Infection

A lot of parents stress over the choice of deciding wither or not to vaccinate their children. The reason why deciding to vaccinate children is so difficult is due to the wide range of myths and side effects that are connected with vaccinations. Examples of myths spread to parents all over the United States is that the diseases don’t even exist anymore, rumors of vaccinations weakening a child’s immune system, and the risk of a child becoming autistic due to thimerisol in vaccinations causing autism.

Side effects also scare parents out of getting their children vaccinated like brain damage, seizures, or allergic reactions. But then parents are pulled back to the thought of the possibility of their child or children catching a very serious life threatening disease. Any of these terrible things occurring in a child’s life makes it very easy for a parent to steer clear of the whole situation, and in ending result, not get their child vaccinated.

When children aren’t vaccinated, they are left defenseless against diseases like hepatitis B, measles, mumps, chicken pox, polio, pertussis (whooping cough),  rubella, and more. All these diseases have the ability to easily kill a child within days, and if it weren’t for the vaccines protection over many children in the United States, the spread of these diseases would travel rapidly. There are a lot of people that do not recommend or get vaccinations for children because they think it is unnecessary to vaccinate for a disease that is no longer around.

But let’s look at the big picture. If everyone stopped getting the vaccinations what would happen? Todd Neale from Medpage today inquires in San Diego 2008, “ Although the rate of two-dose immunization against measles was 95% in the area, a single case of measles from a 7-year-old child returning from overseas sparked an outbreak that exposed 839 people and sickened 11 other children”. If those 839 people weren’t protected with strong immune systems or vaccinations, there would have been a drastic dilemma.

This is a perfect example of how fast a disease can get out of control. When parents think that its o. k. not to vaccinate because the diseases aren’t around anymore, they are really relying on other children who are vaccinated to keep their own children healthy, which is a gamble. In other words, According to the Children’s hospital of Philadelphia, if the immunizations rates drop only a little bit, outbreaks of diseases would sweep across the country rapidly. Another reason parents don’t want to vaccinate is because of the rumor of he vaccinations weakening children’s immune system. According to the Children’s hospital of Philadelphia “If 11 vaccines were given to infants at one time (which they aren’t), then about 0. 1 percent of the immune system would be used up, but because B cells and other lymphocytes are constantly replenished, a vaccine never really uses up a fraction of the immune system. For example, the immune system has the ability to replenish about 2 billion lymphocytes each day. Also a study in Germany revealed that 496 vaccinated and unvaccinated children who received immunizations within the first three months of life had fewer infections with vaccine-related and unrelated pathogens than the non-vaccinated group. So here is the proof that vaccinations will not affect a child’s immune system. Then there is the big scare of vaccines containing the ingredient thimerisol causing autism in children. According to FDA, thimerosal is a mercury containing preservative found in vaccines that prevents bacterial and fungal growth which might occur with repeated puncture of multi dose vials.

A lot of controversy has been held between doctors and parents because of prediction of autism being linked to thimerosal. According to the Centers for Disease Control and Prevention Vaccine Safety Datalink, “Preliminary results from the VSD Thimerosal Screening Study published in 2003 did not find an association between thimerosal exposure and autism risk and recent ecological studies has not found a correlation between thimerosal content of vaccines and autism rates”.

Numerous studies by many scientists have been done and prove that Thimerosal and autism are not related. Examples: Vaccine Education Center at The Children’s Hospital of Philadelphia, “Multiple studies have shown that thimerosal in vaccines does not cause autism”. Another reason people do not get their children vaccinated is because of risks associated with getting the vaccinations. Scary examples of some of the side effects associated with vaccinations include: seizures, brain damage, high fevers and even death.

Let’s take the vaccine for hepatitis B as a good example. The Children’s Hospital of Philadelphia states, “About one of every 600,000 doses of hepatitis B vaccine is complicated by a severe allergic reaction called anaphylaxis. The symptoms of anaphylaxis are hives, difficulty breathing and a drop in blood pressure. On the other hand, every year about 5,000 people die soon after being infected with hepatitis B virus. According to Car Accident Statistics from Edgar Snyder and Associates,” Each year, lmost 250,000 children are injured in car crashes, meaning nearly 700 kids are harmed every day. But this doesn’t stop people from putting their children in cars. The chicken pox vaccine is another example that side effects are very rare. According to Medic 8, “A macular or accine rash usually consisting of a few lesions at the injection site is reported in 3% of children and 1% of adolescents. Cases of allergic reactions to children are very low and should hold any parent back from getting children vaccinated.

So in conclusion, the diseases that vaccines are made to treat are still around, and it is very easy for a disease to spread. Vaccines do not weaken a child’s immune system because of B cells and lymphocytes being constantly replenished by immune system. Numerous studies have been conducted proving that thimerisol does not cause autism. And The risk of a child having a adverse reaction to a vaccine is so low that its safer than driving down the street in a car. Protect your children from deadly diseases, get them vaccinated.

Introduction

Section 1. Search strategy

Describe the strategy you used to retrieve the right resources to help you write your assignment. You must include the key words you used, the databases used and other sources of your literature such as websites, the years searched and the type of literature you were looking for.

Approximate word count: 150-200

Your answer here:

Keywords used in the search engine are: diabetic, foot, ulceration, risk, prospective, aetiology, prevalence, cost, infection, dressing, treatment, amputation, wound, management, policy, guidelines, UK, Philippines, South Asia, Europe, which were consecutively joined together, using the Boolean Operation of adding AND and an asterisk to each terms. The main databases used were CINAHL plus and PubMed. Another source of evidence that the researcher used is the official website of the National Institute for Health and Clinical Excellence in which a clinical guideline was used deemed necessary for the said topic. The World Health Organization and the National Health Services websites were also used in collecting data for statistics as well as the Department of Health website in the Philippines. Peer reviewed articles have been searched using the said databases and have been sources of information. Limitations in this search have been identified. These are as follows:

The search has been limited for ten years only to make the search more manageable and clinically up to date while capturing key information.
The search is only applicable for humans aged 65 and up, regardless of gender. This bracket has been chosen because according to the World Health Organization (2006) diabetic foot ulceration is rampant in this age group.
The search is limited for peer reviewed journals only.
The search is not confined to the United Kingdom only; hence, statistics from Asia were also gathered.

Section 2. Wound aetiology

Select a common wound type (e.g. diabetic foot ulceration, pressure ulcer, leg ulcer, fungating wound, dehisced surgical wound.

