Lippincott microbiology download

Read the quick review below and download the PDF by using links given at the end of the post. We provide the link for educational purpose and hope you will fin this book helpful. To mastering essential microbiology concepts is easier with this vividly illustrated review resource. Part of the popular Lippincott Illustrated Reviews series, this proven approach uses clear, concise writing and hundreds of dynamic illustrations to take students inside various microorganisms and ensure success on board exams.

Lippincott Microbiology 4th edition, straightforward lecture-style outlines streamline the review process, accompanied by hundreds of colorful illustrations that make complex concepts more accessible and bring microorganisms to life in vibrant detail. This edition makes exam preparation more efficient than ever with an emphasis on exam-relevant content, as well as hundreds of board-style review questions that help students confidently prepare for the USMLE.

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Developed for fast content absorption, these high-yield cards support course learning and board exam preparation. We have uploaded a genuine PDF ebook copy of this book to our online file repository so that you can enjoy a blazing-fast and safe downloading experience.

Download Link. Kindly support us by sharing this Post with your friends. You may send an email to admin cmecde. Save my name, email, and website in this browser for the next time I comment. Borrelia species are unusual among bacteria in that their genome is comprised of a linear chromosome and numerous linear and circular plasmids.

Like T. Primary syphilis presenting as painless chancres of the penis Figure II Indicates first-line drugs. Borrelia Species A. Pathogenesis Rodent Lyme disease is caused by the spirochete B. This blood meal results in a heavily engorged tick. Lyme disease is currently the most common arthropod-transmitted disease in the United States with approximately 30, reported cases per year. Lyme disease in Europe and Asia can be caused by other Borrelia species, including Borrelia garinii and Borrelia afzelii, which are associated with different late-stage symptoms.

Clinical significance The first stage of Lyme disease begins days after a tick bite, when a characteristic red, circular lesion with a clear center erythema migrans appears at the site of the bite Figure The organism spreads via the lymph or blood to musculoskeletal sites, skin, CNS, heart, and other tissues and organs.

Weeks to months after the onset other symptoms such as arthritis, arthralgia, cardiac complications, and neurologic complications including meningitis can occur. Lyme disease is rarely fatal but can result in a poor quality of life if untreated.

Laboratory identification Unlike T. Serologic tests have been used to diagnose Lyme disease, but false-positive results are common. Such tests should be used only as confirmation of a strong clinical suspicion. Erythema migrans: A red, circular rash with a clear center Figure Spirochetes D.

Treatment and prevention m Endemic tickborne Doxycycline is the most recommended treatment for the early stages of the disease see Figure If arthritic symptoms have already appeared, longer courses of antibiotics ceftriaxone are used. Prevention of infection includes use of insect repellents and wearing clothing that sufficiently protects the body from tick bites; there is no current vaccine for human Lyme disease.

Relapsing fever is characterized by several cycles of apparent recovery, each followed by a relapse. A most striking property of the relapsing fever spirochetes is their ability to change surface protein antigens.

This ability accounts for the relapsing nature of the disease because, with each relapse, a new antigenic variant arises. Pathogenesis Distinctions can be made between endemic and epidemic relapsing fever. Endemic relapsing fever can be caused by a variety of Borrelia species, occurs in most areas of the world, and is transmitted by softbodied ticks. Endemic relapsing fever is a zoonosis, because it is transmitted from small mammal reservoirs to humans by vectors.

The tick vectors also serve as reservoirs because the Borrelia species are maintained in the tick population by transovarial passage. By contrast, epidemic relapsing fever is transmitted from human to human by body lice Figure Epidemic relapsing fever is associated with crowded, unsanitary, louse-infested environments.

Endemic vs epidemic relapsing fever by Borrelia recurrentis. Clinical significance The first symptoms of relapsing fever appear days after exposure to an infected arthropod Figure These symptoms include an abrupt onset of high fever accompanied by severe headache, u..

Relapsing Fever Spirochetes muscle pain, and general malaise. During this febrile period, which lasts days, abundant spirochetes are present in the blood.

