Tuesday, May 7, 2013

What are two instances where Scout displays her maturity in Chapters 29-31 in the novel To Kill a Mockingbird?

At the end of Chapter 30, Sheriff Tate explains to Atticus, without mentioning his name explicitly, that Boo Radley was responsible for killing Bob Ewell. Sheriff Tate goes on to say that he refuses to tell the town that Boo Radley saved Jem and Scout because that would bring unwanted attention on Boo, who is extremely shy. Tate says that it would be a sin to force Boo into the limelight by exposing the truth. Scout tells Atticus that she understands and says that Mr. Tate was right for what he did. Atticus then asks Scout, "What do you mean?" (Lee 370). Scout says, "Well, it'd be sort of like shootin' a mockingbird, wouldn't it?" (Lee 370). Scout's response displays her maturity because she fully understands the concept of protecting innocent beings. She comprehends the lesson of never killing a mockingbird to metaphorically represent that it is considered a sin to harm an innocent being. Boo Radley is a symbolic mockingbird, and Scout understands Sheriff Tate's motivation not to expose Boo into the town's limelight because it would be harmful to Boo.


Another scene that portrays Scout's maturity takes place in Chapter 31 after she walks Boo Radley home. Scout stands on Boo's porch and looks out at the town. She begins to view Maycomb like she never has before. Scout reminiscences and thinks of the various seasons that Boo Radley watched them grow up from inside his house. Scout says,



"Atticus was right. One time he said you never really know a man until you stand in his shoes and walk around in them. Just standing on the Radley porch was enough" (Lee 374).



Scout has developed the ability to perceive situations from other people's point of view. Scout no longer views Boo Radley as the "malevolent phantom," but rather a sympathetic, caring individual who just happens to be extremely shy.

How are X-rays able to determine the positions of atoms in a protein crystal structure?

Monday, May 6, 2013

In the book Confessions of Saint Augustine, translated by Garry Wills, what are the main points, perspectives, and angles discussed in Book VIII?

In Book VIII of the Confessions, Augustine finally converts, and this book recounts what moves him to take the final step toward conversion. As the book begins, he says of God, "Of Thy eternal life I was now certain, though I saw it in a figure and as through a glass" (page 116). To convince himself of God's existence, he visits Simplicianus, his pious friend, to help him. At this point, Augustine no longer delights in making profits and, next to the "beauty of Thy house" such pursuits as making money seem like a "burden" to him (page 116). Simplicianus tells him about the Roman rhetorician Victorinus, who was so esteemed that he even taught Roman senators. Victorinus's conversion leads Augustine to want to emulate him. 


One of the themes of this chapter is Augustine's struggle between what he calls his "two wills...one carnal, one spiritual" (page 122). In other words, he speaks about the battle between the soul and the flesh related to his inner struggle about whether to convert. Later in this book, he visits his friend Alypius and is still debating about whether to convert. In a frenzy, Augustine beats himself and tears at his hair, and he wonders why his body can obey his mind while his spirit cannot obey what his mind wants it to do (page 129). However, this duality seems too Manichean to Augustine, so he rejects it. This touches on the theme of free will--in other words, can humans force their minds to do what they want? In a torment, Augustine hears a child from a neighboring house say to him, "Take up and read" (page 134). He thinks that God is speaking to him through the child, and he picks up the Bible and reads a verse that says "make not provision for the flesh" (page 134). He immediately converts and tells his mother that he has done so. The main point of this part of the book is that he believes God speaks to him through a child and moves him towards conversion. 

Sunday, May 5, 2013

What are ear infections and disorders?


Causes and Symptoms

The hearing mechanism, one of the most intricate and delicate structures of the human body, consists of three sections: the outer ear, the middle ear, and the inner ear. The outer ear converts sound waves into the mechanical motion of the eardrum (tympanic membrane), and the middle ear transmits this mechanical motion to the inner ear, where it is transformed into nerve impulses sent to the brain.