Now explain and discuss:

What your chosen wound type is
How this type of wound develops (including contributory factors)
How this type of wound is recognised (common characteristics)
Who it affects
Prevalence in UK and home country (if known)

Approximate word count: 800-1000

Your answer here:

The type of wound that the author chose is diabetic foot ulceration. This was chosen because this type of wound is prevalent in the nursing home that the author is currently working at and Diabetes itself is a serious health issue worldwide. Consequently, diabetic foot ulceration is considered to be one of the most significant complications of diabetes, representing a worldwide issue of medical, social, and economic problem greatly affecting the patient’s quality of life. (World Health Organization, 2004) Earlier definitions of diabetic foot ulceration dated back to 1985 by the World Health Organization stating that it is an infection, ulceration, and/or destruction of deep tissue related with neurological abnormalities and various degrees of peripheral vascular disease in the lower extremities. This has been argued by Brownlee (2005) that the term ‘diabetic’ foot signifies that there are specific qualities about the feet of the individual with diabetes that sets this disease apart from other conditions that affect the lower extremities. However they added that anything which affects the foot in those with diabetes can also affect the foot in those without the disease. Thus the definition by De Heus-van Putten (1994) best neutralise those views, stating that diabetic foot ulcers is the many different lesions of the skin, nails, bone, and connective tissue in the foot which occur more often in diabetic patients than non-diabetic patients, such conditions like ulcers, neuropathic fractures, infections, gangrene, and amputation. This is supported by the contemporary study of Vileikyte (2001), presenting that the diabetic patients are statistically more likely to develop foot ulcer that usually leads to disablement and leg amputation. The aetiology of diabetic foot ulceration comprises many components. A multicentre study by Rathur and Boulton (2007) attributed 63% of diabetic foot ulcers to diabetic neuropathy and peripheral vascular disease to be the main causative factors of diabetic foot ulceration. Peripheral neuropathy is a complication of diabetes that is the result of overtime damage of the nerve due to high blood sugar levels (Jerosch-Herold, 2005). This complication consequently contribute to the cause of diabetic foot ulcer for the nerves that relay messages of pain and sensation to the lower limb are generally affected, leading to numbness or even complete loss of sensation in the legs and feet. Losing sensation would also mean not knowing if the feet are hurt or damage. This explains why diabetic patients are usually prone to problems like minor cuts, bruises and blisters without them feeling it.Furthermore, another risk factor is the peripheral vascular disease wherein there is narrowing of the arteries caused by fatty deposits that accumulate in the lining of the arteries resulting to poor blood circulation to the feet (Medina, Scott-Paul, Ghahary & Tredget-Edward, 2005). Inadequate blood supply to the wound means decrease healing and is likely to be damaged. This explains why even a mild injury like stepping in small object or a small scratch in bare foot can eventually become ulcer for a diabetic patient. Moreover, according to Veves, Giurini, and LoGerfo (2006), predisposing factors that may act in combination to the two main risk factors are the unrecognised trauma, the biomechanical abnormalities or deformity, the limited joint mobility, and the increased susceptibility to infection. Demographic factors also play an effect on diabetic foot ulceration, such as age, gender, ethnicity and lifestyle (Medina, Scott-Paul, Ghahary & Tredget-Edward, 2003). According to the World Health Organization (2004) Diabetic foot ulcerations are common on individuals who have Type 1 and Type 2 Diabetes and who are in the age bracket of 65 years old and above. This statistics is not only relevant here in the UK but also worldwide. People who have diabetes for a longer period or manage their diabetes less effectively are more likely to develop foot ulcers. Smoking, not taking exercise, being overweight and having high cholesterol or blood pressure can all increase diabetes foot ulcer risk (Diabetes UK, 2004). Previous foot ulcers and diabetes complications can increase foot ulcer likelihood, as can ill-fitting shoes or previous foot problems such as bunions, etc.

Diabetic foot ulceration usually located in increased pressure points on the bottom of the feet. However, ulcers related to trauma can occur anywhere on the foot (Diabetes UK, 2004) Anatomical distribution of diabetic foot ulceration comprises 50% of ulcers are on the toes; 30-40% are on the plantar metatarsal head; 10-15% are on the dorsum (sole) of the foot; 5-10% are on the ankle; and up to 10% are multiple ulcers (Department of Health, 2002). According to the National Diabetes Support Team (2006), the appearance of a diabetic foot ulcer generally has a base with pink/red or brown/black, depending on the patient’s blood circulations, and with a border of ‘punched-out’ like appearance while surrounded by callous skin. It has a bed with necrotic cap or ulcer (underlying tissues are exposed). Ulcers with a mainly neuropathic aetiology will have a healthy granulating bed whilst those with a significant arterial component will have a necrotic bed (Reiber, 2001). The International Diabetes Federation (2005) accounts that there are 170 million cases of diabetics reported worldwide. By 2025, this figure is expected to rise to 300 million. These diabetics patient have a 12-25% risk of suffering a foot ulcer at some time in their life. According to Reed (2004), elderly people with diabetics have twice the risk of developing foot ulcer, three times the risk of developing foot abscess and four times the risk of developing osteomyelitis. Similarly, diabetics were at greater risk of either local amputations or higher amputations (Hall & DeFrances, 2003). Since different regions of the world have populations that at variance in body builds, footwear, habits and lifestyles, the differences in the prevalence of diabetic foot ulceration is expected. Such differences are likely to be found in Asia, Africa and America for developing countries will experience the greatest rise in the prevalence of Type 2 diabetes in the next twenty years (Stanley & Collier, 2009). Thus, people living in these countries will be expected to have greater risks of ulceration in the later years. However, Abbott et al (2005) focused on Type 2 diabetics among migrant populations of South Asia and African-Carribean populations, compared with data from Europeans living in the UK, and revealed a three to four times higher incidence of ulceration in the Europeans. The lower risk of South Asians was attributed to the lower rates of foot deformity, peripheral vascular disease and neuropathy.

In the Philippines on the other hand, the author was not able to find statistics regarding the prevalence of diabetic foot ulcerations on individuals with either Type 1 or Type 2 Diabetes. Apparently, the Department of Health Philippines website does not have relevant statistics regarding the above matter however, according to the World Health Organization (2004), the prevalence of people having diabetes in Asia is fast rising and it may comprise to 75% of all diabetics in 2025 worldwide.

Section 3. Wound Assessment

Identify one feature of your chosen wound type that is commonly identified during the assessment process and critically discuss different ways of assessing this problem. Your discussion must make clear which aspect of wound assessment you have chosen e.g. exudate, odour, infection, and include an exploration of the different options available for measuring, describing and documenting it. You must link your discussion to the contemporary wound care literature.

Approximate word count: 800-1000

Your answer here:

When a diabetic patient develops an ulcer, it is very essential to know that the ulcer presents in the perspective of the diabetic. However, in the case of a diabetic patient, the skin usually in the feet does not heal efficiently and is prone to develop an ulcer as discussed on the previous section. This is what the writer believes to be the foremost feature of the diabetic foot ulceration that needs major consideration for it can eventually result to infection.

Assessing the delay wound healing of a diabetic foot and its relation to the aspect of infection involves thorough evaluation, thus, a general assessment by the multidisciplinary care approach of the patient with diabetic foot ulcer is fundamental. This includes evaluating for evidence of retinal and cerebro-vascular pathology that could relate to foot and ankle problem (Pham et al, 2000). The said evidence can play a part to falls, traumatic injury and poor foot hygiene of the patient and can aid in appropriate treatment of the wound. The renal and cardiac disease evaluation is another pathological assessment that can contribute to the evaluation of poor healing potential (Stanley & Collier, 2009). The standard observations of blood pressure, heart rate and temperature are also requisite assessment for these can reveal overriding features of sepsis such as pyrexia, tachycardia and general malaise (Costigan, Thordarson & Debnath, 2007). Stanley and Collier (2009) also added that inspection of the diabetic foot such as the characteristics of the skin, nails, and web spaces, is important for it can reveal pathology of the nails (Paronychia) or the cause of the spread of infection. Generally, limb-threatening infections can be defined by cellulitis extending 2cm from the ulcer perimeter, as well as deep abscess, osteomyelitis or critical ischemia (Frykberg et al, 2002). The existence of odor and exudates, and extent of cellulitis should be properly noted for these are indicative of osteomylitis which could indicate infection (Frykberg et al, 2002). In the case of neurological assessment, Jerosch-Herold ‘s (2005) assessment review stated that Semmes-Weinstein monofilament is considered to be the most reliable test for evaluating any loss of protective sensation done in the sole of the feet. The test is not only relevant in assessing loss of sensation; it also evaluates foot deformity, risk for ulceration and signs of infection.

