Infection

The study also revealed that most infections occur about two weeks after surgery, not one week as physicians previously thought. “It’s not what we expected to find,” said Michael A. Acker, M. D., the study’s lead researcher and professor and chief of cardiovascular surgery at the University of Pennsylvania Medical Center in Philadelphia, Pa. In abstract 12247, researchers analyzed more than 5,100 patients in a heart surgery registry.

Patients, average age 64, were treated at nine U. S. academic medical centers and one Canadian center. The median time to major infection was 14 days after heart surgeries. Forty-three percent of all major infections occurred after hospital discharge. “Half of these patients had no evidence of infection before they were discharged from the hospital,” Acker said. “Then they had to return because of the new infection. One implication is that patients must be followed more closely after discharge. In this study, which excluded patients who were infected before surgery, researchers found 761 infections: 300 were classified as major infections (occurring in 6 percent of patients) and 461 were minor (in 8. 1 percent of patients).

Of the major infections:  Pneumonia, infection of the lungs, occurred in 2. 4 percent of all patients.  difficile colitis, an intestinal infection, occurred in 1. 0 percent.  Bloodstream infections occurred in 1. 1 percent.  Deep-incision surgical site infections occurred in 0. percent. Minor infections included urinary tract and superficial incision site infections. The most commonly performed procedures were isolated coronary artery bypass graft and aortic and mitral valve surgeries. Seventy-four percent were elective surgeries and 26 percent were non-elective or emergency surgeries. Several risk factors appeared to increase the risk of developing infection, including congestive heart failure, hypertension, chronic lung disease, corticosteroid use prior to surgery, and length of cardiopulmonary bypass time. In the next level of analysis, the focus will be on differences in care, from the types of dressings, the types of antibiotics, and the types of surgical preparations, to show what processes of care are associated with decreased incidence of infections,” Acker said. “The registry will allow us to modify our best practices to manage post-operative infections. ” The National Heart, Lung, and Blood Institute, National Institute of Neurological Disorders and Stroke and Canadian Institutes of Health Research funded the study.

Skin preparation reduces cardiac implantable device infections In another study (abstract 10041), special skin preparations for 3,700 patients significantly reduced infections from cardiac implantable electronic devices. Researchers at a Milwaukee hospital washed patients’ skin with a special antibacterial solution the night before and morning of the procedure. They also included a strict three-minute drying time for the surgical skin preparation. These steps decreased implant infection rates from 1 percent to 0. 24 percent at a year following the implant placement.

More staphylococcal bacterial infections are occurring after implantation procedures, said Renee Koeberl, R. N. , M. S. N. , lead author of the study.  Pneumonia not a deep incision surgical site infection  is the most common serious infection after heart surgery, according to new research presented at the American Heart Association’s Scientific Sessions 2011. So we need to be aware and curious to everything around us, to secure our good health.

In comparison with the four hospitals the higher waste Is generated In Dacha Medical College Hospital and lowers waste Is The intrinsic vulnerability of waste generated from the hospital is pathogens and sharps. It is apparent that a very few fraction of about 13%-25% of hospital waste requires special treatment for destroying the pathogens. However careless management of this waste may compromise the quality of patient care. Hospital staffs involved with handling, collection, storage, transportation, treatment and disposal system, waste pickers and scavengers are more likely to come in direct contact with the contaminated waste. Hence the incidence of diseases like AIDS, Hepatitis, Tuberculosis, Diphtheria and Cholera among these community increases subsequently.

Even their improper transportation and disposal can cause serious pollution to the surrounding environment. Through this survey it was revealed that poor waste management prevails in almost al hospitals and clinics. In absence of adequate laws and regulation, waste is generally dumped together in a public place or open DDCD bin near the hospital premises. Hospital authorities are not aware nuisance causing from waste. Waste segregation at source is very poor. Rapid growth of hospitals along with dumping of infectious waste with other municipal waste is making the situation detrimental. Therefore proper management of healthcare waste with adequate policy is essential for the environment and for the community as a whole.

Hepatitis is a symptomatic infection that affects the liver. The most common types of Hepatitis virus are A, B, C, D and E. The history of hepatitis dates back to ancient times and the success of modern medicine have improved the prevention and treatment of most types of Hepatitis. The high risk groups include injectible drug users, hemodialysis patients, and those who have sexual contact with infected people. Hepatitis B and C are the leading cause of chronic liver disease and liver cancer in the United States.

History

History of Hepatitis is believed to go back as far as the ancient times. With today’s modern medicine scientists have discovered a major breakthrough in 1963 that identified a serum hepatitis known as Hepatitis B Virus (HBV). Ten years later, they found the cause of hepatitis infection and called it Hepatitis A Virus (HAV). In 1989, Hepatitis C Virus (HCV) was discovered. Hepatitis Delta Virus (HDV) was known in the 1970’s, but was better understood by scientists in the 1980-1990’s. Later the Hepatitis E Virus (HEV) was discovered in 1990.

Etiology

Hepatitis A (HAV) the least serious form and may develop as an isolated case of an epidemic. It is estimated that one out of every 3 people has been affected by HAV. Transmission of HAV is associated with close personal contact or contaminated food or water (Wilson, p. 13). Hepatitis B (HBV) is transmitted primarily by contact with infected blood, semen, and other bodily fluids. Injectable drug users, people with multiple sexual partners and homosexuals are at higher risk for contracting the B virus. Hepatitis B can severely damage a person’s liver, resulting in cancer (Nordqvist, 2009).

Hepatitis C (HCV) is the most serious blood borne infection in the United States. The disease is often passed between drug users who share needles. People who are on dialysis and sexual contact are also at risk. The hepatitis virus is the leading cause of liver cancer and the most common reason for liver transplants (Wilson, 2005). Hepatitis D (HDV) is a defective virus that only if the people who are infected with Hepatitis B. The virus is transmitted through contact with infected blood, unprotected sex, and piercing of the skin with infected needles.