The fever abates along with the number of spirochetes. Apparent recovery is experienced for a period of O days but is followed by a recurrence of the initial symptoms. There may be as many as ten such recurrences, generally with decreasing severity. In fatal cases, the spirochete invades many organs of the body eg, heart, spleen, liver, and kidney , with death generally because of myocarditis with shock.

Diagnosis and treatment Diagnosis is usually based on the appearance of loosely coiled spirochetes visualized with Giemsa or Wright stain in the blood during the febrile stage of the disease. Tetracyclines, erythromycin, and penicillin have proven effective treatments Figure However, the relapsing nature of the disease makes it difficult to distinguish spontaneous remissions from response to therapy. No vaccines are available. D Indicates first-line drugs.

Spirochetes VI. Many serovars have been characterized based upon polysaccharide differences in the LPS component in the outer membrane, and these serovars are specific to distinct geographic locales.

It can, however, survive for weeks in slightly alkaline water. Epidemiology and pathogenesis Figure Dark-field micrograph of Leptospira interrogans. Electron micrograph of one end of a negatively stained Leptospira interrogans showing the axial fibril.

Leptospirosis is essentially an animal disease that is coincidentally transmitted to humans, primarily by water or food contaminated with animal urine. Entrance to the body can also occur via small skin abrasions or the conjunctiva. Although leptospirosis occurs worldwide under various local names, such as infectious jaundice, marsh fever, Weil disease, and swineherd disease , the incidence of the disease today in developed countries is very low. Fewer than cases of clinically significant L.

Clinical significance Fever occurs weeks after infection, at which time spirochetes appear in the blood. These symptoms decrease after about 1 week. However, in cases of biphasic disease ie, the disease having two stages , spirochetes reappear, accompanied by invasion of the liver, kidneys, and CNS. This second stage of the disease, which lasts 3 or more weeks, involves a rise in circulating immunoglobulin M antibodies. Protective immunity develops following disease, but it is serovar-specific.

Diagnosis and treatment Although L. Penicillin or doxycycline is useful if administered during the first stage of the disease, but both are ineffective later Figure Severe leptospirosis is treated with penicillin-G or ceftriaxone. No vaccine is currently available. Prevention of exposure to potentially contaminated water and food helps control the transmission of L. Leptospirosis Pinta Relapsing fever Yaws Syphilis Any of these mechanisms are conceivable with various degrees of plausibility.

The weight of evidence, however, favors the mechanism whereby new antigenic variants arise that elude, for a period, the host's immune defenses, to then be replaced by another variant. Borrelia hermsii is one of several species of Borrelia that cause relapsing fever, when it is transmitted by ticks.

Pinta, yaws, and syphilis are transmitted by direct human-to-human contact, whereas leptospirosis is transmitted via water contaminated with animal urine. The endoflagella are thought to be responsible for the corkscrew motion of spirochetes. The other structural features are not specific to spirochetes. Spirochetes Physical examination shows a firm, raised, red, nontender chancre midway between the base and glans. Which of the following is the most appropriate course of action for the physician?

Test a serum sample for antibodies to herpes simplex virus. Swab the chancre and culture on Thayer-Martin agar. Swab the chancre and perform a Gram stain. Perform a dark-field examination on a swab of the active lesion. Swab the chancre and culture on blood agar. These constitutional symptoms were accompanied by a spreading, circular rash on the child's back. Travel and recreational history indicated that the boy had recently been camping in rural Connecticut.

The boy was unaware of any abrasions, bites, or other injury. Which of the following characteristics is unique to the organism that is the most likely cause of this infection? The outer membrane contains lipopolysaccharide. The outer surface is composed of mycolic acids. The genome is composed of one linear chromosome and a series of circular and linear plasmids. The disease is caused by elaboration of a potent exotoxin.

The disease is transmitted by the bite of a body louse. The patient most likely has primary syphilis rather than herpes simplex virus because the penile chancre is not tender. Herpes lesions are typically very painful. Treponema pallidum, the etiologic agent of syphilis, cannot be readily cultured in the routine clinical microbiology laboratory. Treponemal spirochetes from primary and secondary lesions can be detected microscopically using immunofluorescent stain or dark-field illumination.

