, 58% (39/67), were defined as persistent carriers of S. aureus, considering culture results from both sites. Of the 39 persistent carriers, 15 individuals were culture positive from only the throat on more than half of the sampling occasions (these are called preferential throat carriers) while only 5% (two individuals) were preferential anterior naris carriers by use of the same definition. Typing of the collected S. aureus isolates by pulsed-field gel electrophoresis revealed that the same strain of S. aureus was present, over time, in the throat of an individual at least to the same extent as in the anterior nares. Throat carriage was at least as persistent as carriage in the anterior nares.

Besides being a major human pathogen (14), Staphylococcus aureus colonizes large proportions of human populations (27). The anterior nares are considered to be the primary colonization site (11, 14), and approximately 30% of healthy people carry the bacteria in their anterior nares. Carrier rates close to 60% have been described previously for certain populations (11). The human throat is less well studied as a carriage site, and various isolation rates have been reported previously. Boe et al. reported an isolation rate of 31% in patients admitted to a medical ward (4), and Uemura et al. reported an isolation rate of 29% in a group of healthy adult volunteers (22). Berkovitch et al. found the bacteria in the throats of 10% of healthy children under the age of 2 years (3). There have also been observations of higher-than-expected rates of methicillin-resistant S. aureus (MRSA) in infants’ throats (9). The perineal region seems to be a common carriage site but is rarely the only site to be colonized (4). Also, carriage in various skin areas has been described previously. However, this seems to be secondary to carriage or infection at other sites since removal of nasal colonization with topical treatment in most cases eliminates skin carriage (16, 20).

Three main carriage patterns have been described when individuals are repeatedly sampled in the anterior nares for S. aureus over longer periods. Between 6 and 60% have been reported never to carry the organism (noncarriers), and 14 to 33% have been repeatedly culture positive (persistent carriers). The remaining individuals yield positive cultures from time to time and are characterized as occasional or intermittent carriers (6, 10, 27). The variation between studies might be due to different sampling techniques and/or variations in the definitions of the different carrier states. Persistent carriers tend to carry the same phage type or genotype over time more often than the intermittent and occasional carriers (6, 27). To our knowledge, the carriage pattern over time has not been investigated for any sampling site other than the anterior nares.

The aim of this study was to determine the frequency and persistence of throat carriage in relation to that of anterior naris carriage of S. aureus. We used a sensitive culture technique to minimize errors arising from low recovery rates. All isolates were genotyped by SmaI pulsed-field gel electrophoresis (PFGE).

MATERIALS AND METHODS

Patients and

S. aureus sampling.

All samples were collected as a routine infection control surveillance scheme at the County Hospital of Halmstad, Sweden.

Specimens were collected using a rayon-tipped swab with Amies charcoal transport medium (114C.US) (Copan, Italy). The anterior nares were sampled by rotating the swab tip in both nostrils, and the throat was sampled by rotating the swab tip on both tonsils.

Patients admitted to the orthopedic ward at the County Hospital of Halmstad, Sweden, from March to September 2003 were sampled in both the anterior nares and the throat by staff upon arrival and investigated for the presence of S. aureus. Among the 259 patients sampled, 62% were females, with a mean age of 74.4 years, and 38% were males, with a mean age of 64.3 years. Twenty patients were sampled in March, 72 in April, 57 in May, 20 in June, 17 in July, 38 in August, and 35 in September.

Hospital staff in the orthopedic ward were instructed to sample themselves by rotating a swab in both anterior nares and a separate swab on both tonsils. Samples were taken from all staff members on duty during 1 week each month between March and September 2003 (except for June and July, when the ward was closed most of the time) and then during 1 week in November 2003, March 2004, and April 2005, nine occasions in total. Not all staff members were available at all times, and new staff members were included during the study period. In total, 87 individual staff members were sampled at the orthopedic ward (70 females, with a mean age of 40 years, and 17 males, with a mean age of 34 years).

A group of 67 individuals were repeatedly sampled from the anterior nares and throat for up to 24 months. The group consisted of 34 staff members from the orthopedic ward and 33 staff members from the Department of Clinical Microbiology and Infection Control at the County Hospital of Halmstad, Sweden. Of these 67 individuals, 63 were females and 4 were males, with a mean age of 44 years at the time of the first sampling occasion. They were sampled at least five times during the period between March 2003 and March 2005 (mean, 7.8 times; range, 5 to 10). In total, 384 isolates of S. aureus were collected and their clonal relationships were determined by PFGE analysis.

S. aureus isolation.

All swab samples were incubated for 16 to 18 h at 37°C in a shaker (100 rpm) under aerobic conditions in 3 ml enrichment broth with the following composition: 15.0 g proteose peptone (Oxoid, Basingstoke, England), 2.5 g liver digest (Oxoid), 5.0 g yeast extract (Oxoid), 25.0 g NaCl, 10.0 g mannitol, 16 mg/liter phenyl red, and 8 mg aztreonam in a final volume of 1 liter (final pH, 7.0 ± 0.1). A portion (10 μl) of the broth was then plated on a blood agar plate and incubated at 37°C overnight. Suspected colonies were isolated on a blood agar plate and identified as S. aureus by use of DNase testing and a Staphaurex latex test (Remel Europe Ltd., Dartford, England). When these methods disagreed, the presence of the thermostable nuclease gene was assayed by PCR as described by Nilsson et al. (15). One single isolate of S. aureus was isolated from each sample. The possible presence of more than one strain in each sample was not taken into account. All isolated strains of S. aureus were collected and stored at −70°C for further analysis.

PFGE.

The strains collected in the study were analyzed by PFGE as described by Bannerman et al. (2). The banding patterns from the isolates were analyzed using Molecular Analyst software, version 1.6 (Bio-Rad Laboratories, Hercules, Calif.), with the unweighted-pair group clustering method using average linkages and Dice coefficient. Strains with more than 80% similarity were grouped into clonal groups and named with a capital letter from A to X. Isolates from the same individual but collected on different occasions were also compared to each other. In all cases, when they belonged to the same clonal group, they were within three band differences (21). This means that isolates from different individuals but named with the same letter had at least 80% similarity by the computerized clustering analysis, while isolates from one individual and with the same name had <4 band differences.

Calculations and definitions.

Carrier index (CI) was defined as the number of positive swabs divided by the total number of swabs for each individual, as described by Eriksen et al. (6). However, the definitions of carrier states differ from those used by Eriksen et al. In our work, a persistent carrier is defined as an individual with a CI of >0.5; for an occasional carrier, 0 < CI ≤ 0.5; and for a noncarrier, CI = 0. The study period was defined as the number of months between the first and last samples, and the carrier time was the number of months between the first and last positive samples during the study period for an individual. The time an individual carried the same strain was defined as the number of months an S. aureus strain within three band differences by PFGE was sampled from the individual. Intervening negative samples were tolerated, but intervening findings of strains with more than three band differences by PFGE were not.

RESULTS

S. aureus carriage in patients and staff.

During the study period from March 2003 to September 2003, 259 patients admitted to an orthopedic ward were sampled at admittance, both in the anterior nares and in the throat. The rates of S. aureus isolation from the different sites are presented in Table . In total, S. aureus was isolated from 125 of the 259 patients (48%) from either of the sites. The most common site of isolation was the throat (40% of the patients), followed by the anterior nares (31% of the patients). The difference in isolation frequency between the anterior nares and the throat was statistically significant (P = 0.037). If anterior nares had been the only screening site, 64% (80/125) of S. aureus carriers would have been identified, while sampling from only the throat would have identified 83% (104/125). No significant differences between men and women concerning isolation rates from the different sites were found (data not shown).

TABLE 1.

S. aureus isolation rates in the anterior nares and the throat among patients and staff of an orthopedic ward

Result for naresa Result for throata No. (%) of individuals with result


Patients Staff Patients and staff
Pos Pos 59 (23) 24 (28) 83 (24)
Pos Neg 21 (8) 7 (8) 28 (8)
Neg Pos 45 (17) 23 (26) 68 (20)
Neg Neg 134 (52) 33 (38) 167 (48)
Total 259 87 346

During the study period, all members of the staff on the ward were prompted to sample anterior nares and throat each month. In Table , we have summarized the rates of S. aureus isolation from the first sampling occasion of the 87 staff members. Sixty-two percent (54/87) were positive in either of the sites. As with the patient group, the most common site of isolation was the throat (54% positive, compared to 36% in the anterior nares; P = 0.023).

In total, 346 patients and staff members were screened; 32% were positive in the anterior nares (95% confidence interval, 27 to 37%) and 44% were positive in the throat (95% confidence interval, 38 to 49%). The difference in isolation frequency between the anterior nares and the throat was statistically significant, with a P value of 0.003.

Figure shows the isolation rates in staff and patients for each month. The total numbers of individuals sampled were 67 in March, 114 in April, 99 in May, 82 in August, and 76 in September. No data are presented for June and July because the ward was closed during most of that time. The overall carriage rate was highest in March (66%) and lowest in August (48%). Also, throat carriage tended to drop, from 58% to 38% over the same period. On every sampling occasion, throat carriage was more frequent than nasal carriage.

S. aureus isolation rates among staff and patients at the orthopedic ward from March to September 2003.

Carriage over time.

To study S. aureus carriage patterns over time, a group of 67 individuals was repeatedly sampled from the anterior nares and the throat for up to 24 months. In total, 521 swabs were taken from anterior nares and throat; 152 (29%) turned out positive for S. aureus in the anterior nares and 232 (45%) in the throat.

The 67 individuals were grouped into persistent carriers, occasional carriers, and noncarriers based on CIs calculated from culture results from the anterior nares alone, results from the throat alone, and the combined results from both sites (Table ). Based on the results from the anterior nares alone, 25% (17/67) of the individuals were classified as persistent carriers, compared to 58% (39/67) when the results from the throat swabs were added. The culture results on each sampling occasion for the 39 individuals classified as persistent carriers are presented in Fig. .