Moreover, a vital part in this assessment is the classification of diabetic foot ulcer itself. This is supported by Frykberg et al (2002) stating that classifying ulcer is important in order to facilitate a logical approach to treatment and aid in the prediction of outcome.

In line with that, there are several wound classification guidelines used universally to assess the diabetic foot ulcer. One of this is the Wagner ulcer classification system (1987) is the most widely accepted descriptive classification of diabetic foot ulcerations. It categorises wound depth according to 6 wound grades. These include: grade 0 (intact skin), grade 1 (superficial ulcer), grade 2 (deep ulcer that includes tendon, bone, or joint), grade 3 (deep ulcer with abscess or osteomyelitis), grade 4 (forefoot gangrene) and lastly grade 5 (whole foot gangrene). However, the downside of the Wagner classification system is that it does not specifically address the aspect of infection and circulation problem, which are actually the important parameters of diabetic foot ulceration. However, this method is not really very reliable in assessing ischemia and infection because only useful guidance in the management of each class of ulcer is provided. Nonetheless, a more comprehensive scale has been developed at the University of Texas, which includes risk stratification and expresses tissue breakdown, infection and gangrene separately. According to Abbott et al (2005), this system is generally predictive of the outcome for it uses four grades of ulcer depth (0 to 3) and then stages them into four stages (A to D) basing on the presence or absence of ischemia and infection. The classification system assesses the depth of ulcer penetration, the presence of wound infection, and the presence of clinical signs of lower-extremity ischemia. Similarly, the International Working Group on the Diabetic Foot (2004) has proposed the PEDIS classification which grades the wound on a 5-feature basis: Perfusion (arterial supply), Extent (area), Depth, Infection, and Sensation. Finally, according to the Infectious Diseases Society of America guidelines (2004), the infected diabetic foot is sub-classified into the categories of mild (restricted involvement of only skin and subcutaneous tissues), moderate (more extensive or affecting deeper tissues), and severe (accompanied by systemic signs of infection or metabolic instability).

In addition to that, another form of assessment for infection is the surface swab. But according to Bowker and Pfiefer (2001), it is inadequate for identifying the type of bacteria causing limb-threatening deep infection. The most accurate and reliable technique involves removing exudates from the ulcer, getting a little tissue biopsy from the base of the ulcer and sending the sample to the laboratory in appropriate aerobic and anaerobic culture material. Plain film radiographs should also be obtained to look for tissue, gas and foreign bodies and to evaluate the infected ulcer for bone involvement. (Sutter & Shelton, 2006) Probing to bone using aseptic technique is also done to find out if osteomyelitis is present.

Section 4. Wound Management

Using the same wound feature that you identified in Section 3; critically discuss the different ways there are of managing this problem.

Your discussion must include:

The different types of wound care dressings, products and treatments that could be used to manage this problem
Other appropriate/related aspects of patient care such as nutrition and positioning
How the patient experience can be improved

Approximate word count: 800-1000

Your answer here:

After a comprehensive assessment, an ulcer management plan must be developed to direct treatment goals. In the treatment of diabetic foot ulceration, the primary goal is to attain wound closure and to control infection (Frykberg et al, 2002). In order to achieve this goal good wound care techniques are required. Part of this wound technique are dressings. Wound dressings represent a part of the management of diabetic foot ulceration. Ideally, dressings should alleviate symptoms, provide protection for the wound and promote healing. (Hilton, Williams, Beuker, Miller & Harding, 2002) In line with that, the NHS (2002) released a guide for useful dressings which included dressings for infected diabetic wound. Dressings that are low or non-adhering must be used on infected diabetic wounds with daily dressing changes. According to Foster, Greenhill, and Edmonds (2007), the ideal dressing for infected diabetic foot ulcers are those that fit in the shoes and does not take up too much room, it could withstand shear forces and carry out properly in an enclosed environment, does not increase the risk of infection, absorbs exudates suitably as well as allow drainage and it can be changed frequently and can be removed easily. Hydrocolloids are the best example of such dressings. They contain gel-forming agents, such as gelatin, so when the dressing comes into contact with wound exudate it absorbs ?uid and forms a gel which creates a moist healing environment (Heenan, 2008). According to Pudner (2001), it is advisable to use hydrocolloids in a diabetic foot ulcer as they absorb exudates and can give a visual indication of the need to change dressing. This kind of dressing can be easily removed by gently lifting an edge of the dressing and pulling carefully upwards to reduce the seal of the dressing on the skin and thus minimise trauma to the wound bed and surrounding skin. (Pudner, 2001) Regular dressing changes are done to monitor deterioration of the ulcer. Dressings with Inadine, Iodoflex or Iodosorb are also used to reduce bacterial inhabitation in the ulceration. Daily Flamazine dressings are also recommended for the treatment of Pseudomonas infection. (Sibbald et al, 2003) When the infected diabetic wound become heavily exudated, foams and alginate may be used because they are highly absorbent. Hydrogels facilitate autolysis and may be beneficial in managing ulcers containing necrotic tissue. Dressings containing Inadine and Silver may aid in managing wound infection. Occlusive dressings should be avoided for infected wounds. All dressings require frequent change for wound inspection. (Armstrong, Lavery & Harkless, 2003)

Another management is debridement. The purpose of this is to remove dead or devitalised tissue. (Bowker & Pfeifer, 2004) It is also recognised as one of the most important methods of wound bed preparation because it promotes the release of growth factors which contribute to progressive wound healing. (Leaper, 2002) Ulcer debridement is performed to remove unhealthy tissues such as necrotic, callus and fibrous tissue and recondition them back to bleeding tissues in order to facilitate full image of the extent of the ulcer and its underlying problems like abscesses or osteomyelitis (National Diabetes Support Team, 2006). Offloading must also be part of the management plan for the infected diabetic foot ulcers to relieve pressure from the wound to allow healing to take place. (Doupis & Vevies, 2008) However, offloading devices might be impractical for diabetic individuals who are frail or susceptible to falls, and a disadvantage of devices that cannot be removed is interference with bathing and showering. (Caravaggi, Faglia, & De Giglio, 2000)

In addition to the management stated above, antibiotic treatment is also necessary. The antibiotic regimen should be based on the anticipated spectrum of infecting organisms. (Chantelau, Tanudjaja & Altenhofer, 2006) The combination of an aminopenicillin and a penicillinase inhibitor has the required activity but other options include a quinolone plus either metronidazole or clindamycin. (Tentolouris, Jude & Smirnoff, 2003) In addition to antibiotic therapy, It may also be necessary to promote non weight bearing strategies such as bed rest and or use of wheelchair, crutches, walker, or cane. Diabetic individuals may also be advised to replace or modify their footwear. The lack of sensation associated with neuropathy can result in the tendency to buy shoes that are too small or too tight. It is necessary to accommodate any foot changes or deformities. Orthoses or custom-made shoe inserts may be required for pressure reduction. (Armstrong, Lavery, Harkless, 2003) In selecting devices, the ability of a device to remove or redistribute pressure, the ease of application, cost-effectiveness, and ability to gain compliance must be taken into consideration.