The outer ear consists of the visible portion, the ear canal, and the eardrum. The middle ear is a small chamber containing three tiny bones—the auditory ossicles, termed malleus (hammer), incus (anvil), and stapes (stirrup)—which transmit the vibrations of the eardrum (attached to the hammer) into the inner ear. The chamber is connected to the back of the throat by the Eustachian tube, which allows equalization with the external air pressure. The inner ear, or cochlea, is a fluid-filled cavity containing the complex structure necessary to convert the mechanical vibrations of the cochlear fluid into nerve pulses. The cochlea, shaped something like a snail’s shell, is divided lengthwise by a slightly flexible partition into upper and lower chambers. The upper chamber begins at the oval window, to which the stirrup is attached. When the oval window is pushed or pulled by the stirrup, vibrations of the eardrum are transformed into cochlear fluid vibrations.


The lower surface of the cochlear partition, the basilar membrane, is set into vibration by the pressure difference between the fluids of the upper and lower ducts. Lying on the basilar membrane is the organ of Corti, containing tens of thousands of hair
cells attached to the nerve transmission lines leading to the brain. When the basilar membrane vibrates, the cilia of these cells are bent, stimulating them to produce electrochemical impulses. These impulses travel along the auditory nerve to the brain, where they are interpreted as sound.


Although well protected against normal environmental exposure, the ear, because of its delicate nature, is subject to various infections and disorders. These disorders, which usually lead to some
hearing loss, can occur in any of the three parts of the ear.


The ear canal can be blocked by a buildup of waxy secretions or by infection. Although
earwax serves the useful purpose of trapping foreign particles that might otherwise be deposited on the eardrum, if the canal becomes clogged with an excess of wax, less sound will reach the eardrum, and hearing will be impaired.


Swimmer’s ear, or
otitis externa, is an inflammation caused by contaminated water that has not been completely drained from the ear canal. A moist condition in a region with little light favors fungal growth. Symptoms of swimmer’s ear include an itchy and tender ear canal and a small amount of foul-smelling drainage. If the canal is allowed to become clogged by the concomitant swelling, hearing will be noticeably impaired.


A perforated eardrum may result from a sharp blow to the side of the head, an infection, the insertion of objects into the ear, or a sudden change in air pressure (such as a nearby explosion). Small perforations are usually self-healing, but larger tears require medical treatment.


Inflammation of the middle ear, acute
otitis media, is one of the most common ear infections, especially among children. Infection usually spreads from the throat to the middle ear through the Eustachian tube. Children are particularly susceptible to this problem because their short Eustachian tubes afford bacteria in the throat easy access to the middle ear. When the middle ear becomes infected, pus begins to accumulate, forcing the eardrum outward. This pressure stretches the auditory ossicles to their limit and tenses the ligaments so that vibration conduction is severely impaired. Untreated, this condition may eventually rupture the eardrum or permanently damage the ossicular chain. Furthermore, the pus from the infection may invade nearby structures, including the facial nerve, the mastoid bones, the inner ear, or even the brain. The most common symptom of otitis is a sudden severe pain and an impairment of hearing resulting from the reduced mobility of the eardrum and the ossicles.


Secretory otitis media is caused by occlusion of the Eustachian tube as a result of conditions such as a head cold, diseased tonsils and adenoids, sinusitis, improper blowing of the nose, or riding in unpressurized airplanes. People with allergic nasal blockage are particularly prone to this condition. The blocked Eustachian tube causes the middle-ear cavity to fill with a pale yellow, noninfected discharge which exerts pressure on the eardrum, causing pain and impairment of hearing. Eventually, the middle-ear cavity is completely filled with fluid instead of air, impeding the movement of the ossicles and causing hearing impairment.


A mild, temporary hearing impairment resulting from airplane flights is termed aero-otitis media. This disorder results when a head cold or allergic reaction does not permit the Eustachian tube to equalize the air pressure in the middle ear with atmospheric pressure when a rapid change in altitude occurs. As the pressure outside the eardrum becomes greater than the pressure within, the membrane is forced inward, while the opening of the tube into the upper part of the throat is closed by the increased pressure. Symptoms are a severe sense of pressure in the ear, pain, and hearing impairment. Although the pressure difference may cause the eardrum to rupture, more often the pain continues until the middle ear fills with fluid or the tube opens to equalize pressure.