S. aureus carriage in the anterior nares and the throat among 39 persistent carriers. A red box represents positive results only from the anterior nares on that sampling occasion, an orange box positive from the anterior nares and the throat, a yellow box positive only from the throat, a blue box negative in both locations, and a gray box means no sample was taken. The letter(s) in each box designates the clonal type(s) of the isolated S. aureus strains as determined by PFGE. In orange boxes (positive in anterior nares and throat), the first letter gives the clonal type in the anterior nares and the second in the throat. “$” represents a clonal type unique for that individual. Sampling times are indicated at the top with the following abbreviations: M3, March 2003; A, April 2003; Mj, May to June 2003; Jn, June 2003; J, July 2003; Au, August 2003; S, September 2003; O, October 2003; N, November 2003; D, December 2003; J, January 2004; F, February 2004; M4, March 2004; A5, April 2005.

TABLE 2.

Results from 67 individuals repeatedly sampled in the anterior nares and the throat at least five times over 25 monthsa

Group No. (%) of individuals in group, classified by culture from:


Nares Throat Nares or throat
Persistent carriers 17 (25) 31 (46) 39 (58)
Occasional carriers 21 (31) 18 (27) 14 (21)
Noncarriers 29 (43) 18 (27) 14 (21)

Based on the most frequent carriage site over time, the 39 persistent carriers could be grouped into the following groups: preferential anterior naris carriers, i.e., individuals positive in only anterior nares on more than half of the sampling occasions; preferential throat carriers, i.e., individuals positive in only throat on more than half of the occasions; preferential anterior naris/throat carriers, i.e., individuals positive in anterior nares and throat on more than half of the occasions; and indeterminable carriers, persistent carriers with a mixed pattern of carriage based on the sampling site. With these definitions, 5% of the persistent carriers were preferential anterior naris carriers (individuals 1 and 2 [Fig. ]), 38% were preferential throat carriers (individuals 3 to 17 [Fig. ]), 28% were preferential anterior naris/throat carriers (individuals 18 to 28 [Fig. ]), and another 28% had a mixed pattern of carriage based on sampling location (individuals 29 to 39 [Fig. ]) (Table ).

TABLE 3.

Results from 39 S. aureus persistent carriers grouped by most frequent carriage site(s)

Groupa No. (%) of individuals in group Avg no. of samplings Avg CI Avg study period (mo) Avg carrier time (mo) Avg no. of mo same strain carried in:


Nares Throat
Pref. naris carriers 2 (5) 7.0 0.8 25 25 15 0
Pref. throat carriers 15 (38) 7.8 0.8 21 17 0 13
Pref. naris/throat carriers 11 (28) 7.8 1.0 25 25 21 19
Indeterminable carriers 11 (28) 7.1 0.8 22 18 6 7
All 39 7.6 0.8 23 20 8 12

PFGE analysis of the collected S. aureus isolates showed that carriage in the throat was stable over time. The 39 persistent carriers spent, on average, 20 months as S. aureus carriers during the 25-month study period. The average time spent with the same strain in the anterior nares was 8 months, compared to 12 months in the throat (Table ). The 11 preferential anterior naris/throat carriers spent, on average, 21 months with the same strain in the anterior nares, compared to 19 months in the throat. Four of the individuals classified as preferential throat carriers carried the same strain of S. aureus throughout the study period of 25 months (Fig. ) (individuals 5, 9, 12, and 13 [Fig. ]). The majority of the preferential anterior naris/throat carriers carried the same strain of S. aureus at both sampling sites, but three individuals maintained separate strains in the anterior nares and the throat over several months (individuals 18, 21, and 22 [Fig. ]). In total, the 39 persistent carriers were positive in anterior nares and throat on 94 sampling occasions. Different strains of S. aureus were recovered from the two sites in an individual on 26/94 sampling occasions.

SmaI PFGE band patterns for S. aureus strains isolated from four individuals defined as preferential throat carriers (individuals 5, 9, 12, and 13 [Fig. ]). Sampling times are indicated above the samples with the following abbreviations: m3, March 2003; A, April 2003; M, May 2003; J, June 2003; Au, August 2003; S, September 2003; N, November 2003; m4, March 2004; a5, April 2005. Individual 5 was positive in the anterior nares and the throat on two occasions. The samples from the anterior nares are underlined.

DISCUSSION

S. aureus was isolated more frequently from the throat than from the anterior nares in two unrelated populations. Since the 259 patients were sampled upon admission to an orthopedic ward, their colonization status is probably unrelated within the group or to the 87 members of the staff in the same ward who were also sampled. The mean age of the patient group was much higher than the mean age of the staff group. Females were overrepresented in both groups, but no significant difference in isolation rates was observed between males and females in the patient group (data not shown). We therefore do not think our findings are related to sex or age, and we do not think the findings present a phenomenon in one single population.

Our results demonstrate that S. aureus rarely was carried only in the anterior nares. If the anterior nares were colonized, the bacteria were, with few exceptions, also present in the throat. This could have some important implications. Since anterior naris carriage of S. aureus is a well-documented risk factor for S. aureus infections (11), prophylactic decolonization of carriers has been tried with different patient groups (12). The spread of MRSA among patients and staff in health care institutions also calls for effective regimens for decolonization. A commonly used protocol includes topical treatment of the anterior nares with mupirocin, sometimes combined with application of disinfecting agents for the skin. For most patient groups, studies have not been able to show significant reduction of infection (12, 26). Some exceptions are hemodialysis patients (5), peritoneal dialysis patients (1), and general surgery patients (18). Recolonization with the same strain of S. aureus after the treatment period has been observed to occur (17, 27). The source of bacteria in these cases could be other carriage sites on the patient (for example, the throat) or people or items in the patient’s environment. Repeated treatment has been shown to result in development of resistance to mupirocin (13, 23). During treatment of the anterior nares, low concentrations of mupirocin in the throat have been observed (24). Furthermore, the effect of nasal mupirocin treatment on throat colonization has been questioned (8, 25). Taken together, this might mean that the standard protocol for decolonization of S. aureus might create a situation favoring development of mupirocin resistance in the throats of treated individuals. Residual bacteria in the throat could also be one reason (of several) for recolonization after treatment. Kluytmans and Wertheim proposed that one way to increase efficacy of future treatment regimens could be to eliminate S. aureus also from extranasal sites (12). Considering our results, a treatment also targeting the throat might reduce problems with mupirocin resistance and recolonization and possibly lead to better efficacy in terms of infection reduction.

A large group was preferentially colonized only in the throat, in most cases with the same strain over several months and even years. Obviously, these individuals would not have been detected as carriers if only the anterior nares had been sampled. Nasal carriage seems to have a central role in S. aureus epidemiology and pathogenesis of infection (11, 12), and the risks associated with throat carriage are largely unknown. Half of the preferential throat carriers were culture positive in the anterior nares at least once during the study period. Further studies are needed to determine what risk this group of S. aureus carriers constitutes in terms of spread of the organism and infection. Meanwhile, it seems reasonable to use an enrichment broth (15) and to include the throat when trying to identify MRSA and S. aureus carriers in different situations. If only one site is to be sampled, the throat is probably a better choice than the anterior nares.

In this study, 39 of 67 individuals, or close to 60%, were characterized as persistent carriers. This is roughly twice or even three times as many as the number described earlier (27). This discrepancy is probably due to the combination of a sensitive screening technique, the inclusion of the throat as a carriage site, and a different definition of persistent carriage (CI > 0.5). The change of definition is mainly due to the group of preferential throat carriers. Intervening negative samples reducing the CI for this group were probably due to false-negative results and not the fact that the individual had become a noncarrier. This conclusion seems reasonable since in most cases the same strain was recovered before and after negative sampling occasions. The observed lower CI for preferential throat carriers means that sampling of the throat yields fewer organisms than sampling of the anterior nares either because the sampling technique is suboptimal or, more probably, because there are small numbers of organisms present at the sampling site. A probable reason for the higher-than-expected rate of S. aureus in the throat (compared to the rate in the anterior nares) is that we increased the sensitivity by using an enrichment broth. Usage of the same broth with methicillin increased the rate of MRSA isolation by 35% in a previous study (15).

We observed almost 20% higher carrier rates of S. aureus during the spring months of March and April than in the summer month of August. The higher rate was more pronounced for the throat. Since colonization and adherence of S. aureus (and other bacteria) to the pharynx increase during viral infection (7, 19), an explanation might be that the peak of upper respiratory tract infections during spring in Sweden results in a greater number of individuals colonized. Alternatively, viral infections cause an increase in the number of bacteria in the throat, thereby increasing the chance of a positive culture. This seasonal variation is probably also the explanation for the observation of a more than 10% higher carriage rate among staff than among patients. The first samples from most of the staff were taken in March, but patients were sampled from March through September. To our knowledge, a seasonal variation of S. aureus carriage has not been described before but deserves further attention.

In conclusion, the throat has to be considered as an important carriage site for S. aureus and should be included when screening for S. aureus, including MRSA. Our results also show that S. aureus carriage in the anterior nares in most cases indicates presence of the organism in the throat, although in lower numbers. This has to be taken into account when designing decolonization protocols.

Acknowledgments

This project was funded in part by a research grant from the County Council of Halland, Sweden.

We are grateful to the staff at the orthopedic ward and the clinical microbiology department of the County Hospital of Halmstad, Sweden, for help with sample collection. The pulsed-field gel electrophoresis experiments were performed with great skill by microbiologist Usama Nazar.

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Methicillin-Resistant Staphylococcus aureus (MRSA) – Medical District of Southern Nevada

What is MRSA?