Proper footcare and general skincare must also be implemented. Feet should be checked daily for further cuts, sores, blisters, bruises or dry skin to prevent further ulcer formation. Bringing blood glucose levels within normal range is essential. (International Diabetes Federation, 2009) Strictly managing diabetes is the first stage in treating all the other complications and even the condition itself. Diet and exercise will almost certainly play a role in preventing as well as treating diabetes. (Embil, 2003)

Section 5.

Identify a contemporary source of evidence based guidance (i.e. a clinical guideline) which could be used as a basis for providing a high standard of care to patients with this type of wound. Critically discuss how the guidance given in this document might influence your nursing practice including whether you believe there are any omissions or recommendations made that would be difficult to manage in your own placement. Please also comment on whether the Guideline recommendations could be implemented in your home country e.g. Philippines, Sri Lanka, Malaysia, China.

You must clearly state the title your chosen guideline document and link your work to other healthcare literature where appropriate.

Approximate word count: 400-500

Please start this section by stating the name of your chosen Clinical Guideline.

Name of Guideline: Clinical Guidelines for Type 2 Diabetes Prevention and management of foot problems

A very crucial statement in the guideline states that diabetic individuals should have their feet and legs examined for specific problems at least once a year. This is highly recommended and should be implemented. Diabetic individuals need help to detect problems when they develop neuropathy and lack of protective pain sensation. If this is carried out, prevalence of infection and other diabetic complications will surely go down.

With regards to the whole healthcare setting, the NICE guideline recommends that health care professionals who carry out examinations must be properly trained but specific details of the training are not given. Nurses as well as other members of the healthcare team would need specific trainings most especially on handling equipments as well as imparting management to the affected individuals.

It was also mentioned that diabetic individuals with active problems will be seen by the multidisciplinary foot care team that consists of highly trained podiatrists and orthotists, nurses with training in dressing diabetic foot wounds and diabetes specialists with expertise in lower limb complications. However, there is currently a shortage of podiatrists, nurses and other specialised members of the healthcare team. Lack of clarity about the membership of the multidisciplinary team may affect in the implementation of the guideline.

Regarding ulcer management, there is a further problem with the section in the NICE guidelines on how ulcers should be managed. One or more interventions are suggested, including dressings, antibiotics to treat infection, and pressure relief by the use of special shoes or total contact casts. However, there is little guidance as to which intervention should be chosen and in which circumstance. Unfortunately, this could lead to a reinforcement of current practice where many patients with diabetic foot ulcers have dressings applied to their ulcers with no further interventions until the ulcer deteriorates. (Rathur & Boulton, 2007) Nurses caring for patients with diabetic foot ulcers should understand that, in addition to dressings, patients need effective pressure relief and management of infection.

As with regards to the author’s workplace which is a nursing home, although the guideline is flawed, as all guidelines are, the author believes that it will be really helpful in the management of diabetic foot problems since almost all of the residents who have diabetes are experiencing foot problems already. However, it will be better if the guideline made recommendations regarding services exclusive to nursing homes to address to the specific needs of the diabetic residents.

The author believes that this guideline is not achievable to the Philippines. In view of the current health care setting of the country, it will be very had to implement the guideline due mainly to lack of funding and a huge shortage of specialist health care professionals. The Philippines is one of the countries in South East Asia that prevalence rate of diabetic foot ulcerations and infections are fast rising (WHO,2004) but unfortunately, the country is also understaffed and underfunded.

The author believes that for the NICE guidelines to be implemented whether in the placement or for the whole healthcare setting, it will be necessary to recruit and train a lot of diabetic foot professionals or better yet, educate existing health care professionals. Careful monitoring of the diabetic individuals will be essential as well as imparting proper lifestyle change and management.

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Abbott, C.A., Garrow, A.P., Carrington, A.L., Morris, J., Van Ross, E.R. & Boulton, A.J. (2005). Foot ulcer risk is lower in South-Asian and African-Caribbean compared with European diabetic patients in the UK. The North-West Diabetes Foot Care Study, Diabetes Care, 28(8), 1869–1875.

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Introduction

Measles is a highly contagious disease caused by an enveloped RNA virus of the genus Morbillivirus in the family of Paramyxoviridae (Griffin et al, 1994). It is a major cause of child morbidity and mortality, particularly in developing countries, despite the introduction of attenuated measles virus vaccines which have greatly reduced the incidences since the 1960s (WHO, 2009). The window period of infection for infants lies between the disappearing maternal antibody protection and vaccine administration (Manchester and Rall, 2001). In 2008, 164,000 measles deaths were reported and the majority were children under five years old (WHO, 2009).

Affected individuals combat measles by generating cell-mediated immunity to clear the virus and humoral immunity to provide long-term protection (Manchester and Rall, 2001). However, the measles virus (MV) induces immunosuppression during infection and for weeks after recovery, rendering infected individuals susceptible to secondary infections (Griffin et al, 1994). The evidence of immunosuppression caused was first recognized in 1908 when von Pirquet reported that children lost positive skin tests for tuberculin antigen during MV infection (von Pirquet, 1908).

Research has been carried in vitro and in vivo to define the pathogenesis pathways of MV. Immune responses to MV have been described on transgenic mice and cynomolgus monkeys models (Sato et al, 2007) suggesting that multiple potential mechanisms are linked to the virus-induced immunosuppression (Schneider-Schaulies et al, 2002).

Infection

Measles is transmitted via airborne exposure from coughing and sneezing or close contact with nasal and throat secretions. MV remains active in the air for up to two hours. It enters the body through the respiratory system and spreads systemically by infecting lymphoid cells. Infection and spread is a complex process. The structure and proteins of MV are important determinants of virus tropism and pathogenesis (Yanagi et al, 2006).

Measles virus consists of a non-segmented single negative-strand RNA genome (16,000 ribonucleotides) with a diameter of 150 to 300 nm. The outer envelope comprises the inner matrix protein to form a lipid bilayer surrounding the viral genome. It encodes six structural proteins and two nonstructural proteins which are important for attachment of the virus to the host, replication, and spreading of the virus in the body (Horikami et al, 1995).

The infection process involves four steps:

1. Attachment

When the measles virus enters the respiratory tract, the initial infection begins with viral attachment to host cellular receptors by the haemagglutinin (H) protein. The most studied receptors are CD46 and signaling lymphocytic activation molecule (SLAM/ CD150) (Ferreira et al, 2010). CD46 is a complement regulatory molecule and is present on all nucleated human cells whereas SLAM is only expressed on thymocytes, mature dendritic cells, and T and B lymphocytes (Hsu et al, 2001). Other cell surface proteins such as moesin and substance P receptors were also proposed in MV binding (Kehren et al, 2001). The primary target for early-stage infection has not been clearly defined. It was originally thought that respiratory epithelial cells were firstly infected (Griffin, 2001) but following the discovery of SLAM, some studies suggested that SLAM-positive immune cells should be the initial targets (Yanagi et al, 2002). Leonard et al. (2008) suggested the presence of a basolateral epithelial receptor (EpR) is necessary for the entry of MV into the respiratory epithelium and infection of the epithelial cells is required for shedding and transmission.

2. Fusion

The interaction of both H and F proteins with human receptors is important for the virus to gain access to the host cell. Fusion (F) protein mediates the fusion of viral envelop with the cell membranes. Figure 1 (c) demonstrated the fusion process. When the tetramer H protein binds to its receptor, it generates a conformational change within the F protein which is composed of two subunits F1 and F2 linked by a disulfide bond. The activated F protein inserts the hydrophobic fusion peptide into the target cell membrane and provides entry of the viral genome into the host cell interior (Weidmann et al, 1999).