The effects of HDV are more serious and progresses to chronic liver disease more frequently than virus A, B, or C. Hepatitis E (HEV) is the leading cause of epidemics around the world, but cases in the United States are rare. Primarily HEV is spread by fecal contaminated drinking water and there is no evidence that HEV progresses to chronic liver disease (Wilson, 2005). There have been no cases of HEV reported in the United States. Patients with Hepatitis A and B typically experience sudden unset of fever, malaise and fatigue, nausea and abdominal pain. Anorexia and jaundice may also be present.

Hepatitis C is less forgiving as symptoms may not appear until the patient’s condition has progressed to cirrhosis or cancer (Neighbors & Tannehill-Jones, 2006). Populations affected by Hepatitis In the United States approximately 1. 2 million are living with Hepatitis B and 3. 2 are living with Hepatitis C. Estimated 25,000 people become infected with Hepatitis A. Many people do not know the virus infection exist in the body (CDC, 2009). The Center for Disease Control (2009) estimates 180 million people over the world is infected with HCV, of which four million are identified as cases in the United States.

Each year 26,000 cases of HCV are diagnosed in the United States alone, and 10,000 to 12,000 deaths are contributed to HVC (Centers for Disease Control [CDC], 2009, p. 1). The hepatitis virus is the leading cause of liver cancer and the reason for liver transplants. In the United States approximately 1. 2 million are living with Hepatitis B and 3. 2 are living with Hepatitis C. Estimated 25,000 people become infected with Hepatitis A. Many people do not know the virus infection exist in the body (CDC, 2009).

Treatment

In July of 1982 the Hepatitis B vaccine was approved for use and thirteen years later (1995) the HAV vaccine was approved for use. These significant scientific breakthroughs have led a steady decline in the number of HAV and HBV cases in the United States. There is not a vaccine available for HCV but scientists are working hard to develop one. In addition to the vaccines some treatment options are available. HAV usually resolves itself and no specific treatment is needed. Treatment for HBV is Interferon which slows the progress of the disease in about 40% of patients (Neighbors & Tannehill-Jones, 2006).

In addition to treating HBV Interferon is very effective for treating HCV. This antiviral slows the disease process about 30% of the time (Neighbors & Tannehill-Jones, 2006). There is not an effective treatment for HDV or HEV. Treatment for end stage cirrhosis or cancer caused by hepatitis may result in a liver transplant. Conclusion Hepatitis is a disease that causes an inflammation of the liver. There are several viruses that cause cirrhosis or cancer of the liver. Hepatitis A is a mild disease that typically resolves itself.

The hepatitis B virus is more severe than A and less severe than C. The availability of vaccines for Hepatitis A and B has decreased the number of cases while Hepatitis C continues to infect high risk populations. Scientists continue to strive for a cure for Hepatitis C but in the meantime a people need to be aware of the disease and take steps the reduce the possibility of exposure.

References

1. Centers for Disease Control. (2009). Morbidity and Mortality Weekly Report. Retrieved from http://www. cdc. gov/mmwr/PDF/ss/ss5803. pdf
2. Neighbors, M. & Tannehill-Jones, R. (2006). Viral diseases acquired through alimentary and other routes. In Human diseases (pp. 201-203). Retrieved from https://ecampus. phoenix. edu/content/eBookLibrary2/content/eReader. aspx
3. Nordqvist, C. (2009, April). What is Hepatitis? Symptoms, Causes, and Treatment. Medical News Today, (), Retrieved April 13, 2010 from http://www. medicalnewstoday. com/articles/145869. php
4. Wilson, T. (2005). The ABCs of hepatitis. The Nurse Practitioner, 30(6), 12-18. Retrieved from Retrieved from CINAHL Plus with Full Text database.

Prostitution and Venereal disease Prostitution: ?Prostitution is the act or practice of providing sexual services to another person in return for payment. Venereal disease: ? A disease that is contracted and transmitted by sexual contact, caused by microorganisms that survive on the skin or mucus membranes, or that are transmitted via semen, vaginal secretions, or blood during intercourse. Because the genital areas provide a moist, warm environment that is especially conducive to the proliferation of bacteria, viruses, and yeasts, a great many diseases can be transmitted this way. Type of STD

Chlamydia: ?is a bacterial infection caused by pathogen (germ) Chlamydia trachomatis that usually infects the genitals of both men and women, but can also infect the throat, rectum and eyes. CHANCROID (SHANG-kroid); ? A bacterial infection that results in sores on the mouth, throat, lips, anus, tongue, vagina, or penis. CRABS (Pubic Lice): ?Tiny insects that live off human blood. Although they’re often found around the genitals, they can live in any part of the body with hair. Gonorrhea: ?is a highly contagious sexually transmitted STD bacterial infection, sometimes referred to as the clap.

The nickname of the clap refers to a treatment that used to clear the blockage in the urethra from gonorrhea pus, where the penis would be ‘clapped’ on both sides simultaneously. HEPATITIS: ?There are five types of hepatitis — A through E — all of which cause inflammation of the liver. Type D affects only those who also have hepatitis B, and hepatitis E is extremely rare in the United States. HERPES (Herpes Simplex) ?Two types of a viral infection characterized by periodic outbreaks of painful sores. Stress, sunburn, and certain foods are the primary causes of a herpes outbreak.

AIDS: ?is the acronym for the Human Immunodeficiency Virus, a virus that attacks the body’s immune system, leading to full-blown AIDS (Acquired Immunodeficiency Syndrome). AIDS is devastating because it leaves the body susceptible to life-threatening infections and certain kinds of cancers. HPV / Genital Warts: ? Human Papilloma Virus (HPV) – a group of more than 70 viruses, some of which can lead to cervical cancer. Several strains of HPV cause external genital warts. SCABIES (SKAY-beez): ? A mite that burrows under the skin and lays eggs.

