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Production phase Leaf 4 Grain filling: In this six to seven week period generic 30mg nimotop with mastercard, up to 80% of yield comes from photosynthesis nimotop 30 mg low cost. For example safe nimotop 30mg, by Spore lands Fungus penetrates Fungus grows Symptoms appear spring, septoria tritici is present on the on leaf leaf inside leaf on leaf lower leaves of most crops. Disease development Infection is followed by a ‘latent period’ Latent period when the fungus grows within the leaf but the leaf exhibits no symptoms. Fungal growth beyond Fungicides effective in this period chemical control The cycle of leaf emergence, infection, latent period and symptom expression No disease symptoms visible applies to all foliar diseases. The latent period varies considerably between Latent periods can be as short as 4–5 days for mildew and brown rust. Strategies pathogens and is affected by to manage these diseases depend largely on protecting leaves as they emerge. Many modern fungicides can control disease after a leaf becomes infected but only for about half of the latent period. In the summer, septoria tritici may have a latent period of 14 days, but fungicides provide Latent periods, fungicide activity and spray timing eradicant control for only about seven Example based on septoria tritici days. Latent First spores arrive infection First spores arrive (no symptoms) Infection from within crops Leaf 1 Leaf 1 (flag leaf) As stems extend and upper leaves First spores Latent infection Latent Leaf 2 emerge, the crop tends to grow away arrive (no symptoms) Leaf 2 infection First lesion (no symptoms) from the disease. Leaf 3 Leaf 3 lesion Leaf 3 Leaf 3 10–14 days 10–14 days 10–14 days However, the crucial final three leaves Severe are at risk as soon as they emerge. By lesions this stage, most inoculum comes from within the crop and spore movement from other fields is much less Leaf 4 and below Leaf 3 infected but Leaf 3 may now be Symptoms now visible important. Rusts and powdery mildew already showing disease still in latent showing symptoms – on leaves 2 and 3, not have very short latent periods and can symptoms. In the absence of fungicide use, the Leaf 3 can be Leaf 2 infected but still protected. Instances where a T0 spray may be considered include: Spray window The ‘spray window’ for effective disease control on a – To delay septoria tritici development particular leaf layer is relatively narrow. The optimum spray – Where mildew, yellow or brown rusts are active timing is when a leaf has just fully emerged. Effects of spray timing on disease control For more information, see The optimum T1 spray gives maximum The optimum T2 spray gives maximum disease control on Cereal growth stages – a disease control on leaf 3, and provides the flag leaf and eradicates any latent infections on leaf 2 some protection for leaf 2. In spring and summer, lesions are usually June rectangular and confined by leaf veins. Leaf lesions are often Mild winters and wet, windy surrounded by areas of leaf yellowing or death. Unusually dry weather throughout May need to be monitored regularly for disease, as new races can and June may reduce losses. Higher rainfall areas in the south occur that could potentially overcome the resistance. Cultural The national survey, reported by CropMonitor, showed that Avoid very early sowing of susceptible varieties. This is the lowest incidence of septoria tritici recorded Control relies on using robust rates of azole fungicides at T1 since 2011. Resistance to For more information, strobilurin products Life cycle see Topic Sheet 113. These ascospores infect leaves to produce leaf spots provide adequate from mid-autumn onwards and then spread by rain splash and control. Some systemic Heavy rainfall encourages rapid spore movement from lower to seed treatments upper leaves during stem extension. Wheat disease management guide 12 Foliar diseases – Septoria nodorum Septoria nodorum Life cycle The pathogen survives in crop residues, volunteers and wild Phaeosphaeria (Stagonospora) nodorum grasses. Airborne ascospores from Sometimes known as leaf and glume blotch wheat stubbles spread infection to newly-emerged crops. Secondary spread occurs when pycnidiospores, produced within leaf spots, are dispersed by rain splash. The disease can develop very rapidly in warm temperatures (20–27ºC) with long periods (6–16 hours) of high humidity. Leaves and ear infected by contact and rain splash In spring, crops also infected by pycnidiospores and ascospores pycnidiospores ascospores Seed infection Overwinters on crop debris, grass weeds and volunteers Seed infection causes damping off and early infection of plant Risk factors