3. RNA Replication and Assembly of Viral Particles

The polymerase allows replication and transcription of the genome within the cell. The negative-sense RNA is copied into a complementary positive-strand which, in turn, acts as a template for the negative strand. Viral components are translated in the cell and are assembled at the cell surface (Yanagi et al, 2006).

4. Release of Virus

MV leaves the host cell in a budding form (Yanagi et al, 2006).

Spread

The viremic spread from the respiratory tract is carried out by infected immune cells including monocytes, dendritic cells, B, and T cells which travel through the local lymphatics and are transported to the secondary lymphoid tissue where further viral replication occurs. A secondary viremia occurs when infected cells enter the circulation and viral replication continues in the endothelia and epithelia of other organs including the skin, gastrointestinal tract, liver, kidney, and central nervous system (Ferreira et al, 2010). A systemic spread is favored by the immunosuppression following infection. Multiple mechanisms are involved in the development of immunosuppression and a brief description below focuses on some of the important pathways.

1. Changes in Lymphocyte Number and Function

Lymphopenia of B and T cells during viremic and post-clinical recovery stages is demonstrated by many studies.

Bieback et al. (2002) showed that MV can bind to Toll-like receptor (TLR) 2 on monocytes, inducing SLAM expression, and interleukin-6 (IL-6) production. Also, binding of SLAM can induce Fas (CD95)-mediated apoptosis of uninfected CD4+ and CD8+ T lymphocytes.

The extracellular composition of CD46 is characterized by four short consensus repeat (SCR) and an STP domain. SCRs 2, 3, and 4 are binding regions for C3b and C4b, thereby preventing them from causing autologous complement lysis. The attachment of MV to SCRs 1 and 2 alters the normal signaling pathway resulting in the down-regulation of CD46, eventually leading to increased C3b-mediated complement lysis (Manchester and Rall, 2001).

MV also inhibits lymphoproliferation by causing cell cycle arrest in the G0/G1 phase in dividing lymphocytes (Niewiesk et al, 1999) and interferes with NF-kB signaling pathways and anti-apoptotic B cell lymphoma 3 (Bcl-3) proteins (Bolt & Berg, 2002). Furthermore, Nucleoprotein of MV binds to the Fc-gamma receptor on antigen-presenting cells and impairs their ability to stimulate T cell proliferation (Hehren et al, 2001). Figure 2 summarized the main pathways leading to immunosuppression.

2. The Shift in Cytokine Profile

Early evasion of the innate immune responses is the interference of interferon-alpha/beta signaling pathways (Naniche et al, 2000) due to inhibition of STAT1 and STAT2 phosphorylation by proteins V and C. However, IFN-gamma production is not affected in the acute phase of measles (Takeuchi et al, 2003).

Cross-linking of CD46 by MV and direct binding of MV to CD46 on monocytes and dendritic cells inhibit the production of IL-12 (Karp et al, 1996) and hence suppress macrophage activation, T cell proliferation, and delayed-type hypersensitivity (Atabani et al, 2001). The loss of IL-12 also decreases type 1 cytokines TNF-alpha and IL-2, leading to a transition to type 2 cytokines IL-4, IL-5, and IL-10 by CD4+ T cells (Moss et al, 2002).

Th1 to Th2 shift leads to a change of cell-mediated immunity to a dominant humoral immunity which is not sufficient to combat new infections (Kemper et al, 2003).

3. Impaired Antigen Presentation

Dendritic cells are critical for the antigen presentation to naive T lymphocyte. MV infected dendritic cells fail to undergo differentiation to become mature effector cells and some of them are susceptible to Fas-mediated apoptosis (Servet-Delprat et al, 2000). Marttila et al (2001) reported that antigen processing of other viruses such as rubella virus and coxsackie B4 virus is compromised in MV-infected human mononuclear cells, suggesting impaired antigen presentation to T cells.

Symptoms

The clinical presentation is induced by immune responses. The initial encounter of the virus activates the innate immunity with high levels of IFN-? and IL-8 but it is not efficient to clear the virus, leading to rapid multiplication of the virus (Sato et al, 2008). Figure 3 illustrates the timeline of the viremia and the appearance of symptoms.

The early symptoms of measles, listed below, usually appear after an incubation period of 10 to 12 days and last for 2 to 4 days due to inflammatory reactions affecting the respiratory tract and conjunctiva (Griffin, 1995).

• Fever
• Malaise
• Coryza
• Cough
• Small white spots in the oral cavity (Koplik’s spots)
• Conjunctivitis
• Rash

The appearance of maculopapular rash reflects the immune complex formation in the skin. It correlates with viremia and the onset of adaptive immune responses. The rash starts on the face and upper back after 14 days of exposure and spreads to the entire body over the next 3 days and finally fades after 5 to 6 days indicating that Cytotoxic T lymphocytes destroy infected host cells and clear the virus. Measles antibodies also appear in the circulation around this time with IgM on day 10 and IgG at day 14. They reduce the measles viral load through serum neutralization. IFN-? and IL-8 levels decrease at convalescent as cytotoxic T cells decline (Heffernan and Keeling, 2008).

Immunosuppression

The most important pathologic feature of the measles virus is immunosuppression. Most measles-related deaths are caused by secondary bacterial and viral infections. Malnourished children with weakened immune systems and vitamin A deficiency are at high risk of developing complications which include blindness, diarrhea, bronchitis, encephalitis, ear infection, and pneumonia. Patients with impaired cell-mediated immunity may not develop the rash and they are susceptible to giant cell pneumonia (Manchester and Rall, 2001)

Vaccination

There is no antiviral therapy for measles although medications can reduce complications. Vaccination is currently the best method to prevent the disease. The first MV called Edmonston strain was isolated in 1954 on primary human kidney cells and it was subsequently adapted to chicken embryo fibroblasts and become the progenitor for currently used attenuated live vaccines. Composition of vaccines is important to elicit long-term protective immunity but not immunologic reactions and clinically significant immunosuppression. The measles vaccine is now usually given as part of a trivalent combined vaccine, MMR which is also against mumps and rubella (Hilleman, 1999). The World Health Organization has recommended infants should have the first administration of the measles vaccine at 9 to 12 months because immunity requires a Th1-type response. For countries with high measles transmission, a second dose should be given at age 15 to 18 months (WHO, 2009).

Vaccination campaigns are effective in promoting the use of vaccination and reducing measles deaths. Between 2002 and 2008, measles vaccination has significantly reduced 78% of measles deaths from an estimated 733 000 in 2000 to 164 000 in 2008. However, many developing countries, particularly parts of Africa and Asia, still suffer from this preventable infection due to the poor access to vaccinations and lack of facilities to properly store vaccines (Manchester and Rall, 2001). Ohtake et al (2010) has reported a spray drying method was successful to produce heat-stable measles vaccine powders. However, further tests are required to demonstrate the feasibility of these dry vaccines. Molecular epidemiology is a useful tool to monitor measles and genomic study of the measles virus can provide insight into the development of new and safe vaccines (Ohtake et al, 2010). The World Health Organization is making an effort to monitor outbreaks and increase immunization coverage and hopefully can eventually eradicate the virus in the future.