Chronic otitis media may result from inadequate drainage of pus during the acute form of this disease or from a permanent eardrum
perforation that allows dust, water, and bacteria easy access to the middle-ear cavity. The main symptoms of this disease are fluids discharging from the outer ear and hearing loss. Perforations of the eardrum result in hearing loss because of the reduced vibrating surface and a buildup of fibrous tissue that further induces conductive losses. In some cases, an infection may heal but still cause hearing loss by immobilizing the ossicles. There are two distinct types of chronic otitis, one relatively harmless and the other quite dangerous. An odorless, stringy discharge from the mucous membrane lining the middle ear characterizes the harmless type. The dangerous type is characterized by a foul-smelling discharge coming from a bone-invading process beneath the mucous lining. If neglected, this process can lead to serious complications, such as meningitis, paralysis of the facial
nerve, or complete sensorineural deafness.


The ossicles may be disrupted by infection or by a jarring blow to the head. Most often, a separation of the linkage occurs at the weakest point, where the anvil joins the stirrup. A partial separation results in a mild hearing loss, while complete separation causes severe hearing impairment.


Disablement of the mechanical linkage of the middle ear may also occur if the stirrup becomes calcified, a condition known as otosclerosis. The normal bone is resorbed and replaced by very irregular, often richly vascularized bone. The increased stiffness of the stirrup produces conductive hearing loss. In extreme cases, the stirrup becomes completely immobile and must be surgically removed. Although the exact cause of this disease is unknown, it seems to be hereditary. About half of the cases occur in families in which one or more relatives have the same condition, and it occurs more frequently in females than in males. There is also some evidence that the condition may be triggered by a lack of fluoride in drinking water and that increasing the intake of fluoride may retard the calcification process.



Tinnitus
is characterized by ringing, hissing, or clicking noises in the ear that seem to come and go spontaneously without any sound stimulus. While tinnitus is not a disease of the ear, it is a common symptom of various ear problems. Possible causes of tinnitus are earwax lodged against the eardrum, a perforated or inflamed eardrum, otosclerosis, high aspirin dosage, or excessive use of the telephone. Tinnitus is most serious when caused by an inner-ear problem or by exposure to very intense sounds, and it often accompanies hearing loss at high frequencies.


Ménière’s disease is caused by production of excess cochlear fluid, which increases the pressure in the cochlea. This condition may be precipitated by allergy, infection, kidney disease, or a number of other causes, including severe stress. The increased pressure is exerted on the walls of the semicircular canals as well as on the cochlear partition. The excess pressure in the semicircular canals (the organs of balance) is interpreted by the brain as a rapid spinning motion, and the victim experiences abrupt attacks of
vertigo and nausea. The excess pressure in the cochlear partition has the same effect as a very loud sound and rapidly destroys hair cells. A single attack causes a noticeable hearing loss and could result in total deafness without prompt treatment.


Of all ear diseases, damage to the hair cells in the cochlea causes the most serious impairment. Cilia may be destroyed by high fevers or from a sudden or prolonged exposure to intensely loud sounds. Problems include destroyed or missing hair cells, hair cells that fire spontaneously, and damaged hair cells that require unusually strong stimuli to excite them. At the present time, there is no means of repairing damaged cilia or of replacing those that have been lost.


Viral nerve deafness is a result of a viral infection in one or both ears. The mumps virus is one of the most common causes of severe nerve damage, with the measles and influenza viruses as secondary causes.


Ototoxic (ear-poisoning) drugs can cause temporary or permanent hearing impairment by damaging auditory nerve tissues, although susceptibility is highly individualistic. A temporary decrease of hearing (in addition to tinnitus) accompanies the ingestion of large quantities of aspirin or quinine. Certain antibiotics, such as those of the mycin family, may also cause permanent damage to the auditory nerves.


Repeated exposure to loud noise (in excess of 90 decibels) will cause a gradual deterioration of hearing by destroying cilia. The extent of damage, however, depends on the loudness and the duration of the sound. Rock bands often exceed 110 decibels; farm machinery averages 100 decibels.