SYPHILIS (SIFF-i-lis): ? A bacterial infection caused by an organism called a spirochete. Trichomoniasis: ?is a common sexually transmitted disease (STD) that affects both men and women. Trichomoniasis is caused by a protozoan parasite called Trichomonas vaginalisand is a cause of vaginal infections in women and urethral infections in men. Trichomoniasis is an STD that affects approximately 5 million people in the US every year. Trichomoniasis is one of the most common, curable causes of vaginal infections in women. By: Bobby P. Galleros

Introduction

Mycobacterium avium races paratuberculosis ( MAP ) is the causative agent of an incurable, infective, chronic, granulomatous enteritis in ruminants, called Johne ‘s disease or paratuberculosis. The direct effects of Johne ‘s disease on animate being public assistance and productiveness may look insignificant and are frequently masked by the mostly subclinical character of the disease in domesticated farm animal ( incubation period prior to the oncoming of clinical marks by and large ranges from 2 to 10 old ages ) { { 1 Lepper, A.W. 1989 } } { { 2 Chiodini, R.J. 1984 } } .The economic impact of JohneA?s on dairy cowss industries is significant. Estimated costs as a consequence of reduced weight addition, milk production loss, premature culling and decreased carcase value add up to an one-year sum of $ 250 million ( USD ) in the United States industry entirely { { 3 Ott, S.L. 1999 } } .

More recent in-depth estimations indicate a important relationship being between Johne ‘s disease position and decreased milk production { { 51 Smith, R.L. 2009 } } , increased hazard of being culled { { 40 Smith, R.L. 2010 } } and a reduced calving rate in high sloughing animate beings.

The on-going contention refering the possible function of MAP in Crohn ‘s disease ( human inflammatory intestine disease ) suggests that MAP itself might be of great public wellness significance { { 17 Hermon-Taylor, J. 2000 } } .

Transmission of MAP

Cattles are most susceptible to infection as calves from birth to a few months of age { { 27 Taylor, A.W. 1953 ; 55 Windsor, P.A. 2010 } } , but can besides be infected as grownups { { 28 Doyle, T.M. 1951 } } .Transmission of MAP can happen by a assortment of paths in dairy cowss ; horizontally by consumption of MAP from the environment, or vertically from dike to calf. Evidence of intrauterine transmittal and sloughing of MAP in milk and foremilk has been reported by several surveies { { 5 Nielsen, S.S. 2008 ; 25 Seitz, S.E. 1989 ; 24 Sweeney, R.W. 1992 } } .

Although calf-to-calf transmittal has besides been demonstrated in several experimental scenes where calves are being housed together { { 52 RANKIN, J.D. 1961 ; 53 new wave Roermund, H.J. 2007 } } horizontal infection from cattles to calves and perpendicular infection from dike to calf are believed to be the most common and most of import infection paths in dairy cowss. Previous surveies besides describe that calves born from positive tested dikes were at a significantly higher hazard of going Map infected than calves without this risk-profile.

Besides calves turning up with a future high spiller and calves being born shortly following the freshening of an septic dike were at higher hazard being infected { { 29 Benedictus, A. 2008 } } .

Treatment & A ; control

Presently, there is no satisfactory intervention for the disease. No disinfectants are approved for the intervention of Johne ‘s disease because of their deficiency of efficiency and their failure to supply bacteriological remedy. A vaccinum for Johne ‘s disease exists but is non really normally used because it interferes with the reading of the current TB tegument trial and its inability to wholly forestall infection { { 44 Muskens, J. 2002 } } .

Consequently JohneA?s disease is presently controlled via control plans that implement a assortment of production patterns. The most cost-efficient option for cut downing the prevalence of MAP infection in herds is application of hazard direction steps to interrupt known transmittal paths { { 6 Groenendaal, H. 2003 ; 16 Kudahl, A.B. 2009 } } . Current MAP control plans are risk-based. Management-wise, animate beings are divided into high and low hazard animate beings, by looking at the consequences of 4 one-year showings that test all lactating cattles for MAP specific antibodies in the milk { { 47 Nielsen, S.S. 2011 } } . Particular production pattern recommendations are provided for pull offing bad animate beings and these recommendations chiefly focus on within-herd MAP transmittal { { 46 Nielsen, S.S. 2007 } } .According to recent surveies, implementing patterns that can minimise the exposure of MAP to newborn calves should take precedence in control plans { { 45 Pillars, R.B. 2011 } } .

However, control steps are really expensive and non cost-effective. Current control steps do non take into history that MAP can be transmitted vertically and ignores the possibility that there is familial fluctuation in cowss associated with differential susceptibleness to Johne ‘s doing girls of septic dikes more likely to be infected even if hygiene steps are implemented absolutely at birth.

Heritability of susceptibleness

Considerable work on linkage between genetic sciences and the opposition, tolerance or susceptibleness to Mycobacterium avium races paratuberculosis. Heritability of susceptibleness to infection with MAP has been estimated from 0.06 to 0.159 { { 18 Koets, A.P. 2000 ; 31 Mortensen, H. 2004 ; 37 Hinger, M. 2008 ; 38 Attalla, S.A. 2010 } } . The broad fluctuation in these extimates can be explained by differences in definition of infection and nosologies ( blood or milk ELISA, faecal civilizations, tissue civilizations ) , sample sizes, survey population ( breed ) and statistical theoretical accounts ( assorted animate being theoretical account, beget theoretical account ) used.