Subacute Sclerosing Panencephalitis (SSPE)

SSPE is a fatal disease caused by a persistent infection with a defected form of measles virus in the brain. The common mutated components are the matrix (M), the fusion (F), and the haemagglutinin (H) proteins. Mutations can be point mutations, deletions, and biased hypermutations and are mostly found in the M gene (Gutierrez et al, 2010).

SSPE has a slow progression and usually develops in an interval of 5 to 10 years after the initial infection. It is very rare. The incidence rate varies between countries but the average is about one per million. The age and sex of infected individuals can affect the frequency of SSPE. Infection before the age of 2 years is associated with higher occurrences and boys are 2 times more likely to acquire SSPE (Gutierrez et al, 2010).

The development of SSPE is caused by an incomplete eradication of MV due to inadequate cell-mediated responses caused by genetic polymorphisms (Yentur et al, 2005) and high levels of IL-4 but low levels of IL-12. These cytokines favor humoral response and predispose to viral replication (Hara et al, 2006).

MV enters neurons by binding to host receptors CD46 and CD9 using the F protein. It replicates inside the cells and spreads to neighboring neurons by neurokinins synaptic receptors (Makhortova et al, 2007). Also, sequence analysis of viral RNA showed that the virus was entered from one point and disseminate throughout the brain. The defective structural envelope proteins assist them to escape from the immune system as the mutated M, F, and H proteins failed to assemble and bud out the cells. Thus, the viral particles are not recognized for many years. However, inflammatory responses are finally triggered when the virus damages the host DNA and induces apoptosis (Oldstone et al, 2004).

Histological examination of the brain tissue shows evidence of widespread demyelination, infiltration of immune cells, and blood-brain barrier damage. Glia cells and astrocytes may be activated with increased expression of MHC class II molecules and tumor necrosis factor-?. The appearance of inclusion bodies in brain tissue is also common (Akram et al, 2008).

Patients are often diagnosed based on presentation and clinical findings of electroencephalography, magnetic resonance imaging, and CSF serology (Koppel et al, 1996). SSPE has four clinical stages (Table 2) and most patients died within 3 years of diagnosis (Gutierrez et al, 2010).

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Bloodless Surgery| [Type the document subtitle]| Michael Jones| Abstract There have been many court cases that has made, parent who deny their child blood transfusion, to have to get one. Most time the courts will side with the parents, but if their decision not to is life threatening, the court side with the hospital. Most times it is for religious reasons that parent don’t want their child to have blood transfusion. There are many risks associated with blood transfusion, some parents don’t want to take that risk. Some of the diseases you can get are hepatitis B and hepatitis C.

HIV and AIDS can also be contracted through blood transfusion. It can even lead to death of a recipient. Is it ethical for parents to chose for their kids not to have blood transfusion. There is an alternative to blood transfusion. There are many tools and techniques to prevent the need for blood transfusion. Many doctors today are moving more towards bloodless surgery. The growth of bloodless surgery can be largely due to the number of Jehovah’s Witness patients. It is beneficial for both the patient and the hospital. More cost effective and faster recovery.

I will talk about how preoperative planning is important for a successful bloodless surgery. I will touch on technique like cell savaging and Normothermia. Also introduce you to a cool tool called Cyber-Knife. I will show how Jehovah’s Witnesses and their Hospital Liaison Committee help my family when it came to bloodless surgery. Blood transfusions have been known to have many dangers. In most cases the cons outweighs the pros, causing many people to consider alternative measures. Today one of the most innovative and effective alternatives is bloodless surgery.

In the event that you are faced by such a challenging yet important decision such a surgery, allow me to enlighten you on some of the statistics, procedures and benefits of bloodless surgery to assist you in making an informed decision. As we look at some of the dangers that are associated with blood transfusion alongside modern methods, equipment and benefits of bloodless surgery. We will see how these procedures have progressed over the years, and how the increase in use of bloodless surgery can be attributed to a small group of people known as Jehovah’s Witness.

Witnesses as patients will not accept blood transfusion, under any circumstances. This has caused doctors to look for other solutions. The reasons why you should use bloodless surgery are the risk associated with blood transfusion. Transfusions have been used for over fifty years in clinical medicine. Within those fifty years it has become apparent that the risk such as infectious viruses, bacterial infections and even death has been linked to blood transfusion. Infectious viruses include but are limited to blood borne pathogens like hepatitis B and C.

The Blood bank reports “for screened units of blood in 2007, 1 in 137,000 had hepatitis B, fewer than 1 in 1,000,000 for hepatitis C” (Nagarsheth, N. P. , Sasan, F. 2009) Blood transfusions have been associated with higher incidence of bacterial infections. “Bacterial infection was 2 percent non-transfusion patients, 15 percent for those with up to 2 units of blood red blood cells transfused, 22 percent with three to five units of blood, and 29 percent for patients transfused with 6 or more units of blood. ” (Nagarsheth, N. P. , Sasan, F. 009) The more blood received in a transfusion, the more likely you are to get a postoperative infection. Many People today receive multiple transfusions. Transfusion in time develops allergenic immunization. This limits the supply of compatible blood. These numbers may seem like lottery chances, but why take the chance. Ultimately there is death. Death is not a foreign outcome of blood transfusion. Transfusion related acute lung injury or TRALI, was first reported in the early 90’s. It’s a life threading reaction following a blood transfusion.

TRALI is now known to cause many deaths each year. However, experts believe that the number of death is much higher than what is reported in relation to TRALI, because many doctors are unaware of the symptoms. The cause for such a reaction is conclusive. New scientist states “The blood that causes TRALI appears to come primarily from people who have multiple transfusions. TRALI is the top reason for blood transfusion death in the world. Jehovah’s Witnesses have benefited greatly from their faithful course.

Although their reason for not having blood transfusions are not because of the negative reasons that derive from it, but because of their devout belief in God and the Bible. They obey scripture such as Acts 15; 20 which states “abstain from blood” and Leviticus 7; 26 “you must not eat any blood. ” Jehovah’s Witnesses respect Gods authority and has taken their stand against blood transfusions, regardless of the outcome. If you do not agree with such a point of view, let’s examine the benefits to bloodless surgery and its advancing technology.

Over the years the tools and techniques of surgery without blood transfusion has improved greatly. One tool or technique used for surgeries with a lot of blood lost is called cell salvage. This involves recovering the blood lost by a patient, cleaning it, and putting it back into the patient. This is done non-stop during surgery. “Technological advances have increased system automation… offering higher processing speeds and better end product. ”(Lawrence Goodnough. 2003 Vol. 4) Cell salvaging is also cost effective for the hospital and the patient.

If there is a surgery with lots of blood lost, it is cheaper to use cell salvage than the units of blood used in a transfusion. Also the recovery time is faster reducing the time and money a patient spends at a hospital. How can blood loss during surgery be lowered in order to lessen the chance for need of a blood transfusion? The key is preoperative planning for a successful bloodless surgery. The first thing to be considered is the amount of red blood cell (RBC) that will lost before a transfusion is needed. This is called the transfusion threshold.

Another thing that can be done before surgery is to “increase the patients RBC mass. ” (Watchtower Bible and Track Society, 2004) RBC mass can be increased by injection of iron into the patient. Also erythropoietin(EPO). EPO is a protein hormone produced by the kidneys. “This synthetic hormone acts like the natural erythropoietin found in our kidneys and stimulates the bone marrow to send new, fresh red cells into the bloodstream. ” (Watchtower. org)EPO is normally given 10 to 20 days before surgery. If you increase the RBC mass and lower the transfusion threshold, it allows for an even greater acceptable amount of blood loss.