High – Susceptible varieties Moderate – High rainfall during and after ear emergence Low Symptoms On leaves, symptoms are mainly oval brown lesions with a – South-west and coastal small yellowish halo. Pale brown, rather than black, pycnidia locations distinguish septoria nodorum from septoria tritici. The indistinct brown pycnidia may be only visible when lesions are held up Control to the light. Under high disease pressure, leaf symptoms can Varieties include small purplish-brown spots. All varieties need to be monitored regularly for disease, as new races of pathogens can occur that could Importance potentially overcome the resistance. In 2015, septoria nodorum was recorded for the first time since 2009 in the national survey, reported by CropMonitor. Cultural When severe attacks occur, it is usually in association with Ploughing or cultivation to bury crop residues after harvest high rainfall at ear emergence (eg in the south west). Fungicides T1 and T2 sprays applied to control other diseases usually control septoria nodorum on the leaves. Under hot, dry conditions – or after – Cold winters with several frosts fungicide use – pustules may be difficult to detect. In untreated susceptible varieties, yellow be monitored regularly, as new races can occur which could rust can reduce yields by over 50%. Outbreaks often occur in coastal areas from Essex Sometimes this is not possible – with the incursion of the to the Borders and central England. Life cycle Susceptible varieties should be grown alongside more Epidemics are associated with mild winters that enable the resistant varieties to limit the spread of the disease. Control volunteers that provide a ‘green bridge’ between In early spring, distinct foci may occur; secondary spread is harvest and emergence of new crops. Cool Fungicides (10–15ºC), damp weather, with overnight dew or rain, Azole and most strobilurin products are very effective; some provides optimum conditions for disease development. Symptoms appear 7–14 days after infection so leaf tips may show symptoms before leaves fully For yellow rust population emerge. During autumn and winter, a few for epidemic progress pustules, confined to older leaves, may be seen.

In light of the epidemiological transition buy generic nimotop 30 mg line, we also examine the possibility that a divergence in sex ratios between developing and developed countries is simply due to changing compositions of disease nimotop 30 mg otc. If true generic 30mg nimotop amex, such excess deaths would arise not from lack of “similar care” for men and women but from the changing nature of the disease environment. There is a prima facie case for such an argument, simply because Group 1 diseases might discriminate less between males and females, while there may be intrinsic female advantages in surviving Group 2 disease (see Supporting Information for more discussion). Appendix A describes this dataset in more detail, and points out some of its limitations. It is this estimate that exactly explains the overall decline in missing women in sub-Saharan Africa with this alternative benchmark. Therefore, to argue that blacks in the United States form a better reference group, we have to be certain that the reasons for “missing” black women in the United States (relative to developed regions) stem entirely from biological differences and not from the possibility that black women in the United States suffer more discrimination than their white counterparts in developed countries. Likely, it is a combination of these two factors (and perhaps others) which explain missing black women in the United States. In contrast, deaths from injury tend to be the most variable across countries, as well as across communities within countries. Special methodological considerations Recall (3) from Section 2, which yields a “reference” death rate for women by age and disease: dm(a, k) w u (a, k) = dm(a, k)/dw(a, k) and the corresponding expression for excess female deaths by age and disease: w w w mw(a, k) = d (a, k) − u (a, k) π (a), where πw(a) is the starting population of women of age a. If we simply add these numbers up, we obtain an estimate for missing women that excludes compositional effects due to the epidemiological transition (refer to Section 2. The most significant of these is maternal mortality, for which a male death rate is not defined, so equation (8) is invalid. We therefore construct the reference death rate for maternal mortality in each age group by using the ratio of maternal to overall female mortality in each age group in the reference region, and then scaling this by age-specific female mortality for the country in question. That is, dw(a, mm) w w u (a,mm)= d (a), (9) dw(a) where the