Presbycusis (hearing loss with age) is the inability to hear high-frequency sounds because of the increasing deterioration of the hair cells. By age thirty, a perceptible high-frequency hearing loss is present. This deterioration progresses into old age, often resulting in severe impairment. The problem is accelerated by frequent unprotected exposure to noisy environments. The extent of damage depends on the frequency, intensity, and duration of exposure, as well as on the individual’s predisposition to hearing loss.




Treatment and Therapy

The simplest ear problems to treat are a buildup of earwax, swimmer’s ear, and a perforated eardrum. A large accumulation of wax in the ear canal is best removed by having a medical professional flush the ear with a warm solution under pressure. One should never attempt to remove wax plugs with a sharp instrument. A small accumulation of earwax may be softened with a few drops of baby oil left in the ear overnight and then washed out with warm water and a soft rubber ear syringe. Swimmer’s ear can usually be prevented by thoroughly draining the ears after swimming. The disease can be treated with an application of antibiotic ear drops after the ear canal has been thoroughly cleaned. A small perforation of the eardrum will usually heal itself. Larger tears, however, require an operation, tympanoplasty, that grafts a piece of skin over the perforation.


Fortunately, the bacteria that usually cause acute otitis respond quickly to antibiotics. Although antibiotics may relieve the symptoms, complications can arise unless the pus is thoroughly drained. The two-part treatment—draining the fluid from the middle ear and antibiotic therapy—resolves the acute otitis infection within a week. Secretory otitis is cured by finding and removing the cause of the occluded Eustachian tube. The serous fluid is then removed by means of an aspirating needle or by an incision in the eardrum so as to inflate the tube by forcing air through it. In some cases, a tiny polyethylene tube is inserted through the eardrum to aid in reestablishing normal ventilation. If the Eustachian tube remains inadequate, a small plastic grommet may be inserted. The improvement in hearing is often immediate and dramatic. The pain and hearing loss of aero-otitis is usually temporary and disappears of its own accord. If, during or immediately after flight, yawning or swallowing does not allow the Eustachian tube to open and equalize the pressure, medicine or surgical puncture of the eardrum may be required. The harmless form of chronic otitis is treated with applied medications to kill the bacteria and to dry the chronic drainage. The eardrum perforation may then be closed to restore the functioning of the ear and to recover hearing. The more dangerous chronic form of this disease does not respond well to antibacterial agents, but careful x-ray examination allows diagnosis and surgical removal of the bone-eroding cyst.


Ossicular interruption can be surgically treated to restore the conductive link by repositioning the separated bones. This relatively simple operation has a very high success rate. Otosclerosis is treated by operating on the stirrup in one of several ways. The stirrup can be mechanically freed by fracturing the calcified foot plate or by fracturing the foot plate and one of the arms. Although this operation is usually successful, recalcification often occurs. Alternatively, the stirrup can be completely removed and replaced with a prosthesis of wire or silicon, yielding excellent and permanent results.


Since tinnitus has many possible, and often not readily identifiable, causes, few cases are treated successfully. The tinnitus masker has been invented to help sufferers live with this annoyance. The masker, a noise generator similar in appearance to a hearing aid, produces a constant, gentle humming sound that masks the tinnitus.


Ménière’s disease, usually treated with drugs and a restricted diet, may also require surgical correction to relieve the excess pressure in severe cases. If this procedure is unsuccessful, the nerves of the inner ear may be cut. In drastic cases, the entire inner ear may be removed.


Presently there is no cure for damaged hair cells; the only treatment is to use a hearing aid. It is more advantageous to take preventive measures, such as reducing noise at the source, replacing noisy equipment with quieter models, or using ear-protection devices. Recreational exposure to loud music should be severely curtailed, if not completely eliminated.




Perspective and Prospects

For many centuries, treatment of the ear was associated with that of the eye. In the nineteenth century, the development of the laryngoscope (to examine the larynx) and the otoscope (to examine the ears) enabled doctors to examine and treat disorders such as croup, sore throat, and draining ears, which eventually led to the control of these diseases. As an offshoot of the medical advances made possible by these technological devices, the connection between the ear and throat became known, and otologists became associated with laryngologists.


