Control y eliminación de la malaria

Prevention of Healthcare related Infections has been the focus of Infection Prevention and Quality Initiatives for more than two decades, and multidrug resistant organisms are responsible for many of these infections, further messing up their diagnosis. In addition to strengthening antimicrobial stewardship practices, and improving adherence to standard precautions (including hand hygiene), contact precautions for patients colonized or infected with multidrug resistant organisms have been advised and broadly adopted to prohibit horizontal transmission in the acute care healthcare setting. However, the data firming these recommendations derives predominantly from epidemic rather than endemic settings, where the burden of transmission as well as the transmission rate is by definition high. Guidelines underscore the cruciality of a basic multiprong step that includes education around epidemiologically important organisms, hand hygiene, contact precautions, environmental cleaning and antimicrobial stewardship. Additional measures recommended in the outbreak setting, such as active screening for MDR GNR, MRSA and VRE, alerts for previous positives with pre-emptive CP, and cohorting of patients and staff, etc have also been presented on occasion. The presenter will discuss the strengths and weaknesses of these steps when used alone or in conjunction, and will argue that the focus on the primacy of contact precautions in acute care settings is misplaced for most MDR organisms. Alternative focus and practices will be presented.

The occurrence and undesirable complications from health care–associated infections (HAIs) have been well recognized in the literature for the last several decades. The occurrence of HAIs continues to rise at a dramatic rate. HAIs originally referred to those infections related with admission in an acute-care hospital (formerly called a nosocomial infection), but the term now applies to infections acquired in the continuum of settings where persons get health care (e.g., long-term care, home care, ambulatory care). These unanticipated infections happen during the course of health care treatment and result in significant patient illnesses and deaths (morbidity and mortality); prolong the duration of hospital stays; and necessitate additional diagnostic and therapeutic interventions, which generate added costs to those already incurred by the patient’s underlying disease. HAIs are considered an undesirable outcome, and as some are preventable, they are considered an indicator of the quality of patient care, an adverse event, and a patient’s safety issue.

the most frequent types of adverse events affecting hospitalized patients are bad drug events, nosocomial infections, and surgical complexities.1, 2 From these and other studies, the Institute of Medicine reported that adverse events affect approximately 2 million patients each year in the United States, resulting in 90,000 deaths and an estimated $4.5–5.7 billion per year in additional costs for patient care.3 Recent modification in medical management settings have shifted more medical diagnosis and services to outpatient settings; fewer patients are accepted into hospitals. The disappointing fact is that the average duration of inpatient admissions has declined while the frequency of HAIs has increased.4, 5 The true incidence of HAIs is likely to be underestimated as hospital stays may be shorter than the incubation period of the infecting microorganism (a developing infection), and symptoms may not come up until days after patient gets discharged. For example, between 12 percent and 84 percent of surgical site infections are detected after patients are released from the hospital, and most become evident within 21 days after the surgical operation.6, 7 Patients receiving follow up care or routine care after a hospitalization may seek care in a non acute care facility. The reporting systems are not as well networked as those in acute care facilities, and reporting mechanisms are not directly connected back to the acute care setting to document the suspected origin of some infections.

HAI surveillance has monitored continous trends of infection in health care facilities.8 With the application of published evidence-based infection control strategies, a decreasing trend in certain intensive care unit (ICU) health care-associated infections has been reported through national infection control surveillance9 over the last 10 years, although there has also been an alarming increase of microorganism isolates with antimicrobial resistance. These modifying trends can be affected by factors such as increasing inpatient acuity of illness, inadequate nurse-patient staffing ratios, unavailability of system resources, and other demands that have challenged health care providers to continuosly apply evidence-based recommendations to maximize prevention efforts. Despite these demands on health care workers and resources, reducing preventable HAIs remains an imperative mission and is a contagious opportunity to improve and broaden patient safety.