Two genome-wide surveies have identified venue for resistence or susceptibleness to infection by MAP utilizing Illumina Bovine SNP50 assay { { 32 Settles, M. 2009 ; 33 Minozzi, G. 2010 } } . A SNP on chromosome 9 ( BTA9 ) is associated with casting ( being faecal civilization positive ) when genuinely infected ( tissue civilization positive { { 32 Settles, M. 2009 } } and being ELISA positive { { 33 Minozzi, G. 2010 } } . Zanella et Al. performed an association survey on the same dataset as Settles et Al. and found BTA6 to be associated with tolerence to paratuberculosis { { 43 Zanella, R. 2011 } } . Several campaigner cistrons identified by these genome-wide surveies have been examined for farther association with infection.

Attempts to turn up cistrons associated with susceptibleness or opposition to paratuberculosis hold had limited success. Pinedo et al 2009 identified an association of caspase enlisting sphere 15 ( CARD15 ) with infection { { 34 Pinedo, P.J. 2009 } } , while a separate comparative analysis of bovine, murine, and human CARD15 transcripts suggest no important associations between fluctuation in the CARD15 and disease position { { 41 Taylor, K.H. 2006 } } .Toll-like receptor 4 ( TLR4 ) was associated with infection in recent work by Mucha et Al. 2009 but was non associated with infection in a coincident independent analysis { { 49 Pinedo, P.J. 2009 } } . Tendency towards association between infection and variant allelomorphs of the SLC11A1gene ( once NRAMP1 ) { { 34 Pinedo, P.J. 2009 } } is consistent with a population-based familial association survey carried out by Ruiz-Larranaga et Al. { { 42 Ruiz-Larranaga, O. 2010 } } , but conflicting consequences were presented by a population based association survey by Hinger et Al. 2007 { { 39 Hinger, M. 2007 } } . Hinger et Al. and Minozzi used ELISA-tests as a diagnostic step to sort animate beings as septic whereas Pinedo et Al. used a combination of ELISA and faecal civilization to specify infection and Settles et Al used faecal and tissue civilization.

The complexness of the intracellular infective disease Mycobacterium avium races paratuberculosis causes suggests engagement of many different cistrons that perchance interact with one another and with external factors from the environment. In add-on, the different procedures involved in early disease and late disease are yet ill-defined and may besides be reflected in the different venue found to be associated with the categorization of the type of infection. Particularly because pathogenesis of the disease is non to the full understood and sensitiveness of ELISA trials is rather low in latent or low casting animate beings { { 10 McKenna, S.L. 2006 ; 54 Eamens, G.J. 2000 } } { { 50 Nielsen, S.S. 2008 } } , case-control association surveies that use chiefly tissue and fecal nosologies in order to find the true infection position of the cow present the most dependable consequences.

Vertical transmittal

To look into the importance of perpendicular transmittal, old surveies tried to find the prevalence of foetal infection in cowss and estimated the incidence of calves infected via in utero transmittal. On norm, approximately 9 % of foetuss from subclinically infected cattles ( faecal civilization positive ) and 39 % from clinical cattles were infected with MAP prior to deliver { { 4 Whittington, R.J. 2009 } } .

Harmonizing to Whittington and Windsor { { 4 Whittington, R.J. 2009 } } existent prevalence of foetal MAP infection would be higher than reported because some of the methods and protocols used in these surveies to handle and prove samples have really low specificity { { 54 Eamens, G.J. 2000 } } . The estimated incidence of calf infection derived via the in utero path depends on within-herd prevalence and the ratio of sub-clinical to clinical instances among septic cattles. The mean perpendicular infection rates mentioned above are derived from the consequence of five independent surveies published between 1980 and 2003.

Strain typewriting

Current developments in molecular genetic sciences make it possible to disciminate Mycobacterium avium paratuberculosis strains with different fingerprinting techniques { { 36 Motiwala, A.S. 2006 } } . These techniques can besides be used as a tool to look into the possibility of perpendicular transmittal by comparing strains carried by the dike with strains carried by the girl.

When comparing different MAP fingerprinting techniques, the Multi Locus Short Sequence Repeat technique utilizing all 11 venues selected by Amonsin et Al. 2004 has the highest prejudiced power with a Simpsons diverseness index of 0.967 { { 36 Motiwala, A.S. 2006 } } . Harris et Al. 2006 used four of these identified repetitions ( locus 1, venue 2, locus 8 and locus 9 ) to distinguish MAP strains { { 21 Harris, N.B. 2006 } } .

To analyze diverseness of the selected MAP isolates we used these same four venue for MLSSR analysis and added venue 3, venue 5, venue 6, locus 10 and locus 11 in order to observe more diverity among dam and daughter isolates.

Strain typing methods to longitudinal datasets can now supply us with extra penetration into within herd infection kineticss, including the transmittal of MAP from dikes to girls.

Plan of the Investigation The scope of the investigation concerned the magnitude of penicillin and how it helped the allies win World War II (WWII). The researcher scrutinized the invention and process in which penicillin came to be, the different types of penicillin we have and use today, how it was used to help us more than any other drug in history at one point, and how it came to save thousands of lives in WWII.

The researcher’s method was to use multiple primary resources such as articles written by scholars, medical professionals, and historical investigators. The evidence that was found was evaluated and observed for origin, value, and purpose of penicillin and its use in WWII. B. Summary of Evidence In 1928, Sir Alexander Fleming discovered the first natural mold of Penicillin(Tames 5). Even though his “creation” was mostly on accident, Fleming had been itching to discover a new “wonder drug” since he first became interested in being a scientist(5).

Though the knowledge of disease causing bacteria was somewhat understood at the time, medical researchers had yet to find a chemical able to rid the body of the potent bacteria while not harming the body at the same time. Fleming’s first form of Penicillin was just what was needed to kick off the ultimate breakthrough of medicine. Even then, it wasn’t until another decade after this discovery that people really started needing and using Penicillin to save lives(History of Penicillin).