index k = mm stands for maternal mortality. Maternal mortality is very low in developed regions, so that this procedure will treat practically all maternal deaths as excess female deaths, which is as it should be. A second set of exceptions concerns diseases for which relative death rates for devel- oped countries by age are unreliable, because there are so few deaths. Particularly important examples are malaria, childhood cluster diseases (such as measles), diarrhoeal diseases, and tuberculosis. In these cases, we have nothing to base our estimates on and simply use a reference death ratio of 1:1 as a benchmark. We consider all such categories for which there are at least 2000 female deaths in our country of interest. For malaria, the total number of deaths over all ages and over all developed regions was less than 100 in the year 2000. For diarrhoeal diseases and tuberculosis, the situation is somewhat different: there are a substantial number of deaths recorded in developed regions for these two categories of disease, but these primarily occurred at ages 60 or older. Yet in less developed regions, younger age categories account for a large number of deaths from these diseases, particularily in the case of diarrhoeal deaths. We therefore cannot form reliable reference ratios from developed regions in the younger age categories in this case. For a given disease–age category, we consider fewer than 100 female deaths in developed regions to be too small to form reliable reference death ratios. Alternatively, following the same strategy as above, we could have instead used the overall death rates from all communicable diseases within each age group in developed countries to compute our reference death ratios. However, there is an implicit circularity here: to trust the medical estimates, which are often obtained in developing countries, one must believe, a priori, that there is no gender bias in those countries to begin with. General observations We report our estimates in Tables 5 (India), 6 (sub-Saharan Africa), and 7 (China). In a world with accurate data (including reliable reference death rates) for every conceivable disease, these group sub-aggregates would be built by adding up all missing females from the diseases in that group. Intentional 0 2 29 8 10 3 2 0 mwB = 1637 320 64 191 100 139 236 318 83 mwA = 1712 310 93 258 93 120 241 300 113 Notes: Figures are rounded to the nearest thousand. If we did not do this, and treated all diseases as one composite ailment, we would be entirely unable to separate out the influence of a change in the disease composition. By forcing ourselves to add over these categories, we freeze the disease composition to that in the country of interest, and therefore pick up the “within-disease” component of missing women. The epidemiological transition is located in the difference mwA − mwB, as Observation 1 makes clear. The penultimate line records mwB, as discussed above, pro- viding estimates for every age category as well as a total, obtained by adding in the estimate for missing girls at birth. Recall that mwB deliberately eliminates the effect of the changing composition of disease across developed and developing countries, while mwA includes all changes in disease composition. Yet there is little difference between the two sets of totals at most ages, and the two grand totals mwA and mwB practically agree. By Observation 1, we must conclude that few, if any, of the missing women in India can be attributed to the epidemiological transition. First, it is evident that the bulk of missing females at younger ages come from Group 1 diseases. Group 1 disease accounts for fully 260,000 missing females between the ages of 0 and 4, which is over 15% of the total. Of these, about half is due to infectious disease, while the remainder may be attributed to respiratory and perinatal ailments. To provide some idea of how big this number is, consider maternal mortality in India, which is widely acknowledged to be a serious issue (see, e. Maternal deaths account for about 130,000 excess female deaths, no small number, but of the same magnitude as excess female deaths caused by infectious and parasitic diseases within the age 0–4 category alone. As we have already seen, much of the Indian discrepancy is to be found at older ages. At these ages, the excess burden falls mainly on non-communicable Group 2 diseases. Women die at a rate closer to men from cardiovascular disease relative to developed countries. The plight of older women in the Indian subcontinent, especially of widows, has received some attention in the literature (see, e. One rather sinister observation is that the number of excess female deaths from “Injuries” is high in India.