MRSA stands for methicillin-resistant Staphylococcus aureus, a bacterium that is resistant to most antibiotics commonly used for staphylococcal infections. These drugs include:

  • Methicillin
  • Oxacillin
  • Nafcillin
  • Cephalosporins
  • Imipenem
  • Other beta-lactams

What is the MRSA reservoir?

MRSA can affect humans in two different ways:

  • Colonization
  • Infectious Disease

When a person carries bacteria on the skin or nose without showing signs or symptoms of infection, the person is considered colonized.

If a person has signs of an infection with MRSA, the person is considered infected.

Signs of MRSA infection include:

  • Abscesses
  • Infected infections
  • Pneumonia
  • Respiratory infections
  • Blood, stool, or urinary tract infections

How does MRSA spread from person to person?

MRSA is most commonly spread from person to person through direct contact.For example, in healthcare settings, MRSA is most commonly spread from patient to patient by the hands of healthcare professionals.

How can you stop the spread of MRSA?

The single most effective way to prevent the spread of infection is through proper hand washing, i.e. washing with soap and water for at least 20 seconds and rinsing with warm running water. Hands should be washed both before and after contact with the patient.

Other measures include:

  • Use protective equipment to avoid contact with body fluids from another person
  • Gloves should be worn for all changes of clothing
  • Protective equipment should be disposed of after use
  • Hands should be washed after removing protective equipment
  • Separate clean and dirty laundry

Follow a daily environmental cleaning schedule, including disinfecting handrails, IV stands and telephones.Follow your facility’s isolation procedures.

Is MRSA a bigger problem than other infections?

The answer is yes and no. MRSA is not a “super bug” and is no more virulent than Staphylococcus aureus. However, all infections are of interest to healthcare workers and patients.

MRSA is of particular importance because MRSA infections are very difficult to treat. Typically, MRSA infections are treated with an intravenous drug called vancomycin.The side effects of this drug can be quite serious, especially in elderly or immunocompromised patients.

In addition, patients with invasive devices such as catheters, nasogastric or gastrointestinal tubes, or intravenous lines are much more likely to acquire infections, including MRSA.

What can be done to prevent the spread of MRSA?

  1. Inform the patient, if possible, of his / her condition.
  2. Observe universal precautions. Keep drainage lesions covered.
  3. If possible, use established cohorts to care for patients with MRSA. If individual rooms are not available, select patients with MRSA. Make sure that a patient with an MRSA infection does not share a room with a patient prone to infection, as described above.

Where can I get more information?

Contact the Director of the Nursing or Health Department of Southern Nevada, Department of Epidemiology at (702) 759-1300.

Staphylococcus aureus – a common hospital infection

According to official statistics, the number of deaths from one of the most dangerous hospital infections – MRSA (methicillin-resistant Staphylococcus aureus) has increased significantly in recent years, and the number of cases of infection is constantly growing.

What is Staphylococcus aureus (MRSA)?

Staphylococcus is a common family of bacteria. They are present in most people and are part of the normal microflora of the skin, mucous membranes, and the lower intestine.Carriage of staphylococcus is common among medical personnel.

Staphylococcus infection in hospitals and maternity hospitals occurs by airborne droplets and through the contaminated hands of doctors. You can get infected through open wounds, burns, eyes, skin, blood. Transmission of infection is possible with instruments, catheters, dressings, care items, and food.

MRSA is a “modification” of Staphylococcus aureus that is resistant to one or more antibiotics.To date, researchers have identified 17 types of MRSA with varying degrees of antibiotic resistance.

Treatment of MRSA requires the use of a higher dose of drugs, an increase in the duration of treatment, or the use of an alternative antibacterial agent to which this type of MRSA is still susceptible.

MRSA infection can cause a wide range of symptoms depending on the organ being infected. Signs of infection are redness, swelling, and tenderness of the infected area.The clinical manifestations of staphylococcal diseases are diverse – from skin diseases and pneumonia to meningitis and sepsis.

Why does MRSA exist?

Natural selection is still the basic principle of the development of all living things. And bacteria live in this world much longer than we do, so they are especially successful in this. In addition, the genes of bacteria are constantly changing to resist their main enemy – the antibiotic.

The weaker types of bacteria, when faced with an antibiotic, die, while the more resistant ones simply ignore the medicine.This means that the next time you may encounter staphylococcus, which successfully survived the meeting with the antibiotic, and, therefore, acquired resistance to it.

That is why doctors always advise patients to drink the entire course of antibiotics to the end. If the patient does not complete the course of treatment, then most of the bacteria will die, but not all. The survivors acquire resistance (i.e., resistance) to antibiotics. And each subsequent mutation only increases the bacteria’s ability to survive.

The use of a huge number of antibiotics in hospitals and maternity hospitals causes a huge number of mutations in staphylococcus, thereby increasing its resistance to drugs.

Why is it so dangerous?

The fact that in hospitals staphylococcus is infected more often than outside hospitals can be explained.

  • First, hospital residents are generally weaker than the general population, making them more vulnerable to infection.
  • Secondly, the conditions in hospitals, where there are large numbers of people in small areas, are an excellent environment for the transmission of infections.MRSA infection can be very dangerous for debilitated patients and newborns, especially if it is not recognized and treated with the right antibiotics in time.

What are the prospects?

The reports of an increase in infections and deaths due to MRSA are of great concern to doctors. It may happen that a type of staphylococcus is formed that is resistant to all antibiotics. There is already a VRSA or vancomycin-resistant vancomycin-resistant Staphylococcus Aureus.And in the UK, GISA or glycopeptide-resistant Staphylococcus aureus was recorded, respectively, resistant to glycopeptides.

Although new antibiotics are constantly being developed, pessimistic experts believe that it is only a matter of time before it becomes resistant to them.

One of the main reasons for the emergence of drug-resistant microbes is the abuse of antibiotics. Quite often the doctor prescribes antibiotics for patients with a viral infection.However, antibiotics have no effect on viruses. But bacteria in the body from the use of antibiotics feel great – mutate and multiply. Therefore, doctors are now advised to reduce the prescription of antibiotics.

Improving hospital hygiene is an important factor in protecting patients from MRSA. Manual examinations in hospitals are now doing more harm than good, as they spread the infection. The solution to this problem seems to be a thorough hand treatment after each patient.There is also a proposal to introduce a special position of a nurse responsible for cleanliness in the hospital staff (in Russian health care facilities, these duties are usually assigned to the head nurse of the department).

Although the question of whether dirty hands are the source of staphylococcus reproduction is controversial enough. Some people recall that in previous centuries, people – for the most part – did not even know what a bacterial infection was. He took the carrot out of the garden, rinsed it in a puddle and ate it. And no one died from this, a maximum of a couple of days were plagued by an upset stomach.This was because human immunity was naturally stimulated. Now, in the “sterile” conditions of maternity hospitals, where a person goes immediately after birth, this does not happen. Immunity decreases, therefore, susceptibility to various kinds of bacteria, which previously were not even pathogenic, increases.

While doctors are looking for a way to combat MRSA, the number of infections is steadily increasing. And many experts agree that it may take a very major scientific breakthrough, akin to the discovery of penicillin, for humans to be able to effectively resist resistant bacteria.

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  • Alshaya MA., Almutairi NS., Shaath GA., Aldosari RA., Alnami SK., Althubaiti A., Abu-Sulaiman RM. Original Article – Surgical site infections following pediatric cardiac surgery in a tertiary care hospital: Rate and risk factors. // J Saudi Heart Assoc – 2021 – Vol33 – N1 – p.1-8; PMID: 33880325
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How Science Fights Antibiotic Resistant Bacteria – Rossiyskaya Gazeta

We thought that after the discovery of penicillin we would no longer be afraid of germs. But we were wrong. It looks like a real war. Man invents more and more new means of defense against bacterial attacks. In response, microorganisms improve weapons, train fighters, use camouflage and sabotage groups. The problem of antibiotic-resistant infections has become so serious that recently a special meeting of the UN General Assembly was devoted to it.According to the reported data, at least 700,000 people die each year due to drug-resistant infections. Non-exterminating microbes are on a par with global climate change and other problems of a planetary scale.

In the winter of 2003, Ricky Lannetti, a successful 21-year-old soccer player, developed a cough followed by nausea. A few days later, Ricky’s mother made her son see a doctor. All the symptoms pointed to a flu virus, so he did not prescribe antibiotics to Ricky, because they kill bacteria, not viruses.But the disease did not go away, and Ricky’s mother took Ricky to a local hospital – by this time the boy’s kidneys were already failing. He was prescribed two powerful antibiotics: cefepime and vancomycin. But less than a day later, Ricky died. Tests have shown that the killer was methicillin-resistant Staphylococcus aureus (MRSA), a toxic bacterium that is resistant to multiple antibiotics.

Strains such as MRSA are now called super microbes. Like horror heroes, they mutate and acquire superpowers, allowing them to resist enemies – antibiotics.

End of the antibiotic era

In 1928, returning from vacation, the British biologist Alexander Fleming discovered that the Petri dishes with bacterial cultures left by him through inattention were overgrown with mold. A normal person would take it and throw it away, but Fleming began to study what happened to the microorganisms. And I found out that in those places where there is mold, there are no staphylococcal bacteria. This is how penicillin was discovered.

Fleming wrote: “When I woke up on September 28, 1928, I certainly did not plan to revolutionize medicine by discovering the world’s first antibiotic, but I suppose that is what I did.”The British biologist received the Nobel Prize in Physiology or Medicine for the discovery of penicillin in 1945 (together with Howard Flory and Ernst Cheyne, who developed the technology for purifying the substance).