Although Fleming is credited with this important discovery, it took the start of WWII to pursue medical scientists to strengthen the effect the drug had on people. It’s all thanks to a total of 39 different groups of scientists that hundreds of thousands of fighting men’s lives were saved(World War II and Peoria). Penicillin was considered to be the war’s official wonder drug because of the unbelievable effects it had on infections and deadly diseases. The use of this drug is what made WWII different from any previous war(World War II and Peoria).

Before Penicillin was introduced to the allies of the war, soldiers rapidly died from infections such as Staphylococcal(staff), streptococcal(strep), and pneumococcal(pneumonia) (World War II and Peoria). Since death was the ultimate outcome of these infectious diseases, the number of available soldiers to fight dropped immensely and expeditiously. Due to the shortage of men, sergeants called for men to be recruited no matter their experience; as long as they were 18 years old(Inside WWII).

That then led to more deaths of young cadets because of the lack of knowledge of what to do on the battle field. At that point of time, the allies came to the conclusion that what they needed was a wonder drug ready to use when needed. That’s when Howard Florey and Ernst Chain were forced in with their team of scientists to use Fleming’s Penicillin mold and improve it to where it cured a grown man of a life threatening infection or disease; and make a quantity of hundreds of thousands(World War II and Peoria). After a total of 39 separate drug laboratories in the U. S. ad given their all to synthesize inorganic Penicillin, in 1941, they created a version 20 times more potent than what they started out with in 1939(22). By the autumn of 1943 the war doctors were using the drug on only American and Allied military patients with life-threatening infections. Since a single infection usually called for two million units of Penicillin(single ampoules held 100,000 units), rationing who got what treatment was crucial(World War II and Peoria). The scientists shortly discovered that, while the new version of Penicillin was of very good quality, their new focus needed to be directed on quantity of the drug.

By 1945, the team of scientists brilliantly came up with an amazingly effective technique that supplied the allies with 7,952 billion units of the strongest possible version of penicillin at the time(World War II and Peoria). Though the injections were painful(the needles had to be large enough to allow the medicine to flow through) and had to be given every four hours, soldiers agreed it was worth being able to live and continue fighting to the victory of WWII(23). By the end of it all, the magnificent wonder drug saved the lives of hundreds of thousands of warriors and even more citizens in the U. S. and has continued to fulfill its duty all the way up to today’s time(World War II and Peoria). C. Evaluation of Sources “World War II and Peoria” was the title of the article that helped the researcher the most to come to a conclusion on how Penicillin helped the allies win WWII. The article’s purpose was to further inform people about the studies and development of penicillin during WWII. The article talked about the illnesses and wounds the soldiers fighting in WWII came in contact with and how Penicillin helped them fight and survive through it all.

This particular unit differed from the rest because it did not have its focal point on how Penicillin came to be, but rather its purpose and usage in WWII. However, it did have some limitations of information on specific numbers and names of soldiers that were affected by the wonder drug. The point of view that the article used was from a college professor who had dabbled in history as well as medicine. The professor’s name was Jennifer Rosenburg and she had posted this information around 2000. The second most helpful article’s title was “Inside WWII . The purpose of the article being written was to tell a more medical side of the war as opposed to the blood and guts. Although, it still lingered on with the facts and details of the war itself too much, which limited it with important details it should have withheld about the medical side of the war. But, because of the focusing on one little part at a time problem, the researcher ended up to find it very valuable. It stated facts that were focused on the medicine during the war instead of the medicine in general. The origin of this information was found by Dr. Steven Lister.

He was a doctor during the war, so this gave him a personal experience and the researcher found great value in this type of first hand information. D. Analysis During the period of penicillin gaining importance, World War II was going on. This specific war was fought from 1939 to 1945 by the Axis: Germany, Italy, and Japan; and the allies: Australia, Belgium, Brazil, Canada, China, Czechoslovakia, Denmark, Estonia, France, Greece, India, Latvia Lithuania, Malta, The Netherlands, New Zealand, Norway, Poland, South Africa, United Kingdom, United States, USSR, Yugoslavia, and many others(The Axis and the Allies).

The war was fought by more than fifty countries in the world. The main causes of the war for the U. S. and Britain were The Great Depression and the Treaty of Versailles(Wars and Battles 1939-1945). Around 1943, the Allies really started to need help because they were losing so many soldiers due to infections caused mostly by severe battle wounds which ultimately led to the being outnumbered and overtaken by the Axis. That is where Penicillin came in.

Scientists spent over $2,000,000 trying to perfect and learn more about the drug(World War II and Peoria). They eventually found out that what this drug did, once successfully inserted in the body, was it located the source of the infection and fought only the harmful bacteria( Tames 15). As opposed to the other drugs, at the time, which destroyed not only dangerous bacteria, but the vital bacteria used for fighting infections naturally found in the body(16).

The drug, therefore, saved over hundreds of thousands of men(World War II and Peoria). A few months after the Allies received the drug, the Axis groups started to surrender, which officially ended the war in 1945 with the Allies‘ being the victorious group(Wars and Battles 1939-1945). Under the circumstances that the allies started winning after penicillin came into the picture, that was considered to be one of the main, but least recognized, expositions for the victory of the allies.

Of all the evidence the researcher has came up with to support this claim, the three main pieces of evidence are as follows: only two years after penicillin was thoroughly introduced to the war, the allies won; so many lives were saved–on and off the battlefield–how could it not have such a huge impact; and they must have known it was going to be a huge help, otherwise they would not have invested so much money in the whole process of innovating and testing the drug(World War II and Peoria).