The study of ear diseases did not develop scientifically until the early nineteenth century, when Jean-Marc-Gaspard Itard and Prosper Ménière made systematic investigations of ear physiology and disease. In 1853, William R. Wilde of Dublin published the first scientific treatise on ear diseases and treatments, setting the field on a firm scientific foundation. Meanwhile, the scientific investigation of the diseased larynx was aided by the laryngoscope, invented in 1855 by Manuel Garcia, a Spanish singing teacher who used his invention as a teaching aid. During the late nineteenth century, this instrument was adopted for detailed studies of larynx pathology by Ludwig Türck and Jan Czermak, who also adapted this instrument to investigate the nasal cavity, which established the link between laryngology and rhinology. Friedrich Voltolini, one of Czermak’s assistants, further modified the instrument so that it could be used in conjunction with the otoscope. In 1921, Carl Nylen pioneered the use of a high-powered binocular microscope to perform ear surgery. The operating microscope opened the way for delicate
operations on the tiny bones of the middle ear. With the founding of the American Board of Otology in 1924, otology (later otolaryngology) became the second medical specialty to be formally established in North America.


Prior to World War II, the leading cause of deafness was the various forms of ear infection. Advances in technology and medicine have now brought ear infections under control. Today the leading type of hearing loss in industrialized countries is conductive loss, which occurs in those who are genetically predisposed to such loss and who have had lifetime exposure to noise and excessively loud sounds. In the future, protective devices and reasonable precautions against extensive exposure to loud sounds should reduce the incidence of hearing loss to even lower levels.




Bibliography


Canalis, Rinaldo, and Paul R. Lambert, eds. The Ear: Comprehensive Otology. Philadelphia: Lippincott Williams & Wilkins, 2000.



Dugan, Marcia B. Living with Hearing Loss. Washington, D.C.: Gallaudet University Press, 2003.



Ferrari, Mario. PDxMD Ear, Nose, and Throat Disorders. Philadelphia: PDxMD, 2003.



Friedman, Ellen M., and James M. Barassi. My Ear Hurts! A Complete Guide to Understanding and Treating Your Child’s Ear Infections. Darby, Pa.: Diane, 2004.



Greene, Alan R. The Parent’s Complete Guide to Ear Infections. Reprint. Allentown, Pa.: People’s Medical Society, 2004.



Jerger, James, ed. Hearing Disorders in Adults: Current Trends. San Diego, Calif.: College-Hill Press, 1984.



Kemper, Kathi J. The Holistic Pediatrician: A Pediatrician’s Comprehensive Guide to Safe and Effective Therapies for the Twenty-five Most Common Ailments of Infants, Children, and Adolescents. Rev. ed. New York: Quill, 2002.



“Lack of Consensus About Surgery for Ear Infections.” Health News 18, no. 3 (June/July, 2000): 11.



MedlinePlus. "Ear Disorders." MedlinePlus, April 1, 2013.



MedlinePlus. "Ear Infections." MedlinePlus, April 1, 2013.



National Center for Immunization and Respiratory Diseases, Division of Bacterial Diseases. "Ear Infections." Centers for Disease Control and Prevention, May 23, 2011.



Pender, Daniel J. Practical Otology. Philadelphia: J. B. Lippincott, 1992.



Roland, Peter S., Bradley F. Marple, and William L. Meyerhoff, eds. Hearing Loss. New York: Thieme, 1997.

Friday, May 3, 2013

What is the decibel range of audible sound?

Most people are able to hear sound with a frequency between 20 Hz and 20,000 Hz, called the range of audible sound. In a normal, healthy human ear, these sounds are clearly and correctly processed by the inner ear and the brain. Someone who has suffered hearing degradation due to genetics, old age, or exposure to loud sound may have a diminished range of audible sound.


The decibel range of audible sound is anything from 0 to 180 dB. Any sounds of more than 140 dB are painfully loud, and at the extreme of 180 dB, a person suffers irreversible hearing loss. Some loud sounds may temporarily diminish a person's ability to hear either due to minor injury to the eardrum or a processing issue where the brain has adjusted to very loud sounds and may not correctly interpret quiet sounds. 

Thursday, May 2, 2013

What is Jonas's first lie? How does he feel afterwards?