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Summary of historical studies investigating the efficacy of phage therapy of wounds 30 mg nimotop overnight delivery. Reference Affiliation Bacteria Wound type (n) Route of administration Outcome Details McKinley purchase nimotop 30mg online, Baylor University Staphylococcus Open wounds (4) Injected directly into wound 100% success rate Resulted in decreased discharge and 1923 College of spp purchase nimotop 30 mg with amex. Continued Reference Affiliation Bacteria Wound type (n) Route of administration Outcome Details Walker, 1931 Research Staphylococcus Abscess 0. Squibb & experiments) 5 ml intravenous 2 min after the bacterial inoculum Sons injections or once lesions had developed; each route of administration was set up as a separate study Shultz, 1932 Department of Staphylococcus Furunculosis (63) Subcutaneous injections; 70% success rate A 2-year study: appropriate phage Bacteriology & spp. Major burn wounds, involving 15% of care strategy that encourages deep tissue the total body surface area, may look homeostasis, allows the recolonization of superficial but tend to develop into deeper, commensals and ultimately achieves wound full-thickness wounds, where excision of healing. In all cases, repeated irrigation of the necrotic tissue and closure of the wound by wound that removes foreign material and grafing skin over the area is necessary. For superficial irradiation and some medications such as local infections, the appropriate topical corticosteroids and other immunosuppressive antimicrobial(s) and wound dressings may drugs, stress-induced hyperglycaemia, low be all that is required, but for deep wound serum cortisol levels, anaemia and the length and systemic infections, systemic anti- of hospital stay. Individuals with burns microbials are necessary (Percival and Dowd, covering 30% of the total body surface area 2010). Co-morbidities and complications that are at risk of rapid bacterial colonization due modify the strategy needed to treat a to the immunosuppressive effect of the injury particular wound infection include advanced (Rowley-Conwy, 2010). The prolonged age, obesity, poor nutritional status, dys- presence of an open wound or delayed initial vascular diseases such as those seen with burn wound care leads to high incidence smokers and diabetic patients, or circum- rates of morbidity and mortality. The use of broad-spectrum anti- Diabetic wounds biotics for treating these infections tends to favour subsequent colonization by exogenous Acute as well as chronic wounds are common nosocomial organisms, which are generally complications of diabetes mellitus, which is antibiotic-resistant bacteria such as methicillin- one of the most common causes of chronic resistant S. The chronic wound state may occur as Osteomyelitis part of disorders such as diabetes or pressure regions (e. It is most commonly caused by Once infection occurs, it is imperative to bacteria but may also be due to fungi. It can intervene by undertaking an effective wound- occur as a secondary complication of trauma, 190 C. It may also occur by atending physician to use phage therapy on contiguous spread in regions of poor vascular their patient, and a confirmation of staphylo- function, such as diabetic foot infections or cocci being present in their bloodstream. It from a haematogenous dissemination from was noted that a larger number of patients infected skin sores or insect bites, urinary were male, possibly due to a greater exposure tract infections or dental manipulation. Various 416 cases that produced staphylococci isolates types of osteomyelitis require different from patients found that 89% of these medical and surgical strategies, ranging from isolates were susceptible to the phage stock short-term antibiotic therapy and limited preparation employed in this study. The infecting organism may the trial – these were counted as the negative- vary with age and underlying disease. Twenty-five patients received Children suffering from acute haematogenous phage therapy despite their blood cultures osteomyelitis may tend to be infected by becoming negative prior to commencing Streptococcus pyogenes, whereas adults suf- treatment, and seven of them died. This later fering from chronic open wounds to the bone group was considered the positive-control and sof tissue may have P. We also consider the Soviet bination of other measures such as using Union phage-therapy experience. The last large phage-therapy study carried This study, as well as those outlined in out in the West, following the phage-therapy- Table 13. They reported on the use of phage speculated on the presence of bacterial therapy in 500 patients suffering from artefacts in these preparations, they were staphylococcaemia in the years 1931–1940, unaware of bacterial toxins (i. The systemic infection in most of some of the side effects observed from phage these cases had resulted from local infection treatments (see Olszowska-Zaremba et al. A summary showing staphylococcaemia patients included in the phage therapy study by MacNeal et al. The results are described in this phages infecting strict anaerobes, staphylo- section. When we consider that this therapy cocci and streptococci were used to treat was all that was available in the pre-antibiotic patients with gas gangrene. In one study, the era and later that the economics of medical mixture was applied to 767 patients with only care in the Soviet Union only allowed limited a 19% death rate compared with the control access to the variety of antibiotics available in group, which was treated with ‘other the