The first point was the victory of the allies shortly after penicillin came to use in the war. When they fought without the drug, the allies were losing by a drastic amount considering the vast number of men that died every day from infections on their battle wounds and had suffered without the care that penicillin provided(23). The soldiers suffered for a total of about three and a half years before they actually got penicillin shipped in that had an affect on people(World War II and Peoria).

However, when they did get the wonder drug in, they spent about six months learning the different side effects, insertion ways, and preparations needed before they gave the soldiers all they needed to keep them alive and fighting(World War II and Peoria). The second point, was that there was such a large number of people saved by the drug, that it had to have made some kind of a difference in the way World War II ended. In less than a year, penicillin saved 187 lives just of people in America(21). In the war, penicillin took the death toll, caused by wound infections, from over 12 percent down to less than 1 percent on average(23).

That would mean the allies side of the war would have had a 12 percent advantage over the axis in the battle at this time due to the drug keeping the soldiers dying from wound related infections. The last point stated was with all the time, money, and dedication with bettering this drug, penicillin obviously had a huge impact on World War II The U. S. spent over $2,000,000 trying to perfect the drug to make it effective enough to cure a whole army of men versus enough for one or two individual people.

The money not only paid for the equipment needed, but for the 39 different groups of scientists hired to innovate and test the drug to reach the desired goal(History of Penicillin).

Conclusion

When Penicillin started out, it was but a simple form of mold. Then, When Fleming discovered it destroyed bacteria in the human body without harming the human in any way. He then had over 30 different teams of scientists work at improving this mysterious new drug to make it potent enough to help a man overcome pneumonia.

After years and years of experiments and millions of dollars spent, they finally got what they had been working for. They sent as much as they could to the troops fighting WWII at the time. The doctors at the war stations gave it to the men in critical condition and the drug got them back on their feet and fighting in about a week.

Works Cited

1. “The Axis and the Allies. ” The Countries Who Fought in World War Two. Mandy Barrow, 2010. Web. 12 Nov. 2011. .
2. “The Drug Safety. ” The Drug Safety. The Drug Society, 2011. Web. 26 Sept. 2011. .
3. “How Penicillin Came to Be. Alexander Fleming in WWII. J. Miller. Web. 28 Sept. 2011. .
4. “Inside WWII. ” History Learning Site. Chris Trueman, 2000. Web. 28 Sept. 2011. .
5. Prine, Patricia R. “Moma’s Notes. ” Personal interview. 2 Oct. 2011.
6. Tames, Richard. Penicillin: a Breakthrough in Medicine. Chicago: Heniemann Library, 2001. Print. “Wars and Battles, 1939-1945. “
7. United States American History. Web. 12 Nov. 2011. . “World War II and Peoria. “
8. 20th Century History. Jennifer Rosenburg, 2001. Web. 26 Sept. 2011. . “WWII and Medicine. ” Medicine in World War II. 2001. Web. 27 Sept. 2011. .

Margaret E Gibson July 20, 2009 Microbiology Dr. Metera Lab Report 3: Labs 7 and 8- Metabolism and Biochemical Tests Abstract This experiment focused on metabolism and biochemical tests. The goal of performing these tests was to differentiate microbes from one another and to compare how metabolic and biochemical processes differ from species to species.

The tests performed include: the Fermentation of Sugars Test (sucrose, glucose, and lactose), the Urease Test, the Fermentation of Lactose Test, the Sulfide Indole Mobility (SIM) Test, the Nitrate Reduction Test, the Protein Hydrolysis Test, the Catalase Test, and the Cytochrome Oxidase Test. The microbes that were tested during this lab were: Escherichia coli, Bacillus cereus, the unknown, Proteus vulgaris, Staphylococcus epidermis, Enterobacter aerogenes, the control, and Pseudomonas fluorescens.

The microbes tested during these various tests were looking for which would: reduce sulfur/produce sulfate, produce indole, or possess motility, reduce nitrate, and contain protease, catalase and oxidaase. Introduction The purpose of these labs was to observe various metabolic processes by determining the pH of certain bacteria, determining if the bacteria was urease positive or negative, determining which bacteria ferment which sugar(s) during fermentation, and determining if bacteria are lactose fermenters and non-lactose fermenters.

Metabolic processes can also be observed by determining if bacteria reduce sulfur/produce sulfate, produce indole, or possess motility, determining which bacteria are able to reduce nitrate, determining if bacteria contain protease, determining if bacteria contain catalase, and determining if bacteria contain oxidase. The tests performed to determine these metabolic processes include: the Fermentation of Sugars Test (sucrose, glucose, and lactose), the Urease Test, the Fermentation of Lactose Test, the Sulfide Indole Mobility (SIM) Test, the

Nitrate Reduction Test, the Protein Hydrolysis Test, the Catalase Test, and the Cytochrome Oxidase Test. The bacteria tested include: Escherichia coli, Bacillus cereus, the unknown, Proteus vulgaris, Staphylococcus epidermis, Enterobacter aerogenes, the control, and Pseudomonas fluorescens. The different types of microbes studied in this experiment include: Escherichia coli, Bacillus cereus, Proteus vulgaris, Staphylococcus epidermis, Enterobacter aerogenes, and Pseudomonas fluorescens.

Escherichia coli is mainly found in animal feces and comprises their intestines as well (US Food and Drug Administration). Bacillus cereus is a known medium of food poisoning and causes vomiting and abdominal cramps (Todar). Proteus vulgaris is connected with food spoilage of meat, poultry, and seafood and may cause diarrhea in infants (Schenectady Country Community College). Staphylococcus epidermis often infects hospital patients with weak immune systems in catheter wounds (European Bioinformatics Institute).