According to the facts of physics, if temperature progresses, thermal expansion of an object is positive it will expand and with the decline in temperature, it will shrink. Pressure will increase due to an increase in temperature. On the contrary, during fever we can observe blood vessels and skin are shrunk, pressure decreases, body shivers, sleep increases, motion decreases, inflammation increases, body pain increases, blood circulation decreases, dislike cold things etc. In fever, the firing rate of Warm sensitive neurons declines, and the firing rate of cold-sensitive neuron increases. At the same time if we apply hotness from outside by thermal bag or if we drink hot water, our body responds according to the facts of physics: increase of temperature pressure will also increase, expands blood vessels and skin, body sweats, motion will increase, inflammation will decrease, body pain will decrease, blood circulation will increase, like cold substances etc. During fever, why do our body acts against facts of physics? When disease progresses, pressure and temperature will decline. Blood circulation will decrease due to a decrease of pressure. If the essential temperature of the body is going out, essential temperature and pressure will further decline. This will further endanger the life or action of the organ. When disease increases, it is the sensible and discreet action of the brain that tends to respond against facts of physics to sustain life or prevent organ. There is no way other than this for a sensible and discreet brain to prevent the life or organ. We will get a clear answer if we find out the purpose of fever, sensible and discreet action of the brain. No medical books clarify this. During fever, if the temperature of fever is not a surplus temperature or if it is not supposed to be eliminated from the body, the shrinking of skin and blood vessels, shivering of body, dislike towards cold substances etc., are a protective covering of the body to increase blood circulation to important organs of the body it is against the facts of physics.

According to the facts of physics, if temperature increases, thermal expansion of an object if positive it will expand and with decrease of temperature it will shrink. Pressure will increase due to increase of temperature. On the contrary, during fever we can see the following situations - blood vessels and skin are shrunk, pressure decreases, body shivers, sleep increases, motion decreases, inflammation increases, body pain increases, blood circulation decreases, dislike to have cold substances etc. The temperature increasing and decreasing controlled by brain. Disease or cause of diseases signals the brain to create fever and shivering. In temperature increasing hyperthermia, the firing rate of warm sensitive neurons increases, and inhibit cold sensitive neurons. Contrary to this during fever the firing rate of warm sensitive neurons decreases and the firing rate of cold sensitive neurons increases. In temperature decreasing hypothermia, as in fever the firing rate of warm sensitive neurons decreases and the firing rate of cold sensitive neurons increases. If the aim of cold sensitive neurons increasing their firing rates in hypothermia is to increase blood circulation, then the aim of cold sensitive neurons increasing their firing rates during fever is also to increase blood circulation. If the aim of shivering in hypothermia is to increase blood circulation, then the aim of shivering during fever is also to increase blood circulation. If set point is below there is no necessary of shivering to increase temperature. At the same time, if we apply heat from outside by thermal bag or if we drink hot water, our body acts according to the Facts of Physics -which means, if temperature increases pressure will also increase, expands blood vessels and skin, body sweats, motion will increase, inflammation will decrease, body pain will decrease, blood circulation will increase, like to have cold substances etc. We will get a clear answer if we discover the purpose of fever, sensible and discreet action of brain. No medical books have ever clarified this till date. When disease progresses, pressure and temperature will decline. Blood circulation will decrease due to decrease of pressure. If the essential temperature of the body is going out, essential temperature and pressure will further decrease. This will further endanger the life or action of organs. When disease increases, it is the sensible and discreet action of brain that tends to act against facts of physics to sustain life or protect organs. There is no way other than this for a sensible and discreet brain to preserve the life or organ. During fever, if the temperature of fever is not a surplus temperature or if it is not supposed to be eliminated from the body, the contraction of skin and blood vessels, shivering of body, an aversion towards cold substances etc. are a protective covering of the body to increase essential blood circulation to important organs of the body and this action is against the facts of physics. In all diseases, which decreases essential blood circulation, our body will acts against the facts of physics to increase essential blood circulation.