Normothermia is a technique used to keep the patient’s body temperature during surgery. This helps keep the blood flowing properly. Managing the patient body temperature throughout the entire process reduces the surreal shock to the body which reduces the chances of incurring infection. The patient can be warmed by a thermal suit or a machine that infuses warm fluid into the body. The position can also help reduces blood loss during surgery. Local veins pressure changes depending on the field of relativity to the heart. Low pressure goes hand in hand with blood saved.

Stanford University Medical Center is a pioneer in the use of bloodless surgery in neurosurgery. “Without sawing into the skull or so much as cutting the scalp, they are curing patients whose brain and spine tumors were not long ago considered a death sentences. ” (Fillon, Mike 1997) These surgeries are possible with the use of Stanford University’s computer mediated stereotaxis radio surgery known as the Cyber-knife. The Cyber-Knife is basically a robotic x-ray gun that shots small amounts of radiation into the tumor in a lot of different directions.

This kills off the infected tissue without over exposing other parts of the body to radiation. Cyber-knife is a robotic arm that locks the radiation beam on to the tumor and constantly readjusts its aim in response to the patient’s natural small movement. To help doctors in providing treatment without blood transfusions, Jehovah’s Witnesses have developed a helpful liaison service. Presently, more than 1,400 Hospital Liaison Committees worldwide are equipped to provide doctors and researchers with medical literature from a data base of over 3,000 articles related to bloodless medicine and surgery.

Not only Jehovah’s Witnesses, but all patients in general today, are less likely to be given unnecessary transfusions because of the work of the Jehovah’s Witnesses’ Hospital Liaison Committees. In many surgeries which doctors felt that a transfusion was needed. The liaison committee has provided them with medical literature that shows how effective EPO can be. Some did not think that it would work fast enough to make up the amount of blood needed. A number of cases have shown how quickly EPO gets results. In one instance, on the very same day after EPO was administered, the count of new red cells was already four times normal! ”(Watchtower. org) My mother and father got to see how effective the liaison committee, and blood surgery first hand. When my brother was 16 years old, we found out that he had cancer in his knee. At that time there was no hospitals with a committee or doctor that would perform bloodless surgery on Staten Island. So the hospital liaison committee located Mount Sinai Hospital that had one doctor that did do bloodless surgery. My brother was put on EPO, and was the only patient that was.

For all of the doctors this was their first time use EPO, or even doing bloodless surgery. They were extremely surprised how much better he was doing than the other kid’s that were having blood transfusions. “It was really sad to see all those little kids and babies having blood pumped in to them. ” That is what my mother said when I was asking her about my brother surgery. She said “Junior what the only kid that was up walking around, all the other kids was in their beds look like they was about to die. ” Two things happened to my brother. First he lost all his hire because of chemotherapy.

He also lost his leg because that was the only way they could remove all the cancer. It is reasonable to conclude that although blood transfusion has been around for many years. With all its side effects such as, infectious viruses bacterial infections and even death. It is quickly becoming a thing of the past! With strong scriptural basis and its practical benefits, Jehovah’s Witnesses have been the main reason for the growth of bloodless surgery. Today hospitals across the world implanted bloodless programs to help meet the demand for this growing number.

Along with that, doctors have developed many techniques and tools in order to be successful in bloodless surgery. Techniques such as cell savaging and blood recovery and tools like the Cyber-knife. This have allowed for more cost effective surgeries, faster recovery, lower chance for infection and viruses. If ever surgery is something you have to undergo. I hope that I have persuaded you to make the right decision. References Cantrell, S. (2010). New normothermia measure heats up patient- temperature management. Healthcare Purchasing News, 34(3), 22-29.

Retrieved from EBSCOhost. Fillon, M. (1997). Bloodless surgery. Popular Mechanics, 174(1), 48. Retrieved from EBSCOhost. Goodnough, L. , ; Shander, A. (2003). Evolution in alternatives to blood transfusion. Hematology Journal, 4(2), 87. Retrieved from EBSCOhost. Nagarsheth, N. P. , ; Sasan, F. (2009). Bloodless Surgery in Gynecologic Oncology. Mount Sinai Journal of Medicine, 76(6), 589-597. doi:10. 1002/msj. 20146 Watch Tower Bible and track society of Pennsylvania. (2004) Transfusion Alternatives, Document Series. Watchtower. org

Perquisite has made a reemergence In well-vaccinated populations. Pathogenic adaptation and the decrease In strength are most likely the cause of the reemergence of perquisite. There is pressure for vaccine research because of the resurgence of the pathogen. Perquisite remains one of the leading causes of vaccine preventable deaths in infants under 1 year of age. Perquisite is a Gram-negative, bacillus called Bordello perquisite. This bacterium binds to the ciliated epithelial cells in the misanthropy of the upper respiratory tract. Disease presentation depends on age and history of previous Infection or vaccination.

Young Infants present apneas and occasions, with or without disease symptoms. Adults and teens usually show mild symptoms, and have a typical prolonged cough. The human Forestalled are classified as anamorphic, but there is evidence of genetic variation in B. perquisite. As far as vaccines, there are two types of licensed perquisite vaccines. The first generation is whole cell vaccines (Wows), which are killed cells. The second generation Is cellular vaccines (Cave), which contain virulence factors. The Wows contain whole dead cells that can cause more adverse effects compared to Cave, which have been gradually replacing Wows.

Some of the virulence factors that the CAB uses are pertains, filamentous humiliating, two familiar corpses, and chemically detoxified perquisite toxin. Wows induce type 1 helper T cells, which assist isotonic T cells. Wows also induce a broad antibody response against a range of surface antigens. Oafs induce type 2 helper T cells, which assist B cells. It causes a high antibody response against the vaccine antigens presented. Both of these vaccines give satisfactory long-term protection against perquisite. WAC Is estimated to protect for 4-12 years and the PVC could last 5-7 years.

Programs to vaccinate began in the sass with the WAC. This caused a dramatic drop in mortality and morbidity in children. Perquisite disappeared in the industrialized world in the ass and ass. Infants that are too young to be fully vaccinated are at the highest risk for severe disease. Adolescence and adults are prone to mild Illness from perquisite. There has been a steady Increase, since the ass, In cases of perquisite In countries with successful and long lasting vaccination programs. The two key factors responsible for the resurgence in vaccinated are the appearance of new B. Reroutes strain variants, ND the gradual loss of the protective immunity from vaccines. This is all still under investigation and depends on the subpopulation and countries reporting. Antigenic mutations in 8. perquisite have been noted all around the world. The fact that B. perquisite strains are more Isolated in vaccinated populations than In non-vaccinated populations supports the possibility of mutation of the bacteria. Immune pressure on B. perquisite can eventually cause functional inactivation or complete deletion of genes coding for them. B. perquisite strains may be able to evade the effectiveness of vaccines being given.

Human perquisite specific immune mechanisms protect against disease rather than infection, and are not long lived. Ant-perquisite antibodies can minimize Infection by preventing attachment to respiratory epithelial cells by neutralizing toxins and by removing bacteria through postulation and compliment- Perquisite infection induces Gig antibodies. There is a wide interest in human and Maurine T-cell responses specific for B. perquisite. Humeral and cell-mediated responses readily react to B. perquisite. So far no single specificity, type or level of effectors mechanism has been declared for protection.