Enterobacter aerogenes is the source of numerous infections such as bacteremia, lower respiratory tract infections, skin and soft tissue infections, urinary tract infections (UTIs), endocarditis, intra-abdominal infections, septic arthritis, osteomyelitis, and ophthalmic infections (E Medicine). Pseudomonas fluorescens are able to grow in various conditions such as soil, water, and plant habitats (European Bioinformatics Institute). Several hypotheses arise during this experiment due to the many subjects being tested. However, since there are numerous tests being performed, a more general hypothesis can be ascertained.

The hypothesis for all tests in both Lab 7 and Lab 8 is that the outcome of the tests will produce the desired results in order to differentiate various species of bacteria from one another and to reveal certain characteristics of metabolic and biochemical processes. Materials and Methods Lab 7 For Part A of Lab 7, label Escherichia coli, Proteus vulgaris, the unknown, and Enterobacter aerogenes on a blue (sucrose), a green (glucose), and a red (lactose) tube. Then, using aseptic technique, inoculate each bacteria into each color tube by sticking the inoculating loop to the bottom of the tube and twirling it, then pulling it straight out.

Record the results. For Part B, label the tubes Escherichia coli, Proteus vulgaris, unknown, and Enterobacter aerogenes. Using aseptic technique, inoculate each tube with the corresponding bacteria by streaking the surface of the agar slant. Record the results. For Part C, label Staphylococcus epidermis, Proteus vulgaris, and Escherichia coli on the Petri plate with the MacConkey agar. Using aseptic technique, inoculate the labeled parts of the plate. Record the results. Lab 8 For Part A of Lab 8, label each tube Enterobacter aerogenes, Staphylococcus epidermis, and Proteus vulgaris.

Using aseptic technique, “stab” the inoculating loop ? of the way to the bottom of the tube and then pull it straight out to inoculate each tube with the corresponding bacteria. Record the results. For Part B, label each tube Enterobacter aerogenes and “control. ” Using aseptic technique, inoculate each Tryptic Nitrate tube by sticking the inoculating loop to the bottom of the tube and twirling it, then pulling it straight out. Then, add ten drops of sulfanilic acid anddemehtyl-1-napthylamine. If a red color develops after this step, record the record the results. If not, add zinc dust to the tube and vortex it.

Record the results. For Part C, label Enterobacter aerogenes and Bacillus cereus on the milk agar plate. Using aseptic technique, inoculate the plate with the corresponding bacteria. Record the results. For Part D, put a few drops of water on the slide and then inoculate it with Bacillus cereus. Next, add one drop of hydrogen peroxide to the sample. Record the results. For Part E, use a sterile swab to transfer the cells from Enterobacter aerogenes and Pseudomonas fluorescens to a disk. Use a new swab for each sample. Add one drop of water to each disk. Record the results. Results Lab7: Part A [pic] |[pic] | |Figure 1 |Figure 2 | |Figure 1 is the unknown for sucrose. As shown, it had an orange |Figure 2 is Escherichia coli for sucrose. As shown, it was | |ring at the top that fades to yellow at the bottom, was cloudy |orange throughout, had darker solution inside the tube than out, | |all the way through, and had no bubbles. |was very cloudy at the bottom, and had no bubbles. |[pic] |[pic] | |Figure 3 |Figure 4 | |Figure 3 is Enetrobacter aerogenes for sucrose. As shown, it was|Figure 4 is Bacillus cereus for sucrose. As shown, it had a dark| |yellow and cloudy throughout, and had no bubbles. |orange ring at the top and was light orange, it was cloudy at the| | |bottom, and had no bubbles. |[pic] |[pic] | | | | |Figure 5 |Figure 6 | | | | |Figure 5 is Enterobacter aerogenes for glucose.

As shown, it was|Figure 6 is the unknown for glucose. As shown, it had an orange | |all yellow and cloudy (++), and had no bubbles. |ring at the top, was yellow and cloudy (++) throughout, and had | | |no bubbles. |[pic] |[pic] | | | | |Figure 7 |Figure 8 | | | | |Figure 7 is Escherichia coli for glucose. As shown, it was |Figure 8 is Bacillus cereus for glucose.

As shown, it was orange| |yellow, cloudy at the top, and had no bubbles. |throughout and had no bubbles. | |[pic] |[pic] | | | | |Figure 9 |Figure 10 | | | | |Figure 9 is the unknown for lactose.

As shown, it was uniformly |Figure 10 is Enterobacter aerogenes for lactose. As shown, it | |light red and cloudy (+), and had no bubbles. |was light orange and cloudy (++), had a red ring at the top, and | | |had no bubbles. |[pic] |[pic] | | | | |Figure 11 |Figure 12 | | | | |Figure 11 is Escherichia coli for lactose. As shown, it was |Figure 12 is Bacillus cereus for lactose.

As shown, it was red | |yellow, cloudy at the top, and had bubbles. |throughout and had no bubbles. | Lab 7: Part B |[pic] |[pic] | |Figure 13 |Figure 14 | |Figure 13 is the unknown. As shown, it had a red streak of red |Figure 14 is Enterobacter aerogenes. As shown, it had faint | |colonies (+++) and remained the same color. |cloudy colonies (+) and remained the same color. |[pic] |[pic] | |Figure 15 |Figure 16 | |Figure 15 is Escherichia coli. As shown, it had faint cloudy |Figure 16 is Proteus vulgaris. As shown, it was bright pink | |colonies (+) and remained the same color. |throughout, orange at the bottom, and experienced a change in | | |color. | Lab 7: Part C pic] Figure 17 Figure 17 is Staphylococcus epidermis, Proteus vulgaris, and Escherichia coli. As shown, the Staphylococcus epidermis showed no growth, the Pseudomonas vulgaris showed substantial growth (+++), and the Escherichia coli showed substantial growth (+++) and turned pink. Lab 8: Part A |[pic] |[pic] | |Figure 18 |Figure 19 | |Figure 19 is Enterobacter aerogenes.