Modern man is accustomed to the fact that antibiotics are affordable and reliable helpers in the fight against infectious diseases. Sore throat or a scratch on the arm does not cause panic in anyone. Although two hundred years ago, this could lead to serious health problems and even death. The 20th century was the era of antibiotics.Together with vaccinations, they saved millions, maybe billions of people who would certainly have died from infections. Vaccines, thank God, are working properly (doctors do not seriously consider the social movement of vaccine fighters). But the era of antibiotics seems to be coming to an end. The enemy is advancing.

How super microbes are born

One-celled creatures were the first to conquer the planet (3.5 billion years ago) – and continuously fought with each other. Then multicellular organisms appeared: plants, arthropods, fish … Those who retained their single-celled status thought: what if we put an end to civil strife and begin to seize new territories? Inside multicellular organisms it is safe and there is a lot of food.Attack! Microbes moved from one creature to another, until they got to a person. True, if some bacteria were “good” and helped the owner, others only caused harm.

People resisted these “bad” microbes blindly: they introduced quarantine and were engaged in bloodletting (for a long time this was the only way to fight all diseases). It was only in the 19th century that it became clear that the enemy has a face. Hands began to be washed, hospitals and surgical instruments were treated with disinfectants.After the discovery of antibiotics, it seemed that humanity received a reliable means of fighting infections. But bacteria and other unicellular organisms did not want to leave the warm place and began to acquire resistance to drugs.

The super microbe can resist antibiotics in different ways. For example, it is capable of producing enzymes that degrade the drug. Sometimes he is just lucky: as a result of mutations, his membrane becomes invulnerable – a shell on which drugs used to inflict a crushing blow.Resistant bacteria are born in different ways. Sometimes, as a result of horizontal gene transfer, bacteria that are harmful to humans are borrowed from useful defenses against drugs.

Another, more realistic depiction of methicillin-resistant Staphylococcus aureus (MRSA). It spreads more and more every year, especially inside hospitals and among people with weakened immune systems. According to some reports, in the United States, this microbe kills about 18 thousand people annually (it is still impossible to determine the exact number of cases and deaths).Photo: “Schrödinger’s cat”

Sometimes a person himself turns the body into a center for training killer bacteria. Let’s say we treat pneumonia with antibiotics. The doctor prescribed: you need to take the medicine for ten days. But on the fifth, everything goes away and we decide that it’s enough to poison the body with all kinds of nasty things and stop taking it. By this time, we have already killed some of the bacteria least resistant to the drug. But the strongest survived and got the opportunity to reproduce. So, under our careful guidance, natural selection began to work.

“Drug resistance is a natural phenomenon of evolution. Under the influence of antimicrobial drugs, the most sensitive microorganisms die, but the resistant ones remain. And they begin to multiply, passing on the resistance to their offspring, and in some cases to other microorganisms,” explains the World Health Organization.

– The fact that many antibiotics can be bought over the counter without a doctor’s prescription contributes to the emergence of drug resistance. And the doctors themselves are often reinsured and unreasonably prescribe these drugs.Let’s say a person’s temperature rises – they immediately give him antibiotics without doing tests and without figuring out what caused it, – says the professor of the MMSU Yuri Vengerov (infectious disease doctor, doctor of medical sciences, co-author of the books “Infectious and Parasitic Diseases”, “Infectious diseases “,” Tropical diseases. A guide for doctors “,” Lectures on infectious diseases “). – The selection of microbes is especially active in hospitals. People with various infections come into contact there, and many antibiotics are taken there.As a result, hospital pneumonia and other nosocomial infections are now widespread. We are talking not only about bacterial diseases, but also, for example, about fungal diseases. Among mushrooms, already 30% have acquired drug resistance.

Unicellular attack

In the fall of 2016, a meeting of the UN General Assembly is taking place in New York, which is attended by representatives of 193 countries, that is, virtually the entire planet. Usually issues of war and peace are discussed here. But now we are not talking about Syria, but about microbes that have developed resistance to drugs.

“World leaders have shown unprecedented attention to the problem of containing antimicrobial-resistant infections. This means that bacteria, viruses, parasites and fungi develop the ability to resist the action of drugs that were previously used to destroy them and treat the diseases they cause. pledged to take large-scale and coordinated action to tackle the root causes of antimicrobial resistance across a range of areas, primarily health, animal health and agriculture.This is only the fourth time in history that the health issue has been raised by the UN General Assembly, “the WHO website reports.

The forecast is gloomy. “Patients are finding it increasingly difficult to recover from infections as the level of resistance of pathogens to antibiotics and, even worse, reserve antibiotics is steadily increasing. Combined with the extremely slow development of new antibiotics, this increases the likelihood of respiratory, skin, urinary and urinary infections. pathways, blood flow can become incurable, and therefore fatal, “explains Dr. Nedret Emiroglu from the WHO European Office.

– I would definitely add malaria and tuberculosis to this list of diseases. In recent years, it has become increasingly difficult to deal with them, since the pathogens have acquired resistance to drugs, says Yuri Vengerov.

Similarly, Keiji Fukuda, WHO Assistant Director-General for Health Safety, says: “Antibiotics are losing their effectiveness, so common infections and minor injuries that have healed for decades can now kill again.”

Model of a bacteriophage that infects a microbe. These viruses invade bacteria and cause them to lysis, that is, dissolution. Although bacteriophages were discovered at the beginning of the 20th century, it is only now that they have begun to be included in official medical reference books. Photo: “Schrödinger’s cat”

– Bacteria began to resist especially zealously when antibiotics began to be used in huge quantities in hospitals and in agriculture, – assures biochemist Konstantin Miroshnikov (Doctor of Chemistry, Head of the Laboratory of Molecular Bioengineering at the Institute of Bioorganic Chemistry.Academikov M.M. Shemyakin and Yu.A. Ovchinnikov RAS). “For example, to stop diseases in chickens, farmers use tens of thousands of tons of antibiotics. Often for prevention, which allows bacteria to get to know the enemy better, get used to it and develop resistance. Now the use of antibiotics has begun to be limited by law. I believe that public discussion of such issues and further tightening of the law will slow down the growth of resistant bacteria. But they will not stop.

– The possibilities of creating new antibiotics are almost exhausted, and the old ones are failing.At some point, we will be powerless against infections, – Yuri Vengerov admits. – It is also important to understand that antibiotics turn into a medicine only when there is a dose that can kill microbes, but at the same time not harm a person. The likelihood of finding such substances is less and less.

Has the enemy won?

The World Health Organization periodically publishes panicky statements: they say, first-line antibiotics are no longer working, more modern ones are also close to surrender, and fundamentally new drugs have not yet appeared.Is the war lost?

“There are two ways to fight microbes,” says biologist Denis Kuzmin (candidate of biological sciences, employee of the educational and scientific center of the IBCh RAS). – First, to look for new antibiotics that act on specific organisms and targets, because it is the “large caliber” antibiotics, which infect a whole bunch of bacteria at once, cause the accelerated growth of resistance. For example, it is possible to design drugs that begin to act only when bacteria with a certain metabolism enter inside.Moreover, manufacturers of antibiotics – producing microbes – need to be looked for in new places, more actively to use natural sources, unique geographic and ecological zones of their habitat. Secondly, it is necessary to develop new technologies for obtaining and cultivating antibiotic producers.

These two methods are already being implemented. New methods of finding and testing antibiotics are being developed. Microorganisms that can become a weapon of a new generation are searched for everywhere: in rotting plant and animal remains, silt, lakes and rivers, air … For example, scientists managed to isolate an antimicrobial substance from the mucus that forms on the frog’s skin.Remember the ancient tradition of putting a frog in a jar of milk to keep it from souring? Now this mechanism has been studied and they are trying to bring it to medical technology.

Another example. More recently, Russian scientists from the N.N. G.F. Gause researched the inhabitants of edible mushrooms and found several potential suppliers of new drugs.

Scientists from Novosibirsk, working in the Russian-American laboratory of biomedical chemistry of the ICBFM SB RAS, took a different path.They managed to develop a new class of substances – phosphorylguanidines (it is difficult to pronounce, and it is not easy to write it down). These are artificial analogues of nucleic acids (more precisely, their fragments) that easily penetrate the cell and interact with its DNA and RNA. Such fragments can be created for each specific pathogen based on the analysis of its genome. The project is headed by American Sydney Altman (1989 Nobel Prize Laureate in Chemistry (together with Thomas Chek). Professor at Yale University. In 2013 he received a Russian mega-grant and began to work at the Institute of Chemical Biology and Fundamental Medicine of the SB RAS).

But the most popular directions in the search for anti-infection agents are bacteriophages and antimicrobial peptides.

Puddle Allies

From a bird’s eye view, the building of the IBCh RAS looks like a double helix of DNA. And just outside the gate is an incomprehensible sculpture. The plate explains that it is a complex of the antibiotic valinomycin with a potassium ion in the middle. Fifty years ago, employees of the institute understood how metal ions bind to each other and how they then pass through the cell membrane thanks to ionophores.

Now the IBCh is engaged in another topic – bacteriophages. These are special viruses that selectively attack bacteria. The head of the laboratory of molecular bioengineering, Konstantin Miroshnikov, affectionately calls his charges, bacteriophages, animals.

– Phages are good and bad at the same time in that they act on a specific pathogen. On the one hand, we aim only at those microbes that interfere with life, and do not bother the rest, and on the other hand, it takes time to find the right phage, which is usually not enough, ”the zavlab smiles.

There are both bacteria and bacteriophages in every puddle. They are constantly fighting each other, but for millions of years neither side can defeat the other. If a person wants to overcome bacteria that attack his body or potatoes in a warehouse, it is necessary to deliver more corresponding bacteriophages to the breeding site of bacteria. Here is a metaphor, for example: when they were exploring the coast of Golden Sands in Bulgaria, there were many snakes, then they brought many hedgehogs and they quickly shifted the balance of the fauna.