However, syphilis is usually diagnosed serologically by detection of 1 antitreponemal antibodies that are specific to the treponemal surface proteins and 2 nontreponemal antibodies reagin that are directed against normal phospholipid components. Borrelia burgdorferi, the causative agent of Lyme disease, has a unique genome composed of a linear chromosome and a complement of circular and linear plasmids.

The outer sheath of the spirochetes is also relatively unique in that it does not contain lipopolysaccharide or endotoxin. The outer surface does not contain mycolic acids, which are found in the Mycobacterium species. Many patients, however, do not know that they have been bitten by a tick until the characteristic rash appears.

The highest incidence of Lyme disease caused by B. J Northeast and upper Midwestern United States. Instead, they are enclosed in a single plasma membrane. Because of their extremely small size, mycoplasmas frequently pass through bacteriologic filters. Mycoplasma species are widely distributed in nature and include several commensals commonly found in the mouth and genitourinary GU tracts of humans and other mammals.

For these reasons, mycoplasmas are often recovered as contaminants or adventitious flora from biological materials, including clinical samples. Three Mycoplasma species are definitively associated with human disease, namely, Mycoplasma pneumoniae, which is the cause of an atypical pneumonia, and Mycoplasma hominis and Ureaplasma species, which are associated with a variety of GU diseases, such as urethritis, pelvic inflammatory disease PIO , and intrapartum infections Figure However, M.

Mycoplasma genitalium is a recently recognized sexually transmitted pathogen that causes nongonococcal urethritis NGU. Lacking cell walls, mycoplasmas are insensitive to antibiotics that inhibit cell division by preventing cell wall synthesis such as penicillin, see p.

However, they are susceptible to other inhibitors of prokaryotic metabolism. They are, therefore, plastic and pleomorphic and thus cannot be classified as either cocci or rods. Mycoplasmas are also the smallest of known free-living, self-replicating prokaryotic cells.

Infectious virus particles are released following cell lysis. After attachment to and uptake by the host cell, rotaviruses become partially uncoated in a lysosome. The rotavirus genome has 11 segments of linear, dsRNA, each of which codes for a single protein.

Reassortment of the RNA segments see p. After the negative-strand RNA is made, it stays associated with its positive-strand template, giving rise to a dsRNA segment that is packaged in the virion. Rotaviruses are released following cell lysis rather than by budding through the membrane, thus accounting for the lack of a viral envelope.

Clinical significance Following ingestion, rotaviruses infect the epithelial cells of the small intestine, primarily the jejunum Figure Rotaviruses are able to reach the small intestine because they are resistant to the acid pH of the stomach. The incubation period is usually 48 hours or less.

Infection can be subclinical or may result in symptoms ranging from mild diarrhea and vomiting to severe, nonbloody, watery diarrhea with dehydration and loss of electrolytes. Although rotavirus infections are probably equally widespread around the world, the outcomes of infection vary significantly in different regions, and malnutrition dramatically increases the severity of the infection.

Infection results in some degree of lifelong immunity with reinfected adults suffering a much milder illness. Infants who are breastfed also suffer milder disease manifestations. However, in developing countries and areas where medical facilities or personnel may be lacking, the mortality is significant: An estimated 1 million deaths per year worldwide result from rotavirus infection.

Laboratory identification Severe diarrhea, dehydration, and electrolyte loss can be due to a variety of causes. Accordingly, a definitive diagnosis cannot be made on clinical grounds alone. As with many other viral infections, identification can be made by detection of viral capsid antigens in stool samples using enzyme-linked immunosorbent assay see p. An increase in the titer of antiviral antibody in a patient's serum can also be diagnostic.

Electron microscopy of stool specimens, although not a routine diagnostic measure, can aid in the identification of the virus because rotaviruses have a distinctive appearance see Figure Rotavirus 01 Following ingestion, rotaviruses infect the epithelial cells of the small intestine, primarily the jejunum.

Treatment and prevention There is no specific antiviral drug appropriate for treatment of rotavirus infections. The most important clinical intervention is the rapid and efficient replacement of fluids and electrolytes, usually intravenously. Formulations are also being produced that can be used in developing countries so that fluids and electrolytes can be replaced orally. Two oral vaccines containing live attenuated virus have been shown to be safe and highly efficacious in protecting infants against severe rotavirus gastroenteritis.