As shown, it showed |Figure 20 is Staphylococcus epidermis. As shown, it showed no | |substantial growth (+++). |growth. | |[pic] | | |Figure 20 | | |Figure 21 is Proteus vulgaris. As shown, it showed substantial | | |growth (+++), turned black, and exhibited a red ring at the top. | Lab 8: Part B |[pic] |[pic] | |Figure 21 |Figure 22 | |Figure 22 is Enterobacter aerogenes. As shown, it was red ? of |Figure 23 is the control. As shown, it was red ? of the way | |the way through separated by black at the bottom. |through separated by black at the bottom. | Lab 8: Part C [pic] Figure 23

Figure 24 is Enterobacter aerogenes and Bacillus cereus. As shown, Bacillus cereus exhibited a lot of growth (++++). Lab 8: Part D [pic] Figure 24 Figure 25 is Bacillus cereus. As shown, it formed bubbles. Lab 8: Part E [pic] Figure 25 Figure 26 is Enterobacter aerogenes and Pseudomonas fluorescens. As shown, the Pseudomonas fluroescens turned purple. Discussion The results of this experiment prove that the hypothesis was correct: the expected results were obtained and therefore made it possible to differentiate various species of bacteria from one another and to reveal certain characteristics of metabolic and biochemical processes.

For example, in the Fermentation of Sugars test, the unknown’s pH was slightly alkaline and no carbon dioxide gas was given off (Figures 1, 6, and 9). The Escherichia coli had a pH around neutral for all three of the sugars and there were bubbles in the Durham tube for glucose, so the bacteria produced carbon dioxide gas during fermentation (Figures 2, 7, and 11). The Enterobacter aerogenes had a slightly acidic pH and no carbon dioxide gas was given off (Figures 3, 5, and 10).

The Bacillus cereus had a slightly alkaline pH and no carbon dioxide gas was given off (Figures 4, 8, and 12). In the Detection of Urease test, the unknown remained the same color, so it was urease negative (Figure 13). The Enterobacter aerogenes remained the same color, so it was urease negative (Figure 14). The Escherichia coli remained the same color, so it was also urease negative (Figure 15). The Proteus vulgaris turned red, meaning it became alkaline with the production of ammonia, so it was urease positive (Figure 16).

In the MacConkey Agar test, the Staphylococcus epidermis exhibited no growth, meaning it is Gram positive, and it does not ferment lactose (Figure 17). The Proteus vulgaris exhibited growth, so it is Gram negative, and it does not ferment lactose (Figure 17). The Escherichia coli exhibited growth, so it is Gram negative, and it turned red, so it ferments lactose (Figure 17). In the Sulfur Indole Motility test (SIM), Enterobacter aerogenes exhibited growth above the inoculation line, so it is motile (Figure 18). The Staphylococcus epidermis did not exhibit any growth, so it is not motile (Figure 19).

The Proteus vulgaris exhibited growth above the inoculation line, turned black, and showed a red ring at the top of the solution, so it is motile, a phosphorus reducer, and an indole producer (Figure 20). In the Nitrate Reduction test, the Enterobacter aerogenes turned red, so the nitrate was not reduced by nitrate reductase, meaning it was nitrate reductase negative (Figure 21). The control also turned red, so the nitrate was not reduced by nitrate reductase, meaning it was also nitrate reductase negative (Figure 22).

In the Protein Hydrolysis test, the Enterobacter aerogenes did not exhibit any growth, so it was protease negative (Figure 23). The Bacillus cereus exhibited a lot of growth and turned the milk agar clear, so it was protease positive (Figure 23). In the Catalase test, the Bacillus cereus bubbled, so it is catalase positive (Figure 24). In the Cytochrome Oxidase test, the Enterbacter aerogenes did not change color, so it is cytochromoe oxidase negative (Figure 25). The Pseudomonas fluorescens turned purple, so it is oxidase positive (Figure 25).

As expected in all laboratory experiments, this one had the possibility of human error. Mistakes could have been made by failing to sterilize the inoculating loop correctly, which would result in possible contamination of the sample. Another error could have been possibly occurred by mislabeling the plates according to species, which would produce invalid results. Finally, failing to inoculate the SIM tubes ? of the way to the bottom of the tube would result in the inability to observe whether or not the species is motile or not. Although this experiment went rather smoothly, there is always an opportunity for mprovement. An example of how this experiment could be made better is by testing more of the same microbes in each test. In Labs 7 and 8, many of the microbes used in the tests were not consistently present in each one. If the same bacteria were used, it would aid greatly in differentiating the same bacteria from one another and observing how metabolic and biochemical processes differ from species to species. This experiment and its results are important to the scientific community because they ultimately serve as a basis for further study of the subject.

By learning basic metabolism and biochemical tests used to differentiate microscopic organisms from one another, researchers can then develop more advanced and more specific tests that can further distinguish microbial species from each other. This will aid in discovering new microbes and different ways microbes react to certain factors. By doing so, researchers will have a better idea of how to distinguish helpful, potentially life-saving microbes from pathogenic or harmful ones. References

US Food and Drug Administration. Escherichia Coli. 5 Oct. 2006. . . Todar, Kenneth. Bacillus Cereus Food Poisoning. 2006. . . Schenectady County Community College. Proteus Vulgaris, P. Mirabilis.. . . European Bioinformatics Institute . Staphylococcus Epidermis Can Cause Infections in Wounds. 2006-2007. . . E Medicine . Excerpt from Enterobacter Infections. 1996-2006. . . European Bioinformatics Institute . Pseudomonas Fluorescens Is Being Researched as a Biological Control Organism. 2006-2007. . .