– Two years ago we began to cooperate with the Rogachevo agricultural park near Dmitrov. The general director of the organization, Alexander Chuenko, is a former electronics engineer and an enlightened capitalist, not alien to the scientific approach, says Konstantin. – The crop of potatoes was eaten up by pectolytic bacteria – soft rot that lives in warehouses. If left untreated, potatoes quickly turn into tons of smelly goo. Phage treatment of potatoes at least dramatically slows down the development of infection – the product retains its taste and presentation longer both in storage and on store shelves.At the same time, the phages attacked putrefactive microbes and biodegraded – they disintegrated into DNA particles, proteins and went to feed other microorganisms. After successful tests, the management of several large agricultural complexes became interested in such bio-protection of the crop.

– How did you manage to find the necessary bacteriophages and turn them into an antidote? I ask, glancing at the toy phage on top of a stack of books.

– There is a classic double agar method for searching. First, lay a kind of lawn of bacteria on the first layer of agar in a Petri dish, pour water from a puddle on top and cover with a second layer of agar.After some time, a clean spot appears on this muddy lawn, which means that the phage has devoured the bacterium. We isolate the phage and study it.

Miroshnikov’s laboratory, together with Russian and foreign colleagues, received a grant from the Russian Science Foundation for research and diagnostics of potato pathogens. There is work to do here: plant bacteria are much less studied than human ones. However, with our body, too, a lot is unclear. According to scientists, doctors do not examine a person this way: all tests and examinations are sharpened for antibiotics, and other methods are needed for phage therapy.

– Phage therapy is not a medicine in the current sense, but rather a complex service that includes quick diagnosis and selection of the right remedy against a specific pathogen. In Russia, phage preparations are included in the list of medicines, but are not mentioned in the guidelines for physicians. So doctors who are in the subject are forced to use phages at their own peril and risk. And in Poland, for example, the legislation states that if a patient cannot be cured by traditional evidence-based medicine, at least dancing with a tambourine, at least homeopathy, at least phage therapy can be used.And at the Hirschfeld Institute in Wroclaw, phages are used as personalized medical care. And with great success, even in the case of advanced purulent infections. The use of phages is a scientifically grounded and biologically understandable, although not trivial method, sums up Miroshnikov.

Peptides are a family of substances consisting of amino acid residues. Recently, scientists are increasingly considering peptides as the basis for future drugs. It’s not just about antibacterial agents.For example, at Moscow State University. M.V. Lomonosov and the Research Institute of Molecular Genetics of the Russian Academy of Sciences, a peptide drug was created that normalizes brain function, improves memory, attention and resistance to stress. Photo: “Schrödinger’s cat”

And here is the news from the science city of Pushchino. Scientists from the branch of the IBCh RAS, the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences and the Institute of Biochemistry and Physiology of Microorganisms named after V.I. G.K. Scriabin RAS investigated how the bacteriophage T5 enzyme acts on E. coli. That is, they worked not with the bacteriophages themselves, but with their enzyme proteins.These enzymes destroy the cell walls of bacteria – they begin to dissolve and die. But some microbes have a secure outer membrane, and this method does not work on them. In Pushchino, they decided to attract substances that increase the permeability of the membrane to help the enzyme. As a result of experiments on E. coli cell cultures, scientists have found that together the enzyme and the agent destroy bacteria much more efficiently than separately. The number of surviving cells was reduced by almost a million times compared to the control experiment.Cheap common antiseptics such as chlorhexidine were used as a helper, and in very low concentrations.

Phages can be used not only as a medicine, but also as a means of increasing the effectiveness of vaccinations.

– Within the framework of a project supported by the Ministry of Education and Science of Russia, we are going to use bacteriophage proteins to enhance the immunogenic properties of an artificial antigen, says microbiologist Andrei Letarov (Doctor of Biological Sciences, Head of the Laboratory of Microorganism Viruses at the V.I.S.N. Vinogradsky Federal Research Center of Biotechnology RAS). – For this, fragments of the antigen are genetically engineered to link with certain proteins of bacteriophages, which are capable of assembling into ordered structures, for example, into tubes or spheres.

As the scientist explains, such structures with their properties resemble particles of pathogenic viruses, although in fact they do not pose any danger to humans and animals. The immune system is much more willing to recognize such virus-like particles and quickly develops an antibody response.This is the way to create an improved vaccine that, in addition to traditional long-term protection, will provide a quick protective effect to prevent the spread of the disease at the site of infection.

Worm and pig immunity

Pavel Panteleev, a junior researcher at the educational and scientific center of the IBCh RAS (Candidate of Chemical Sciences), loves to ride a bicycle in the mountains. He also loves to study marine invertebrates, more precisely, their antimicrobial peptides, which fight bacteria in living organisms every day.Peptides are the younger brothers of proteins: they also consist of amino acids, only there are no more than fifty of them, and in proteins there are hundreds and thousands.

– At the beginning of each article about peptides, something like this is written: “There is an urgent need to create new antibiotics, because the old ones no longer work due to resistance. And antimicrobial peptides have a wonderful property – resistance from bacteria is produced with great difficulty to them” … The educational and scientific center where I work is looking for peptides that would allow us to resist pathogenic microorganisms, says Pavel.

More than 800 of these peptides are known today, but none of them work in humans. Medicines based on peptides fail clinical trials over and over again: it is not possible to find stable structures that would enter the right amount in the right place and do not cause side effects. They tend to accumulate in the body: for example, they can kill an infection, but not come out with urine, but remain in the kidneys.

“We are studying marine annelids,” says Pavel. “Together with colleagues from the Institute of Experimental Medicine, we isolated two peptides from the Arenicola marina worm (sea sandworm) and studied them.When I was a graduate student, we still went to the White Sea for worms, but we never found new peptides in them. Of course, this may be due to the imperfection of the search method, but, most likely, this worm really only has two peptides, and this is enough to defend itself against pathogens.

– Why worms, are they easier to study?

The fact is that there is a concept according to which the innate immunity system in ancient invertebrates must be very strong, because many of them live in not the most favorable environmental conditions and still exist.Now one of the objects of my research is horseshoe crabs peptides.

Pavel pulls out his phone and shows something with a turtle shell and a bunch of disgusting crab legs. This can only be seen in a horror movie or in a bad dream.

Bacteriophage. Its real height is about 200 nanometers. The bulge at the top is called the head. It contains nucleic acid. Photo: “Schrödinger’s cat”

“However, it doesn’t matter what you study, worms, horseshoe crabs or pigs,” Paul continues.- In all organisms you will examine the same tissues and cells where the peptides are located. For example, blood cells are neutrophils in mammals or hemocytes in invertebrates. It is not yet known why, one can only put forward hypotheses, including humorous ones. A pig is not a particularly clean animal, so it needs more protectors that will prevent bacteria from its mud bath from infecting the body with anything. But there is also a universal answer: in each specific case, there are as many peptides as necessary to protect the body.

– Why are peptides better than antibiotics?

– Peptides are cleverly arranged. Unlike antibiotics, which, as a rule, act on a specific molecular target, peptides are incorporated into the bacterial cell membrane and form special structures in it. In the end, the cell wall is destroyed under the weight of the peptides, the invaders penetrate inside, and the cell itself explodes and dies. In addition, peptides act quickly, and the evolution of the membrane structure is a very disadvantageous and difficult process for bacteria.Under such conditions, the likelihood of developing resistance to peptides is minimized. By the way, in our laboratory peptides are studied not only from animals, but also from plants, for example, protective compounds of a protein-peptide nature from lentils and dill. On the basis of selected natural samples, we create something interesting. The resulting substance may well be a hybrid – something in between a peptide of a worm and a horseshoe crab, says Pavel.

P. S.

Hopefully, in five, ten or twenty years, there will be a new era of germ-fighting.Bacteria are cunning creatures and, perhaps, will create in response even more powerful means of defense and attack. But science will not stand still, so in this arms race, victory will still remain with man.

Man and bacteria. Metaphors

Friends

Staff members are bacteria that live in our body. According to some estimates, their total mass is from one to three kilograms, and their number is greater than that of human cells. They can be employed in manufacturing (production of vitamins), in the processing industry (digestion of food) and in the army (in our intestines, these bacteria suppress the growth of their pathogenic counterparts).

Invited Food Specialists – Lactic acid and other bacteria are used to make cheese, kefir, yoghurt, bread, sauerkraut and other products.

Double Agents – Actually, they are enemies. But we managed to recruit them and make them work for the needs of our defense. We are talking about vaccinations, that is, the introduction of weakened versions of bacteria into the body.

Adopted children are no longer bacteria, but parts of our cells – mitochondria.Once they were independent organisms, but, having penetrated the cell membrane, they lost their independence and since then they regularly provide us with energy.

Workers-prisoners of war – genetically modified bacteria are used for the production of drugs (including antibiotics) and many other useful substances.

Enemies

Invaders – all those who invade our body, parasitize on it and lead to angina, tuberculosis, plague, cholera and many other diseases.

Fifth column – some bacteria that live in our body or on the skin, in normal situations, can be quite harmless. But when the body is weakened, they insidiously rise up and go on the offensive. They are also called opportunistic strains.

Protective fortresses – colonies of bacteria that cover themselves with mucus and films that protect against the action of drugs.

Armored Infantry – Among the bacteria resistant to antibiotics, there are those who know how to make their outer shells impervious to drug molecules.The strength of the infantry is hidden in the lipopolysaccharide layer. After the bacteria die, this layer of fat and sugar enters the bloodstream and can cause inflammation or even septic shock.

Training bases – situations in which the most resistant and dangerous strains survive. Such a training base for bacterial special forces can be the human body, which disrupts the course of taking antibiotics.

Chemical weapons – some bacteria have learned to produce substances that decompose drugs, depriving them of their healing properties.For example, enzymes from the beta-lactamase group block the action of antibiotics from the penicillin and cephalosporin groups.