Statement of the Problem: Heritable susceptibility to tuberculosis (TB) is complicated and polygenic in the nature. 5-10% of humans that come in exposure with the bacterium Mycobacterium tuberculosis (Mt) will get the disease, provided no acquired- or congenital immunodeficiency were present. We still lack a viable explanation for the observed epidemiologic fact.

Method: Activation of macrophages via proinflammatory cytokines IFN-v and interleukin (IL)-17 can kill intracellular bacteria such as Mt. Instead, macrophages stimulated by the Toll-like receptor (TLR)-10 agonists show an anti-inflammatory effect. The TLR-10 acts by inhibiting the TLR-2 signaling from the cell membrane. The TLR-2 is the Mt-binding protein by which activated macrophages can internalize (and finish) Mt. Inactivation of the TLR-2 protein might create a risk for acquiring the disease. This was supported by our finding that TLR2 gene polymorphisms, which either inactivate the TLR2 gene product or have a dominant negative role in TLR-2-signaling, associated with elevated risk for tuberculosis in the Croatian Caucasian population.

Findings: The genome-wide study found that three single nucleotide polymorphisms (SNPs) within the HLA class II loci were significantly related with TB; suggesting that adaptive immunity is of paramount importance for defense against TB. In our studied population, SNP in the TLR10 gene was associated with risk for Tuberculosis, analyzed by the dominant model of inheritance. However, this was contrasted by the fact that SNPs in the IL17A&F genes were not.

Conclusion & Significance: Studying genetic risk by association studies or genome-wide screening led us to propose that clinical manifestation of TB is a state above certain risk-threshold. Threshold is achieved by deposition of seemingly minor susceptibilities divided between the hallmarks of the disease. The model suggests that every human population has its own criteria’s of genetic risks for TB.

Regarding genetic predisposition to tuberculosis, we advice that the maximal risk for clinical manifestation requires complementation of sub-risks divided among the hallmarks of the disease. Clinical tuberculosis would only be known if at least one from each group of the genes encoding putative 5 (perhaps 7) hallmarks of the disease are mutated or changed epigenetically. These mutations/changes could be either sporadic (usually by the influence of the environment like other infection (HIV), nutrition, smoking, radiation etc.) or inherited. Ignorance of the immune attack is one of the hallmarks for TB that is shared with cancer. Perhaps, a similar immunotherapy as the recent one used in treating immunogenic types of cancer (anti-PD1, or/and anti-CTLA4) could be also successful in therapy of (multi-drug) resistant TB.

Consequently, we believe that it is important to study genetic risk factors for TB in every human subpopulation similarly as it is done for cancer, especially now that novel immunotherapies, have opened new ways to treatment of advanced cases

Active tuberculosis is a multi organ disease caused by primary infection or as a reactivation of hidden tuberculosis. Accordingly, active tuberculosis could be primary tuberculosis or reactivation tuberculosis. Primary tuberculosis occurs when the immune system is unable to protect against the Mycobacterium tuberculosis bacterium (MTB) infection. Reactivation tuberculosis, as the name suggests, is the reactivation of contained mycobacterial infection. Reactivation Tb is the most common form of active tuberculosis,revealing 90% of the cases. The lung is the most commonly known organ, other organ systems commonly affected include the gastrointestinal system, the musculoskeletal system, the lymphoreticular system, skin, liver, and the reproductive system.

The World Health Organization (WHO) estimates that, annually, around 8 million people get active tuberculosis globally, and nearly 2 million people die from this disease. Of every 10 people infected with M. tuberculosis, one may develop an active infection at any point of time in their lifetime. The WHO reported in 2017 that the estimated global incidence rate for tuberculosis has decreased by 1.5% each year since 2000. However, despite these substantial gains and drastic global efforts to eradicate tuberculosis, the disease still accounts for significant morbidity and mortality worldwide. Developing countries like India, Pakistan, the Philippines, China, South Africa, Indonesia, and Nigeria experience the highest morbidity and mortality rates. When combined, these countries accounted for 64% of all tuberculosis-related deaths in 2016, according to the WHO.