West, it can be understood that the need methods’ and resulted in 42% deaths. Another to care for patients, by whatever means series, using the same phage mixture available, took precedence over rigorous produced at the Eliava Institute, had 19% scientific methodology. Viewed in this deaths compared with 54% using ‘other context, it is possible to glean some useful medications’. The death/survival rates appeared methods for the intramuscular and intra- to be the end points, with no mention of limb venous use of phage preparations. These studies have been reviewed by were most commonly applied topically at the Chanishvili et al. Three ‘mobile infected with staphylococcus and a 72% brigades’, each composed of six persons positive outcome in 1888 cases, in which the (three surgeons and three bacteriologists), 28% of failed patient treatments was were to test bacteriophage cocktails specific atributed to mixed bacterial infections. These for staphylococci, streptococci andClostridium reports prompted the Soviet Military to perfringens. The first brigade treated 2500 institute the universal use of phage wound wounded soldiers, with the result of only therapy during the Finnish Campaign and 1. Data from of Georgia, was producing 5 t of phage the other two brigades showed that, of 941 products each week primarily for the military. Many such wounds therapy were revealed and it was concluded had abundant pus and complicated infections that ‘in those that were treated earlier, the with surrounding inflammation as well as wounds were clear of infection sooner and necrotic foci, and retained bullet and wood granulation appeared rapidly, temperature fragments. To control serious intoxication due was normalized in a shorter period of time to sepsis and toxaemia, as well as high fever and unpleasant odours did not develop or and gangrenous inflammation, these wounds were insignificant’ (Chanishvili et al. This by wound irrigation with a 2% sodium move allowed a more controlled scientific chloride solution. The wounds were then environment and more standardized tech- sprayed with phages and dressed with niques of blood analysis prior to phage phage-soaked gauze but not packed with therapy. A volume of 5–10 ml of phage was surgical wound manipulation and phage injected simultaneously into the abdominal application were systematically recorded and wall, shoulder or hip. Only three or four such work was published in 1941 in a book writen treatments were normally required to achieve by Professor Tsulukidze entitled Experience of a complete cure and the blood composition the Use of Bacteriophages in Conditions of War was also improved. In summary, he found day of treatment, so that further infection was that, on arrival from the front, mixed bacterial unlikely. Treatment infections were the general rule and were with phage therapy took a number of days unlike infections seen afer long hospital whereas ‘ordinary therapy’ took several stays and prolonged manipulations, which weeks.

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Therefore purchase nimotop 30mg otc, those in author- ity should understand the disease of addiction and use an effective discount 30mg nimotop visa, compassionate approach that will benefit both the addicted nurse and nursing as a whole cheap nimotop 30mg without a prescription. Understanding the biological mechanisms that underlie he concept of alcoholism and other drug dependency as addiction can help others recognize and treat the problem with being a disease first surfaced early in the 19th century. The American Nurses Association estimates that 6% to 8% of nurses have alcohol or drug abuse problems serious enough to impair their judgment, meaning that the disease of Defining Addiction addiction profoundly affects the nursing profession. Addiction is defined as the ongoing use of mood-altering sub- The following description of the disease of addiction has stances, such as alcohol and drugs, despite adverse consequences. Characteristics of alcoholism include continuous or peri- phenomenon of craving in some can also be at least partly at- odic impaired control over drinking, preoccupation with alcohol, tributed to these neurophysiologic mechanisms. Under the direct use of alcohol despite adverse consequences, and distortions in influence of the disease, the addict is in an altered state of con- thinking—most notably denial. To the brain, alcoholism and sciousness, one that is now measurable with the newer imaging drug addiction are the same. The status as a maladaptive pattern of substance use, leading to clinically of “disease” can also assist with the necessary coverage for treat- significant impairment or distress, although they are manifested ment, giving addiction its rightful parity with other diseases in differently. Substance dependence is defined and manifested by three Not everyone accepts addiction as a disease. Some still or more of the following occurring at any time in the same view it as a moral failure or lack of will power. Many nurses 12-month period: remain silent about their addiction to mood-altering substances • A need for markedly increased amounts of the substance to for a number of reasons. The most important reason is denial achieve intoxication or desired effects (Morse & Flavin, 1992). Addicted nurses also experience shame • A markedly diminished effect with continued use of the same and guilt that drive the addiction underground. They do not in- amount of the substance tentionally jeopardize the safety and well-being of their patients • The characteristic withdrawal syndrome for the substance or themselves; in