Camouflage – microbes that change the outer shell and protein composition so that the drugs “do not notice” them.

Trojan Horse – Some bacteria use special techniques to defeat the enemy. For example, the causative agent of tuberculosis (Mycobacterium tuberculosis) is able to get inside macrophages – immune cells that catch and digest wandering pathogenic bacteria.

Super Soldiers – These omnipotent bacteria are not afraid of almost any medicine.

WHO recommendation

Ten Commandments of Antibacterial Behavior

1. Get vaccinated on time.

2. Only use antimicrobial drugs when prescribed by a licensed healthcare practitioner.

3. Once again: do not self-medicate with antibiotics!

4. Remember that antibiotics do not help against viruses.Treating the flu and many types of “colds” with them is not only useless, but also harmful. It seems to be going on at school, but during a study by VTsIOM to the question “Do you agree with the statement that antibiotics kill viruses as well as bacteria?” 46% of the respondents answered yes.

5. Take the medicine in exactly those doses and for as many days as prescribed by the doctor. Do not stop taking even when you feel healthy. “If you do not complete the treatment, there is a risk that antibiotics will not kill all the bacteria that caused your illness, that these bacteria mutate and become resistant.This does not happen in every case – the problem is that we do not know who can end the treatment prematurely and without consequences, “admit the WHO experts.

6. Never share antibiotics.

7. Do not use previously prescribed and remaining antibiotics.

8. Wash your hands. Drink only clean water.

9. Use protective equipment during intercourse.

10. Avoid close contact with patients. If you yourself get sick, show nobility – do not try to infect your classmates, fellow students or colleagues.I mean, stay at home.

Tobacco smoke makes Staphylococcus aureus stronger

As doctors and scientists know, methicillin-resistant Staphylococcus aureus (MRSA), which is resistant to the antibiotics used today, can lead to life-threatening skin and blood diseases and infectious diseases, as well as pneumonia.

At the same time , a recent study showed that in the presence of the MRSA bacteria in the human body, the situation can significantly worsen if the patient smokes.

As scientists have found out, if methicillin-resistant Staphylococcus aureus is exposed to cigarette smoke, it becomes even more resistant to the attempts of the human immune system to resist its influence.

Researchers emphasize – earlier it was possible to irrefutably prove that smoking, undoubtedly, significantly harms the respiratory and immune cells of the human body. And now scientists have discovered the other side of the coin – smoking can promote the spread of invasive bacteria in the human body and make them more aggressive.

To test their hypothesis, scientists used macrophages – immune cells that consume pathogens. The researchers raised two populations of MRSA bacteria — one population “raised” as usual, and the other with cigarette smoke extract. The scientists then left the macrophages to cope with both populations of bacteria.

While observing this process, scientists found that while macrophages were equally capable of consuming both bacterial populations, they had a hard time killing those methicillin-resistant Staphylococcus aureus specimens that had been exposed to cigarette smoke extract during growth.

Researched studied the mechanism that macrophages usually use to kill bacteria – reactive oxygen species that carry out a kind of chemical explosion. As it turned out, MRSA bacteria exposed to smoke were more resistant to this method of destruction – more precisely to antimicrobial peptides, small protein parts of the immune system that are used to make holes in bacterial cells and initiate an explosion.

The effect is dose dependent, which means that the more MRSA bacteria are exposed to the smoke extract, the more resistant they become. These data suggest that cigarette smoke enhances MRSA bacteria by altering their cell walls so that they can better reflect antimicrobial peptides and other charged particles.

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Comparative assessment of the effectiveness of antibiotic therapy for MRSA – associated soft tissue infection in critically ill patients with severe burns

V.V. KULABUKHOV , officeMD, associate professor, A.N. KUDRYAVTSEV, A.G. CHIZHOV , Institute of Surgery named after A.V. Vishnevsky Ministry of Health of Russia, Moscow


Intensive care units can now be considered as an area of ​​high risk of developing nosocomial infections. Gram-positive microflora, especially in specialized surgical departments, can play one of the leading roles in the development of infectious complications of this group, which determine the severity of the patient’s condition, the length of stay in the intensive care unit and nosocomial mortality [13].

INTRODUCTION

Staphylococcus aureus (Staphylococcus aureus) is the second most important pathogen responsible for infectious complications associated with the fact of providing medical care. This pathogen is associated with 30% of cases of infection in the area of ​​surgical intervention, is isolated in 24% of patients with ventilator-associated pneumonia [7]. According to the multicenter study OASIS (2011), in northern and central Italy, 44% of cases of bacteremia were associated with gram-positive flora, of which 35.8% with various strains of Staphylococcus aureus [12].Aureus strains with drug resistance to semi-synthetic penicillins (MRSA) have the greatest clinical significance. They are allocated in 49-65% of all cases of all nosocomial staphylococcal infections. As of 2007, there were 94,360 cases of MRSA-associated infections in the United States. During the year of observation, 18 650 deaths were recorded, determined by this infectious complication [10]. With regard to the forms of localization of an infectious disease caused by MRSA, the most frequently observed are nosocomial pneumonia (34%), soft tissue infection (27%), and bloodstream infection (18%) [8].In the event of the development of soft tissue infection in the areas of burn injury, according to S.V. Yakovleva, 2013, S. aureus is the most frequent pathogen – up to 40.4% of cases, 61.7% of patients have MRSA strains [2].

Staphylococcus aureus, including strains of MRSA, can asymptomatically colonize the skin of both patients, if they seek medical help, and medical personnel providing this assistance. The most important loci of the human body in relation to colonization by Staphylococcus aureus are the skin and mucous membranes of the vestibule of the nasal cavity, the skin of the axillary cavities and the perineum.The period of colonization of MRSA can take quite a long time, on average 56 days, until the infection develops [8]. During this period, a person colonized with MRSA can pose a serious epidemiological hazard by spreading methicillin-resistant S. aureus strains in the environment. According to S.S. Huang, 2011 [8], 24% of patients who underwent an infectious disease associated with MRSA had a recurrence of infection during the year of follow-up, and in half of the patients in the first three months after discharge.The cited data on mortality of patients with identified MRSA colonization require special attention. The authors indicate that within one year after the discovery of MRSA, 46% of patients in this group died. More than one third of all deaths (35%, 94 of 269 patients) were directly attributable to MRSA infection. It is noteworthy that no clear dependence of mortality on the duration of the MRSA colonization period was found, as well as a connection with the duration of hospitalization in these patients.

It should also be noted that the contact mechanism of MRSA spread is the main one in hospital settings. It is realized both directly during direct contacts between a patient or a carrier and a susceptible person, and in a household contact way, through contamination of environmental objects. In rare cases, it is possible to transmit infection by blood contact through contaminated medical equipment during diagnostic and treatment procedures. The facts of the development of resistance to semisynthetic penicillins during the time of S.aureus are very rare.

Similar features of MRSA infection explain the increased attention to this problem by a large number of clinicians. This is leading to the creation of programs to prevent the spread of methicillin-resistant S. aureus strains in health care facilities and in “home” areas where regular outpatient care is provided or where a patient colonized with MRSA is discharged. These programs are based on preventive measures aimed at blocking the pathways of transmission of MRSA.The basic measures of these programs are not MRSA-specific and are aimed at effective prevention of all forms of nosocomial infections. With regard to narrowly targeted measures, it is necessary to highlight early recognition and isolation of MRSA carriers, decolonization strategies, motivation of personnel alertness in relation to MRSA infection, improvement of microbiological diagnostics, epidemiological surveillance of MRSA carriers, etc. Special attention should be paid to early etiotropic therapy in case of development acute form of MRSA infection.Taking into account the above circumstances, its tasks should also include the effective eradication of the pathogen from the patient’s body, preventing the formation of MRSA-carriage in convalescents.

In recent years, vancomycin has been used as the main etiotropic agent for the treatment of MRSA infection [3]. The essential features of the use of this antimicrobial agent are: predominantly bacteriostatic effect (very low bactericidal activity can be achieved with the use of high doses of the drug), lack of activity in structured microbial communities, significant difficulties in selecting the optimal dose, poor tolerance and a high risk of adverse reactions when effective for dosage therapy.These circumstances complicate the eradication of MRSA during treatment with vancomycin [4], which hypothetically suggests the formation of MRSA carriage in survivors of the infection. Difficulties in the selection of optimal dosages of vancomycin are associated with the phenomenon of “creeping” minimum inhibitory concentration (“creep” MIC). The essence of this phenomenon is that during the use of an antibiotic in suboptimal doses, the sensitivity of MRSA to it decreases, which requires an increase in the amount of the drug administered. It is a well-known fact that with an increase in the MIC of vancomycin for MRSA in the range between 1 and 2 μg / ml, an increase in the dosage of the drug can lead to an increase in its concentration in the blood serum of more than 20.8 mg / L.This greatly enhances the nephrotoxic effects of the antibiotic [9]. In addition, M.N. Jeffers et al (2007) noted that long-term vancomycin therapy, even at moderate concentrations, provokes the development of renal dysfunction. Thus, today’s reality compels us to include convalescents of MRSA infection who received vancomycin at risk of MRSA colonization. The peculiarities of the pharmacodynamic profile of the drug, its low safety and poor tolerance in effective clinical dosages do not allow the use of vancomycin in the optimal concentration that can prevent this phenomenon.