  Jonas has a few opportunities to lie after he receives permission to do so. First, in chapter 12, his mother asks if he slept soundly after his first meeting with the Giver. "Jonas simply smiled and nodded, not ready to lie, not willing to tell the truth" (88). Because Jonas dreamed of the memory he received the day before, he couldn't tell his mother about it. She wouldn't understand and he isn't supposed to talk about his training.


Next, in chapter 14, Jonas experiences what it is like to have a broken leg. At home that night, his father asks him what is wrong and if he wants medication; but, Jonas simply denies anything is wrong and dodges the issue. This isn't lying, yet, but he's building his skills for when he does lie. Another deceptive thing that Jonas does is when he accidentally gives Gabe, the baby, a memory to calm him in the middle of the night.



"He wondered, though, if he should confess to The Giver that he had given a memory away. . . He decided not to tell" (117).



At this point, Jonas has developed a pattern for deceit and he is now ready to lie. After receiving the memory about Christmas and grandparents, Jonas asks his parents if they love him. His mother freaks out about precision of language and they explain that they enjoy him, but love is an archaic word and not used anymore. They ask him if he understands that it is inappropriate to use the word love in their community and Jonas lies and says he understands. "It was his first lie to his parents" (127).


Jonas does not like his parents' answer, so he acts out against the community for it by not taking his pill the next morning. The text does not directly state that Jonas didn't like his parents' answer, but it can be inferred by his abrupt disobedience to one of the community's major rules the next morning. The more memories Jonas receives, the more he learns about what he doesn't have in his life. If Jonas can't have love in his life, for example, then he will contradict the community in the only way he knows how--stop taking the pill to see what else might happen. He is starting to realize that he doesn't want to be controlled by people who don't love him and who probably lie to him.

Wednesday, May 1, 2013

What are enterobacter?


Definition


Enterobacter are gram-negative, aerobic, motile bacteria found in soil, water, and the human intestinal tract. Enterobacter is an opportunistic pathogen that is responsible for various infections.






Natural Habitat and Features


Enterobacter is a rod-shaped, gram-negative bacteria that belongs to the family Enterobacteriaceae, which also includes the genera
Klebsiella
,
Escherichia
, Citrobacter, and Serratia. Enterobacter infections exhibit symptoms similar to infections with other gram-negative bacteria.


Not all Enterobacter species cause diseases in humans. Among the most common pathogenic species are E. aerogenes and E. cloacae. Various species can be found in water, plants, plant materials, insects, and dairy products, as well as in human and nonhuman animal feces. E. cloacae has been used in the biological control of plant diseases and of insects on mulberry leaves.



Enterobacter species are rod-shaped bacteria that can be identified by large lactose-fermenting colonies of gram-negative rods that are either raised or mucoid. These mucoid colonies appear pink to purple because of lactose fermentation. Enterobacter strains are mainly fimbriate and slime-forming.


Species of Enterobacter can be differentiated by their ability to ferment particular sugars and by their possession of arginine dihydrolase, lysine, and ornithine decarboxylase. E. aerogenes and E. cloacae can be differentiated by testing for lysine decarboxylase and arginine dihydrolase. Most Enterobacter species grow well at 86 degrees to 98.6 degrees Fahrenheit (30 degrees to 37 degrees Celsius), using eosin methylene blue (EMB) agar. MacConkey agar, when used, will give a red stain to the growing colonies.




Pathogenicity and Clinical Significance

Gram-negative pathogens possess endotoxins, giving them pathogenic properties. The most common pathogenic Enterobacter species are E. cloacae and E. aerogenes. These types of bacteria can cause opportunistic infections in immunocompromised persons. Rarely will Enterobacter become problematic in a healthy person. The urinary and respiratory tracts are the most common sites of infection.


Acquisition of Enterobacter infections can be by either endogenous or exogenous sources. Most nosocomial (hospital-acquired) Enterobacter infections cannot be traced to a single common exogenous source. Endogenous sources of nosocomial Enterobacter infections typically arise from a previously colonized site, such as the skin, gastrointestinal tract, or urinary tract. A person can be colonized with more than one Enterobacter species at any given time.