Re-evaluation of current Reroutes animal models is necessary in perquisite vaccine research and development. Collecting isolates from the population is also extremely important for the treatment of the new strains of B. perquisite. Studying what is happening with the immune system and how the bacteria have mutated will help prevent many cases of perquisite. I chose this topic because I wanted to learn more about the resurgence of perquisite in vaccinated populations. The article was well written. What I have learned in microbiology definitely helped me understand exactly what the article was saying. Isolating the specific reasons that B. Artists has reemerged is an ongoing study. It is extremely important to collect the specific strains from the population getting sick. These strains will help scientist develop better protection from perquisite. This article focuses on the fact that we need animal models to understand why this disease is reemerging. In order to develop effective vaccines for perquisite these studies are necessary. “Resurgence of Perquisite Calls for Re-evaluation of Perquisite Animal Models.

Ginger Ginger is a knotted, thick, beige underground stem (rhizome). The stem extends roughly 12 Inches above ground with long, narrow, ribbed, green leaves, and white or yellowish-green flowers. The Important active components of the ginger root are thought to be volatile oils and pungent phenol compounds (such as gingerers and gasohol). 1. 1 Parasitological examination of stool specimen This Is the examination of intestinal parasites. This aspect of the training was designed to Introduce students to the area of Woolgathering.

Helmets refer to arms and can be divided to 3 groups: a. Nematodes-Round & segmented b. Custodies-Flat & segmented c. Dermatomes-Flat & engorgement’s. During the collection of stool sample, samples to be examined must be freshly passed. The first test carried out on samples is the macroscopic test which involves the use of the unaided eye to see basic morphological features Including the presence of blood or mucus. The next step Is the microscopic test which Involves two steps: 1 Direct wet preparation 2. Concentration techniques. The procedure of the direct wet preparation is as follows: A drop of normal saline is deed to a clean, grease free slide using a Pasteur pipette. With a swab stick, a tiny quantity of the stool specimen Is collected and placed on the slide containing the normal saline, and Is emulsified with it. After emulsification, the slide Is covered with a cover slip and allowed to stand for 30 seconds to a minute and examined under a microscope using both low and high magnifications(ex. and ex.).

It was noticed that the number of parasite eggs determine the degree of infectious parasite that could result. Concentration of the stool specimen allows for easy viewing of hidden micro organisms. Its advantage over the direct wet preparation Is that In cases of light infections, the causative agents can still be viewed and detected. Concentration can be carried out either using brine, or 10% formaldehyde ether. Summarily, brine concentration is a floatation technique employing the use of density.

Some substances will float and stick to the cover slip and will be examined, while 10% formaldehyde ether is a sedimentation technique, where the substance desired to be examined descends to the bottom of a tube after centrifugation. The stain used for 1 . AAA Collection and examination of blood specimen This involves in the collection and examination of blood samples. Collection can occur through either finger prick using a sterile lancet-when little quantity is required, or vein puncture using a syringe-when a relatively larger quantity is required.

After collection, preparation for microscopic examination follows, and this could be done by direct wet preparation, thin film or thick film methods. The direct wet preparation is carried out as follows: With a Pasteur pipette, 2 drops of blood is placed on a clean, grease-free slide and covered with a coveralls and allowed to stand for seconds to minute, and then viewed under a microscope using low and high magnifications. Note that the standing is for easy identification of motile parasites.

In the thin film preparation, a drop of blood is placed on a clean glass slide, CM from the edge (for labeling). Use another slide, inclined at 30-450 as a spreader. (Allowing the blood to spread within the width of the spreader before pushing forward to obtain a monolayer. ) When the thick film method is employed, 2 drops of blood is placed at the centre of a clean slide, and using the edge of another slide, spread the sample in n anti clockwise manner until a diameter of 1 centimeter is obtained. 1. B Staining techniques Staining is employed only when thin or thick layer preparations are used.

Stains include: Wright stain, Leaching stain, Ageism and Field stains. It should be noted that Leaching stain is used for only thin films, while Ageism stain is used for both thick and thin film preparations. 1. C Blood group determination Three antiserum- A, B and D are used to determine the possible blood grouping of a given blood sample. 3 drops of the blood sample is placed on a clean slide. A drop of entities A, B, and D are placed on drops 1, 2 and 3 respectively and the agglutination of any of the spots determine the blood grouping.

Erasures was treatable with penicillin until the sass’s, in 1959 when more the 90-95% of all strains became resistant it was treated with nonmetallic, a stronger form of antibiotic that was used to treat gram positive bacteria. This In turn because resistant to all strains of the bacterium. Nonmetallic is no longer used today but the term for MRS. is still used. Colonization: The organism Is superficially carried on the skin, in the nose, etc. People are not sick and do not require antibiotics.

Infection: A person has a clinical Infection with the organism e. G. Wound Infection, skepticism, urinary Infection etc. Infected persons usually require systemic antibiotics. MRS. is transmitted through skin to skin contact and is carried by 2% of the human population. MRS. rate is very high in New Zealand. There are two types of MRS., HA- MRS. hospital or health care acquired and CA-MRS. community acquired. The most common means of transmission is in a health care environment as patients have lower immune systems and are weak.

MRS. in hospitals and other care settings is easily spread as hygiene practices are not up to scratch from patient/ nurse contact and hygiene with surgical wounds and other intensive devices such as catheters and feeding tubes. Community acquired MRS. can be found in healthy patients that have not been hospitalized. Many patients of MRS. do not understand their infection and its ways of transmission; this can lead to feelings of astigmatism and fear. MRS. itself cannot have any direct psychological impact on patients with MRS. but is in fact other people’s attitudes and the patient’s perception of scrutiny.

Research has hon. that contact with infected hospital patients on average drops by 22% when a person id diagnosed with MRS.. Isolation techniques in infection control are no longer used as they can cause psychosocial effects for patients and their families and Interfere with the home-like atmosphere that a nurse is trying to establish. For these reasons, a system called Body Substance Precautions (BSP) was developed. It focuses on keeping all moist body substances, (blood, feces, urine, wound drainage, tissues, oral secretions, and other body fluids) from the hands of personnel.

This Is accomplished through hand washing and Increased glove use Shown Ms Fairly retirement village where my patient resides has a policy for MRS. and Infection control from the Missouri department of health and senior services section for living term care and the advisory committee on Infection prevention and control. Their infection control guidelines for long term care facilities have an emphasis on body substance precautions. BSP provides a consistent approach to managing body substances from ALL residents and is essential in preventing transmission of potentially infectious agents. Specific situation for the overall reasonable exposure risk associated with the task. Risk factors that should be included in the evaluation include: Type of body fluid with which there is or will be contact. Volume of blood/body substances likely to be encountered Reasonable anticipation of exposure; e. G. , “will my hands touch the resident’s secretions? ” Probable route of exposure; I. E. , hand contact, airborne, droplet, splashing Microbe concentration in fluid or tissue. Some safety precautions include: Gloves,Handwriting ,Face and Eye Protection ,

Apron or Gown Sharps Handling and Disposal ,Employee Health ,Handling Laboratory Specimens, Soiled Linen ,Disposal of Regulated Waste From Resident’s Rooms, Environmental Cleaning, Cardiopulmonary Resuscitation (CPRM) , Resident Placement, Activity Restriction and the Use of Private Rooms for Infection Prevention and Control , Physician’s Role in Implementing the Body Substance Precautions System, Role of Nurses and Other Health Care Workers in Implementing the Body, Substance Precautions System, Precautions for Residents With Airborne Diseases.