The above circumstances determine the interest of clinicians and researchers in other drugs with activity against MRSA. Linezolid, tigecycline, and daptomycin are now the most common. Of the indicated drugs, only daptomycin has a bactericidal effect in therapeutically available dosages. The benefits of the antibiotic include the ability to penetrate structured microbial communities, such as biofilms, to create an effective concentration in infected tissues.The mechanism of antibacterial action is associated with a violation of the integrity of the cell wall of bacteria, which leads to their rapid death. The rate of eradication of MRSA depends on the concentration-dependent killing used. Currently, the highest dose of daptomycin is limited to 6 mg / kg, but in a clinical experiment, even higher doses (10-12 mg / kg) had an adequate safety profile, significantly reducing the time of MRSA eradication [6]. As well as for vancomycin, for daptomycin in research practice the phenomenon of “creeping” minimal inhibitory concentration (“creep” MIC) has been described [3], however, its development is easily overcome due to the significant therapeutic reserve associated with the possibility of safely increasing the dosage of the drug to the level of a satisfactory bactericidal activity.According to P. Lagace-Wiens et al (2011), no clinical confirmation of the MIC creep phenomenon for daptomycin was found [11]. Isolated cases of MRSA resistance to daptomycin have been associated with previous use of other antibiotics with anti-MRSA activity or during long-term use of the drug in an inappropriate dose [5]. The Food and Drug Administration (FDA) has approved daptomycin for the treatment of skin and soft tissue infections, bloodstream infections with bacteremia, and right-sided endocarditis.The Federal Service for Surveillance in Healthcare and Social Development (Roszdravnadzor) of the Russian Federation, in a message dated October 4, 2010, strongly recommends adhering to these indications for the use of daptomycin due to the risk of developing a number of adverse events (reversible eosinophilic pneumonia).

Thus, it seems rational to include daptomycin in the empirical therapy of soft tissue infection in areas of burn injury as a drug of choice that promotes rapid eradication of gram-positive pathogens (incl.h. MRSA) and allowing to prevent their further carriage in convalescents.

In order to analyze the rate of complete eradication of the pathogen when using various antibacterial agents with anti-MRSA activity for the treatment of invasive wound infection in burn areas, we undertook an observational retrospective cohort study. In the course of it, the medical histories of patients with severe burn injuries (Frank index more than 60 units) who were admitted to the intensive care unit of the Department of Thermal Injuries of the Institute of Surgery named after V.I.A.V. Vishnevsky in the period from November 2013 to February 2014 on the 7-10th days after the injury. The criterion for inclusion in the study was the presence in patients of invasive wound infection [1] associated with MRSA, in the complex therapy of which antibacterial drugs with anti-MRSA activity were used: Cubicin (Cubicin®, Novartis Pharmaceuticals UK, Ltd., UK) active substance: daptomycin (daptomycin) and Vankorus® (Vancorus, JSC SINTEZ, Russia) active substance: vancomycin (vancomycin).

The exclusion criteria were the presence of allergic reactions to these medicinal products, the patient’s age up to 18 years.

MATERIALS AND METHODS

The reason for the transfer to the specialized ICU of the burn center of the Institute of Surgery named after A.V. Vishnevsky, all patients had a severe thermal injury (Frank index more than 60 units) with the development of burn disease at the stage of septicotoxemia, complicated by the course of invasive wound infection in the areas of burn injury.

All patients ( Table 1) , 12 people (3 women, 9 men, mean age 42 ± 17.3 years), at the time of transfer to the ICU, underwent complex therapy provided by the recommendations of the American Burn Association (ABA). In all observed cases, there was a prolonged wound infection in the areas of burn injury, the etiology of which was determined retrospectively.

All admitted patients underwent sanitizing surgical interventions in order to limit the pathogenic load from the areas of wound burn infection.In the postoperative period, multicomponent intensive therapy was continued in the intensive care unit. All participants in the study received the necessary therapy, the main components of which were artificial ventilation of the lungs, infusion and transfusion therapy, and the use of anticoagulants. During their stay in the ICU, the patients underwent a comprehensive clinical, laboratory and instrumental examination with the registration of clinical, biochemical blood parameters, hemostasiogram; determination of acid-base parameters, gas composition of arterial and venous blood.

Before starting antibiotic therapy, the patients underwent microbiological studies of the wound discharge. Subsequently, microbiological monitoring was carried out by cultural bacteriological analysis of the discharge of wounds every 48 hours, until the condition was stabilized and transferred from the department. Microbiological studies were performed in accordance with the standards of the Clinical and Laboratory Standards Institute (CLSI).

The prescription of antibacterial drugs was carried out according to the de-escalation scheme during the first 60 minutes of stay in the department, taking into account the previous inpatient treatment and previous data from microbiological studies.Vancomycin as a traditional antibacterial agent and daptomycin, which became available from the moment of its inclusion in the therapeutic practice of the Institute of Surgery, were used as etiotropic therapy for the suspected MRSA infection at the time of admission. Taking into account these circumstances, 6 patients (Vanco group) were selected who received VANCORUS® (VANCORUS) 1 g after 12 hours in the form of a slow intravenous infusion at a rate of no more than 10 mg / min for at least 60 minutes, and 6 patients ( Cubic group), who used CUBICIN® 6 mg / kg of the drug once a day, administered by intravenous infusion over 30 minutes.

The criteria for the effectiveness of the therapy were the timing of the eradication of MRSA according to the microbiological study of the wound discharge.

Statistical processing. For data analysis, a Microsoft Access database and archival materials were used. Statistical processing was performed using the STATISTICA 7.0 system (StatSoft, USA). Samples in the study were compared relative to mean values ​​using a nonparametric alternative to the t-test for independent groups (considering the total number of observations in the study n <100) U - Mann - Whitney test.

RESULTS OF THE STUDY

At the time of connection to the monitor, patients had a course of burn disease in the phase of septicotoxemia, complicated by invasive wound infection in the areas of burn injury. In all patients in the study, positive results were obtained from the microbiological analysis of the wound discharge (Table , Table 2 ). Microbial associations of gram-negative flora with methicillin-resistant staphylococcus were found. Fecal enterococcus was isolated in two cases; Candida albicans fungi were isolated from one patient.

The use of these antibacterial agents was not accompanied by adverse events in both groups of patients. During therapy, the patients showed no signs of renal failure.

The duration of specific anti-MRSA therapy was longer in the Vanco group than in the Cubic group ( Table 3 ). Despite this, it was possible to isolate an average of more than 20 days of observation from the wound discharge of patients of the Vanco MRSA group, which indicated a significantly longer persistence of methicillin-resistant S.aureus compared to the Cubic group.

In two patients of the Vanco group, MRSA continued to exude from the surface of residual burn skin defects after the relief of clinical signs of invasive wound infection and the transfer of the patient from the intensive care unit. MRSA was determined at a concentration of less than 105 CFU. This was considered as continued colonization, which predisposed to the formation of MRSA carriers during the recovery period of burn disease. Complete decontamination of the burn lesion zone was achieved in one patient on the 40th day, and in the other on the 48th day from the moment of admission to the department due to adequate toilet of the remaining skin defects with antiseptics with anti-MRSA activity.

Conclusion

Summarizing the above, it can be noted.

1. MRSA colonization is an additional risk factor for death in patients seeking medical care.
2. MRSA colonization may occur in convalescents of acute MRSA infection due to inadequate use of antibacterial agents with anti-MRSA activity.
3. The most general requirement for antibacterial agents used for the treatment of infection associated with methicillin-resistant strains of Staphylococcus aureus is rapid and effective eradication of the pathogen from the patient’s body, preventing the formation of MRSA-carriage in convalescent patients.
4. Daptomycin, included in the empirical therapy of soft tissue infection in the areas of burn injury, used in moderate therapeutic dosages, has advantages over vancomycin in terms of the rate of eradication of MRSA, prevents long-term persistence of the pathogen in this group of patients.

Literature

1. Krutikov M.G. Pharmacokinetics of antibacterial drugs in burnt [Electronic resource] Internet-journal “Combustiology”, 2003, 16-17.URL: www.burn.ru/all/number/show/?id = 3543 (date of access: 05/31/2014).
2. Yakovlev S.V. Systemic antibiotic therapy of burn disease. Basic Research, 2013, 3 (1): 184-188.
URL: www.rae.ru/fs/?section=content&op=show_article&article_id=10000385 (date accessed: 05/28/2014).
3. Bassetti M. Empiric Therapy of Gram-positive Bloodstream Infections and Pneumonia. M. Bassetti, G. Villa. In: J.-L. Vincent (Ed.). Annual Update in Intensive Care and Emergency Medicine.Springer-Verlag 2012: 264-277.
4. Bassetti M. New approaches for empiric therapy in Gram-positive sepsis. M. Bassetti, F. Ginoccio, D.R. Giacobbe. Minerva Anestesiol. 2011, 77: 821-827.
5. Boucher HW. Perspectives on daptomycin resistance, with emphasis on resistance in Staphylococcus aureus. H.W. Boucher, G. Sakoulas. Clin. Infect. Dis. 2007, 45: 601-608.
6. Figueroa DA. Safety of high-dose intravenous daptomycin treatment: three-year cumulative experience in a clinical program.D.A. Figueroa, E. Mangini, M. Amodio-Groton et al. Clin. Infect. Dis. 2009, 49: 177-180.
7. Hidron AI. Antimicrobial-Resistant Pathogens Associated With Healthcare-Associated Infections: Annual Summary of Data Reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006-2007. Hidron AI, Jonathan RE, Patel J, Horan TC, Sievert DM, Pollock DA, Fridkin SK. Infect. Control. Hosp. Epidemiol. 2008, 29: 996-1011.
8. Huang SS.Methicillin-Resistant Staphylococcus aureus Infection and Hospitalization in High-Risk Patients in the Year following Detection. Huang SS, Hinrichsen VL, Datta R, Spurchise L, Miroshnik I, Nelson K, Platt R. PLoS ONE, 2011, 6 (9).
9. Jeffers MN. A retrospective analysis of possible renal toxicity associated with vancomycin in patients with health care-associated methicillin-resistant Staphylococcus aureus pneumonia. Jeffres MN, Isakow W, Doherty JA, Micek ST, Kollef MH. Clin.Ther., 2007, 29: 1107-1115.
10. Klevens RM. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. Klevens RM, Morrison MA, Nadle J et al. JAMA 2007,298: 1763-1771.
11. Lagace-Wiens P, Adam H, Nichol K, Decorby M, Mulvey M, Karlowsky J. Vancomycin and Daptomycin MIC Creep in Staphylococcus spp.in Canada – Analysis of 4642 S. aureus and 497 S. epidermidis isolates from 2007–2010 : Interscience Conference on Antimicrobial Agents and Chemotherapy.Chicago, USA, 2011.
12. Luzzaro F. Prevalence and epidemiology of microbial pathogens causing bloodstream infections: results of the OASIS multicenter study. Luzzaro F, Ortisi G, Larosa M, Drago M, Brigante G, Gesu G. Diagn. Microbiol. Infect. Dis. 69: 363-369.
13. Wisplinghoff H. Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study. Wisplinghoff H, Bischoff T, Tallent SM, Seifert H, Wenzel RP, Edmond MB.Clin. Inf. Dis. 2004,39: 309-317.