fact, the workplace is often the last place the Volume 1/Issue 2 www. A predisposition alone is generally not Typically, the workplace is the last place the signs and symp- enough to cause the disease. Changes in mood, behavior, social factors, such as peers and societal and familial norms, and and appearance may be gradual or sudden. The signs and symptoms of addiction include: psychological issues, such as a history of physical or sexual abuse, other trauma, and dual diagnosis. Chemical dependency is a primary disease, however, c long sleeves and tinted glasses inappropriate for the setting and is not caused by other diseases. Both diagnoses must be c overuse of cologne and breath fresheners treated fully and equally. The only issue is the use of addicting c severe mood swings or change in personality c withdrawal from family, friends, and coworkers—for substances to treat a chemically dependent person, which may example, refusing social invitations fuel the addiction—for example, treating anxiety disorder with c frequent disappearances during work hours benzodiazepines. A person with a dual diagnosis needs continuity c smell of alcohol on breath during work hours of care and caregivers who understand addiction. Animal studies show that specific alcohol-related traits, • The same substance taken to relieve or avoid withdrawal symp- such as sensitivity to intoxication and sedative effects, develop- toms ment of tolerance and withdrawal, and even susceptibility to • The substance taken in larger amounts or over a longer period organ damage, can have genetic origins. Studies of family ill- than was intended nesses, twins, and adoption support a genetic contribution to • A persistent desire or unsuccessful efforts to cut down or con- alcoholism. The Human Genome Project is also contributing trol substance use to our understanding of the role of genetics in alcoholism. The of the following in a 12-month period: stronger urge to drink in the alcoholic may be related to the G • Recurrent substance use resulting in a failure to fulfill major allele that predisposes people to drug use in general (Gianoulakis, role obligations at work, school, or home Krishnan, & Thavundayil, 1996). In his 2003 editorial in The • Recurrent substance use in situations in which it is physically American Journal of Psychiatry, “A Predisposition to Addiction: hazardous Pharmacokinetics, Pharmacodynamics, and Brain Circuitry,” Dr. Substance dependence and abuse are differentiated for di- Research points to the commonality of all addictive processes, agnostic purposes, but often treated similarly by clinicians. Despite many discussions regarding an addictive personality, research indicates that the personalities of alcoholics are hetero- Causes of Addiction geneous. Certain personality problems, such as impulsivity and A percentage of the population has a biogenetic predisposition poor coping skills, can result from early developmental problems, 32 Journal of Nursing Regulation but these personality deficits can also result from addiction. That Figure 1 is, addiction can interfere with the way people see themselves, Reward Circuitry of the Brain cope with stress, and interact with others. Sometimes, determin- ing whether personality problems are primary or secondary to ad- The reward circuitry of the brain involves the mesolimbic dopamine system, including the prefrontal cortex, the nucleus diction must wait until the addict is sober for an extended period. From a psychological perspective, Khantzian and Mack have described “the heavy reliance on chemical substances to Prefrontal relieve pain, provide pleasure, regulate emotions, and create per- cortex sonality cohesion. It seems logical that the strong connection that can occur among sober addicts plays a pivotal role in addiction recovery. Conversely, disorders that disrupt these attachment and affiliative systems, such as borderline personality disorder, Reward is the term neuroscience uses to describe experi- can pose significant challenges to the treatment of addiction. Before the addiction, a deficit in reward the areas of the brain involved in reward and the neurochem- capacity could create a feeling of deprivation, leading to craving istry of our feel-good chemicals that create reward responses. During active substance use, previ- Neurotransmitters, such as dopamine and beta-endorphins, fa- ous temperament styles are exaggerated, and because of ongoing cilitate communication to the reward center. Eventually, the reward pathway shifts its sensitivities Nurses at Risk to the substance or behavior instead of the neurotransmitters. The risk to nurses is the same as it is for the general popula- In other words, the brain begins to depend on outside chemicals tion, except for one thing: Nurses have better access to opiates. This accessibility, coupled with the culture of relieving pain with mood-altering substances, can create an ideal environment Magical Connection for a person who is genetically predisposed to addiction. Thus, The predisposed brain of the addict is like a lock, and the ad- nurses with a significant family history of addiction should either dicting substance or behavior is the key. When the key opens abstain from working with opiates or have an awareness of the the lock the first time, the experience is extremely powerful, potential for danger and incorporate stress-reducing behaviors even magical. In the mid-1990s, positron emission tomography into their lifestyle as a prevention. These studies and others demonstrate that addicts experience their substances Reward Circuitry of the Brain more intensely than nonaddicts.