Current vaccines are not associated with increased risk of intussusception telescoping of one portion of the intestine into another , which was associated with a previous rotavirus vaccine. Prevention of rotavirus infections requires improved sanitation measures. As a result, the patient experiences a malabsorptive state in which dietary nutrients such as sugars are not absorbed by the small intestine, leading to a hyperosmotic effect that causes diarrhea.

Rotaviruses infect and replicate in the gastrointestinal tract and typically affect infants and very young children. Although rotavirus infections are seen worldwide, significant mortality exists only in developing countries or in situations where good medical treatment '- eg, fluid and electrolyte replacement is not available.

Because rotaviruses contain a segmented genome, infection of a single cell with two different rotaviruses can result in genetic reassortment and the emergence of a new viral strain with some genomic segments from one parent and the remaining genomic segments from the other parent.

Rotaviruses do contain the enzymes required to synthesize viral mRNAs. A, B, D, E: No differences exist between polioviruses and rotaviruses in these characteristics.

The diagnosis of rotavirus infection is readily made by detection of viral antigens in the stool by enzyme-linked immunosorbent assay. Although the diagnosis can be made by electron microscopy, it is not a routine procedure. The clinical presentation is not sufficiently distinctive to make the diagnosis, and there is no specific antiviral treatment for rotavirus infections. There are no specific antiviral treatments for rotavirus infection.

The most effective treatment simply involves fluid and electrolyte replacement. The virus is nonenveloped, and therefore, membrane fusion does not occur.

Metronidazole is used to treat infections with anaerobic bacteria and some parasitic infections. Unlike HIV, rotavirus does not have reverse transcriptase or proteases that are required for virus maturation. OVERVIEW The designation "unconventional infectious agent" refers to a distinctive, transmissible, infectious agent that, although having some properties in common with viruses, does not fit the classic definition of a virus Figure One such highly unconventional infectious agent, the prion, has been implicated as the causative agent of transmissible spongiform encephalopathies TSEs.

These infections are transmissible to uninfected animals and humans. The primary disease manifestation, encephalopathy, should be distinguished from encephalitis. TSEs are characterized by their distinct absence of inflammatory signs, whereas encephalitis is distinguished by inflammation and the infiltration of white cells. Important TSEs of animals include scrapie in sheep, bovine spongiform encephalopathy BSE in cattle popularly called "mad cow disease" , and chronic wasting disease found in deer and elk.

Histologically, these diseases are characterized by spongiform vacuolation of neuronal processes and gray matter; accumulation of a unique protein prion protein, or PrP, as shown in Figure Such diseases are sometimes referred to as transmissible amyloidoses. PRIONS After an extensive series of purification procedures, scientists were astonished to find that the infectivity of the agent causing scrapie in sheep was associated with a single protein species, with no detectable associated nucleic acid.

This infectious protein is designated the PrP. It is relatively resistant to proteolytic degradation and, when infectious, tends to form insoluble aggregates of fibrils, similar to the amyloid found in other diseases of the brain. Fibrillar proteins accumulate in the brains of patients with transmissible spongiform encephalopathy. Presence of prion protein in normal mammalian brain A noninfectious form of PrP, having the same amino acid and gene sequences as the infectious agent, is present in normal mammalian brains on the surface of neurons and glial cells.

It is referred to as PrPc cellular prion protein. Although the function of noninfectious PrPc is Figure Unconventional Infectious Agents al Interaction of the infectious PrP molecule with a normal PrP causes the normal form to fold into the infectious form. The primary structure and posttranslational modifications of the normal and the infectious forms of the protein are closely related or identical. However, specific mutational changes of single amino acids at a few sites appear to be determinants of susceptibility to exogenous infection and the probability for spontaneous conversion of the normal PrPc to the infectious form PrP The key to becoming infectious apparently lies in the three-dimensional conformation of the PrP.