Nosocomial acquisition of Enterobacter is more common than community-acquired Enterobacter. These infections are acquired from prolonged hospitalization, especially in intensive care units, often as a result of poor handwashing technique, invasive procedures, mechanical ventilation (which can cause ventilator-associated pneumonia), hyperalimentation with dextrose, indwelling catheters (such as intravenous catheters), or prior use of antimicrobial agents.


Incubation times for Enterobacter are variable. Symptoms can appear from as early as two hours to three weeks after infection, with the majority of symptoms occurring between two hours and two days.



Enterobacter bacteria associated with skin and soft-tissue infections, burn and surgical-wound infections, intra-abdominal infections, endocarditis, septic arthritis, osteomyelitis, meningitis, and bloodstream infections further complicate an already ubiquitous pathogen. Morbidity and mortality rates with Enterobacter are significant. The most critical factor in determining the risk of mortality in a person with an Enterobacter infection is the severity of the underlying disease. Additional factors include other aspects of treatment and the microorganism’s virulence and resistance. E. cloacae has the highest mortality rate of all Enterobacter infections.




Drug Susceptibility

The goals of pharmacotherapy in the treatment of Enterobacter infection are to reduce morbidity, eradicate infection, and prevent complications. Prior use of antimicrobial agents is the single most frequently cited risk factor for the development of Enterobacter resistance. Initial drugs of choice include aminoglycosides, carbapenems, fluoroquinolones, and fourth-generation cephalosporins. Susceptibility testing is essential because some Enterobacter infections are resistant to the initial drugs of choice, making the choice of appropriate antimicrobial agents more complicated.


Carbapenems (imipenem and meropenem) are often the most effective drugs of choice against E. cloacae, E. aerogenes, and other Enterobacter species. First- and second-generation cephalosporins are virtually ineffective against Enterobacter. Third-generation cephalosporins show good in vitro activity, but they appear to increase the risk of developing drug resistance. The combination antibiotic piperacillin/tazobactam has been shown to lower thirty-day mortality rates.



Enterobacter species contain subpopulations of organisms that produce low levels of beta-lactamase. The subpopulation of these beta-lactamase-producing organisms will predominate once exposed to broad-spectrum cephalosporins. Thus, an Enterobacter infection that initially appears sensitive to cephalosporins may eventually become resistant during therapy.


Antimicrobial drug resistance occurs as a result of the production of
inactivating enzyme, alteration of the drug’s target, and alteration in the
ability of the drug to enter and or accumulate in the cell. Detection of
resistance can be identified as soon as twenty-four hours after initiation and up
to two to three weeks into therapy.



Bacterial resistance to antibiotics continues to be a significant threat. Multiple Enterobacter strains are already resistant to many antibiotics. Infectious-disease specialists are instrumental in determining appropriate antibiotic treatment. Handwashing remains the single most helpful tactic in preventing the spread of Enterobacter infections.




Bibliography


Forsythe, Stephen J., Sharon L. Abbott, and Johann Pitout. “Klebsiella, Enterobacter, Citrobacter, Cronobacter, Serratia, Plesiomonas, and Other Enterobacteriaceae.” Manual of Clinical Microbiology. Ed. James H. Jorgensen et al. 11th ed. Vol. 1. Washington: ASM, 2015. 714–37. Print.



Marcos, Miguel, et al. “Effect of Antimicrobial Therapy on Mortality in 377 Episodes of Enterobacter spp. Bacteraemia.” Journal of Antimicrobial Chemotherapy 62.2 (2008): 397–403. Academic Search Complete. Web. 29 Dec. 2015.



Sanders, W. Eugene, Jr., and Christine C. Sanders. “Enterobacter spp: Pathogens Poised to Flourish at the Turn of the Century.” Clinical Microbiology Reviews 10.2 (1997): 220–41. Web. 29 Dec. 2015.



Tortora, Gerard J., Berdell R. Funke, and Christine L. Case. Microbiology: An Introduction. 12th ed. San Francisco: Benjamin, 2016. Print.

What are hearing tests?

Indications and Procedures Hearing tests are done to establish the presence, type, and sever...