Diseases of Children – Day Medical

General diseases of children and their treatment

The Department of Children’s Health and Disease, also known as Pediatrics, is a branch of science that diagnoses, monitors and treats people involved in the process from birth to adolescence. From 0 to 18 years of age, among children, as persons with certain congenital diseases, after childbirth, regular monitoring of vaccination should be applied, mental, physical and motor development of pediatrics hekimlerinc is recommended to follow.Routine exams conducted in this process are monitored and monitored by many processes, such as height, weight, nutrition and similar development of infants, as well as the development of everyday life skills, expression and understanding, neurological and psychological development.

All children deserve quality medical care. As a parent, it is important to be aware of the most current treatment guidelines so you can make sure your child is receiving the best possible care.

The following information from the Turkish Academies of Pediatrics lists the most common childhood illnesses and their approved treatments.The treatments reviewed here are based on scientific evidence and best practice. However, there may be reasons why your pediatrician has different recommendations for your child, especially if your child has a persistent health condition or allergies. Your pediatrician will talk with you about the changes in treatment. If you have any questions about proper childcare, contact your pediatrician at the day’s medical clinic.

Sore throat

Sore throat is common in children and can be painful.However, the sore throat caused by the virus does not need antibiotics. In these cases, the specific province

Sore throat is common in children and can be painful. However, the sore throat caused by the virus does not need antibiotics. In these cases, no specific medication is required and your child should recover within seven to ten days. In other cases, a sore throat can be caused by an infection called streptococcus.

Streptococcus cannot be accurately diagnosed simply by looking at the throat.a laboratory test or a quick office test for strep that includes a swift throat gland is needed to confirm the diagnosis of strep. If it is positive for streptococcus, your pediatrician will prescribe an antibiotic. Even if symptoms improve or disappear, it is very important that your child takes the antibiotic exactly as prescribed. Steroid medications (such as prednisone) are not an appropriate treatment for most sore throats.

Infants and young children rarely get into strep throat, but if they are in the care of children or have an older brother’s illness, they are more likely to be infected with strep bacteria.Although streptococcus is spread mainly through coughing and sneezing, your child can also get it by touching a toy played by an infected child.

Talk to your pediatrician at the day’s medical clinic when the difference between sore throat, strep and tonsillitis and sore throat is a more serious infection.

Ear Pain

Ear pain is common in children and can have many causes, including an ear infection, swimmer’s ear (infection of the skin in the ear canal), pressure from a cold or sinus infection, and toothache that spreads to the ear and jaw.For a correct diagnosis, your pediatrician will need to examine your child’s ear. If your child’s ear pain is accompanied by a high fever, includes both ears, or if your child has other signs of illness, your pediatrician may order a detailed examination. Many real ear infections are caused by viruses and do not require antibiotics. If your pediatrician suspects your child’s ear infection may be a virus, they will talk with you about the best ways to help relieve your child’s ear pain while the virus does not progress.

Urinary Tract Infection

Urinary tract infections or bladder infections occur when bacteria accumulate in the urinary tract. The infection can be found in children from childhood through adolescence and into adulthood. Symptoms of an infection include pain or burning when urinating, the need for frequent or urgent urination, bedwetting, or accidents with a child who knows how to use the toilet, abdominal pain, or pain in the side or back.

Your child’s doctor will need a urine sample for the sweet before deciding on a treatment. Your doctor may adjust the treatment based on the bacteria found in your child’s urine.

Skin Infection

For most children with a skin infection, a skin test (culture or swab) may be required to determine the optimal treatment. Tell your doctor if your child has a history of MRSA, staphylococcus or other resistant bacteria infection, or if he has contact with other family members or resistant bacteria.

See Tips for treating boils, abscesses and cellulite, as well as viruses, fungi and parasites.

Bronchitis

Chronic bronchitis is an infection of the larger, more central airways in the lungs and is more common in adults. Usually the word “bronchitis” is used to describe a breast virus and does not require antibiotics.

Bronchiolitis

Bronchiolitis is common in infants and young children during the cold and flu season. Your doctor may hear “wheezing” when your baby is breathing.

Bronchiolitis is usually caused by a virus that does not require antibiotics. Instead, most treatment guidelines are designed to comfortably monitor your child for any breathing difficulties, eating, or dehydration symptoms. Medications used for patients with asthma (such as albuterol or steroids) are not recommended for most infants and young children with bronchiolitis. Babies who are born prematurely or have underlying health problems may need different treatment plans.

cold

The common cold is caused by viruses in the upper respiratory tract. Many young children, especially those in childcare, can get 6 to 8 colds per year. Cold symptoms (including a runny nose, congestion, and cough) can last up to ten days.

Green mucus in the nose does not automatically mean that antibiotics are needed; The common cold never needs antibiotics. An eshila generally does not need antibiotics. However, if a sinus infection is suspected, your doctor will carefully decide if antibiotics are the best choice based on your child’s symptoms and physical examination.

Bacterial Sinusitis

Bacterial sinusitis is caused by bacteria that enter the sinuses. Sinusitis is suspected when cold-like symptoms, such as nasal discharge, daytime cough, or both, persist for more than ten days without improvement.

Antibiotics may be needed if this condition is accompanied by a thick yellow runny nose and fever for at least 3 or 4 days in a row.

Cough

Cough is usually caused by viruses and often does not require antibiotics.

Cough medicine is not recommended for children ages 4 and younger, or children ages 4 to 6, unless advised by your doctor. Research has consistently shown that cough medicines do not work in the age group 4 and younger and have the potential for serious side effects. Narcotic cough medicines such as codeine should not be used in children.

If Symptoms Change:

Sometimes mild infections that are viral or bacterial can develop into more serious infections.Call your doctor if your child’s illness changes, gets worse, does not go away after a few days, or if you are worried about new symptoms developing.

Can MRSA transmission occur in public swimming pools? –

Contents:

, Jakarta – Maintaining cleanliness is a must and must be maintained at all times. The reason is that pollution of the body or the environment means that germs, bacteria, viruses or fungi can enter the body.One of the diseases that can be contracted as a result of this bad habit is MRSA or Methicillin-resistant Staphylococcus aureus . To make matters worse, transmission of this disease can occur in hospitals and other public places such as public swimming pools.

MRSA is a type of staphylococcus that is resistant to certain antibiotics. Most of these MRSA infections affect the skin, causing a pimple or boil, which can be thought of as a spider bite; red, swollen, painful, warm to the touch, and festering; also accompanied by fever.Although there have been no reports of MRSA transmission via pool water so far, there are suspicions that MRSA can be easily transmitted. Check out the following reviews!

How is MRSA spread across the pool?

The germs that cause MRSA are easily spread in swimming pool water and other areas through direct or indirect contact with other visitors infected with MRSA. However, MRSA cannot be stored for long in chlorine sterilized swimming pool water at the correct pH (7.2-7.8).Infection can be transmitted immediately if you accidentally or accidentally touch someone’s MRSA infection.

In the meantime, indirect infections can occur when you and the person borrow personal items, such as towels or razors, or touch surfaces such as handrails or changing benches in public swimming pools that are contaminated with MRSA. The most likely condition for MRSA to spread is contact with an open cut or cut in the skin.

So how to prevent transmission of MRSA from public swimming pools?

Not only does this prevent MRSA disease, here are some things to do before entering the pool to avoid contracting the disease.Some things to consider include:

  • See Water Conditions. The pool water should look clean, clear and blue to the bottom. Before deciding to enter, make sure you can see the drain and tile lines at the bottom. Also make sure that the water around the filter is constantly moving and bubbling, which indicates that the filter machine is working.

  • Smell the scent. Chlorine does not usually have a strong odor.If chlorine has a strong odor, it indicates chloramine, a chemical made up of chlorine mixed with body oil, sweat, urine, saliva, lotions, and feces.

  • Touch. Make sure the inside wall of the pool is smooth, not slippery or sticky, and water should not stick to your hands.

  • Do not swallow water. If you are in a safe condition, make sure you do not swallow pool water. Also teach your children and train yourself not to do this, even just sticking your fingers in your mouth.

What are the symptoms of MRSA to watch out for?

Symptoms of MRSA differ depending on the type. However, if you experience any of the following symptoms after swimming, you should be aware of them. These symptoms include:

  • Fever;

  • Trembling;

  • Cough;

  • Difficulty breathing;

  • Chest pain;

  • Headache;

  • Muscle pain;

  • Limp.

Meanwhile, if it attacks the skin, an infection occurs with symptoms such as:

  • Swollen;

  • Redness;

  • Pain

  • Fester.

Are the symptoms mentioned above? See a doctor immediately.