Presumably, this conformational difference confers relative resistance to proteolytic degradation on infectious prions, thereby distinguishing them from normal PrPc in infected tissue. A model for "reproduction" of the agent is shown in Figure Epidemiology The normal mode of transmission among animals eg, among sheep in a flock infected with scrapie has not been elucidated.

It is clear, however, that several diseases of domestic animals have been transmitted via feed prepared from other diseased animals. Bovine spongiform encephalopathy: BSE, commonly called mad cow disease, arose in British cattle presumably caused by their feed processed with animal parts prepared from diseased sheep and cattle. The obvious question raised by this occurrence is whether the BSE from infected cattle can be transmitted to humans.

Although such a risk was originally considered negligible, a study of infectious material from a cluster of histologically distinctive British CJD cases in unusually young patients now referred to as "variant," or vCJD indicated that animal-to-human transmission very likely did take place.

Because the incubation time for symptoms to appear varies from 4 to 40 years, the likelihood of a potential epidemic caused by BSE is unknown.

Kuru: An example of human-to-human transmission of a TSE is found in kuru, a disease in which the infectious agent is acquired by an individual's exposure to diseased brain tissue in the course of ritualistic cannibalism among members of a tribe in New Guinea.

Infection occurs by consuming contaminated brain tissue or via inoculation through breaks in the skin following the handling of diseased tissue. With cannibalism cessation in the late s, the disease is disappearing. Creutzfeldt-Jakob disease: Of more general significance are the documented cases of iatrogenic unintentionally introduced by medical procedures transmission of CJD, for example, by use of prion-contaminated human pituitary-derived growth hormone prepared from individuals who died from CJD.

In addition, corneal transplants, implantation of contaminated brain electrodes, and blood transfusions have resulted in documented cases of disease transmission. Thus far, there has been no evidence of transplacental transmission or transmission by person-to-person contact. Prions the PrP gene. However, most CJD cases are sporadic and have an unknown etiology ie, they occur with no known exposure or mutational change.

Despite the inherited nature of the disease, brain tissues from these patients are nevertheless infectious. Knockout mice lacking the gene that encodes PrPc appear normal but are immune to infection with prions. Pathology Ingestion or other extracerebral exposure to prions results in significant multiplication of prion agents in the follicular dendritic cells within lymphoid tissues and in the spleen, but it is invasion of the central nervous system that results in the typical clinical effects.

The basis for the pathogenic consequences of abnormal PrP 5c deposition has not been clarified. Diseased brain tissue is characterized by accumulation of abnormal PrP 5c in the form of amyloid fibrils in neuron cytoplasmic vesicles see Figure There is, in addition, extensive vacuolation within neurons, neuronal loss, and astroglial proliferation.

The extensive destruction results in the characteristic spongiform appearance of gray matter in histologic sections. Recent evidence suggests that these two proteins may physically interact with one another and participate in the same signaling or transport pathways in neurons. Clinical significance TSEs are a group of progressive, ultimately fatal, neurodegenerative diseases affecting humans and a number of animal species.

The disease process is fundamentally the same in all TSEs, but their clinical manifestations and histopathologies differ. TSEs also share some similarities with conventional infectious diseases, but their differences are striking Figure Molecular basis of inherited TSEs: In each inherited TSE, specific, single amino acid substitutions or insertions of nucleotide repeat sequences are found in the PrP gene.

These are thought to increase greatly 10 6 -fold the probability of transition to the infectious conformation. In the spontaneously occurring, sporadic disease ie, with no known exposure to infectious material and no inheritance of a mutated PrP gene , it is proposed that the altered folding occurs randomly with low probability. Importantly, once formed, the abnormal PrP 5 c acquires both the ability to "multiply," as well as the properties of an infectious agent.

It has been recognized, however, that certain amino acid substitutions at one specific site increase susceptibility to infection. They all can multiply in the infected host. There are characteristic and reproducible pathologic changes and clinical dysfunction in the diseased host. Strains differing in virulence and species specificity can be recovered from different hosts.

No humoral immune or inflammatory response is observed during the course of the TSE disease. No virus-like particles can be seen by electron microscopy or isolated from diseased tissues.

Certain TSEs, unlike conventional infectious diseases, can be inherited. Unconventional Infectious Agents characteristic clinical phenotype.