By I. Sulfock. Gwynedd-Mercy College.

Title of the German edition: registered designs referred to in this book Medizinische Mikrobiologie are in fact registered trademarks or proprie- tary names even though specific reference to ª 2005 Georg Thieme Verlag discount clomid 25 mg on-line atraso menstrual 02 dias, this fact is not always made in the text discount clomid 100 mg mastercard menstruation underpants. Ru¨digerstraße 14 clomid 50mg lowest price menstrual yearly calendar, 70469 Stuttgart, Therefore, the appearance of a name without Germany designation as proprietary is not to be con- http://www. Any use, ex- Cover design: Cyclus, Stuttgart ploitation, or commercialization outside the Typesetting by Mitterweger & Partner narrow limits set by copyright legislation, GmbH, 68723 Plankstadt without the publisher’s consent, is illegal Printed in Germany by Appl, Wemding and liable to prosecution. Usage subject to terms and conditions of license V Preface Medical Microbiology comprises and integrates the fields of immunology, bacteriology, virology, mycology, and parasitology, each of which has seen considerable independent development in the past few decades. The com- mon bond between them is the focus on the causes of infectious diseases and on the reactions of the host to the pathogens. The objective of this textbook of medical microbiology is to instill a broad- based knowledge of the etiologic organisms causing disease and the patho- genetic mechanisms leading to clinically manifest infections into its users. This knowledge is a necessary prerequisite for the diagnosis, therapy, and prevention of infectious diseases. Beyond this academic purpose, its use- fulness extends to all medical professions and most particularly to physicians working in both clinical and private practice settings. This book makes the vast and complex field of medical microbiology more accessible by the use of four-color graphics and numerous illustrations with detailed explanatory legends. Most chapters begin with a concise summary, and in-depth and supplementary knowledge are provided in boxes separating them from the main body of text. This textbook has doubtless benefited from the extensive academic teaching and the profound research experience of its authors, all of whom are recognized authorities in their fields. The authors would like to thank all colleagues whose contributions and advice have been a great help and who were so generous with illustration material. The authors are also grateful to the specialists at Thieme Verlag and to the graphic design staff for their cooperation. Usage subject to terms and conditions of license Kayser, Medical Microbiology © 2005 Thieme All rights reserved. I Basic Principles of M edical icrobiologie and Im unology Macrophage hunting bacteria Kayser, Medical Microbiology © 2005 Thieme All rights reserved. Kayser & Infectious diseases are caused by subcellular infectious entities (prions, viruses), prokaryotic bacteria, eukaryotic fungi and protozoans, metazoan an- imals, such as parasitic worms (helminths), and some arthropods. Definitive proof that one of these factors is the cause of a given infection is demon- strated by fulfillment of the three Henle-Koch postulates. For technical rea- sons, a number of infections cannot fulfill the postulates in their strictest sense as formulated by R. In the medical teachings of Hippocrates, the cause of infections occurring fre- quently in a certain locality or during a certain period (epidemics) was sought in “changes” in the air according to the theory of miasmas. This concept, still reflected in terms such as “swamp fever” or “malaria,” was the predominant academic opinion until the end of the 19th century, despite the fact that the Dutch cloth merchant A. At the time, general acceptance of the notion of “spontaneous generation”—creation of life from dead organic material—stood in the way of implicating the bacteria found in the corpses of infection victims as the cause of the deadly diseases. It was not until Pas- teur disproved the doctrine of spontaneous generation in the second half of the 19th century that a new way of thinking became possible. By the end of that century, microorganisms had been identified as the causal agents in many familiar diseases by applying the Henle-Koch postulates formulated by R. The History of Infectious Diseases 3 The Henle–Koch Postulates 1 The postulates can be freely formulated as follows: & The microorganism must be found under conditions corresponding to the pathological changes and clinical course of the disease in question. However, the fact that these conditions are not met does not necessarily exclude a contribution to disease etiology by a pathogen found in context. In particular, many infections caused by subcellular entities do not fulfill the postulates in their classic form. The Present The frequency and deadliness of infectious diseases throughout thousands of years of human history have kept them at the focus of medical science. The development of effective preventive and therapeutic measures in recent dec- ades has diminished, and sometimes eliminated entirely, the grim epidemics of smallpox, plague, spotted fever, diphtheria, and other such contagions. As a result of these developments, the attention of medical researchers was diverted to other fields: it seemed we had tamed the infectious diseases. Previously unknown pathogens causing new diseases are being found and familiar organisms have demonstrated an ability to evolve new forms and reassert themselves. The origins of this reversal are many and complex: human behavior has changed, particularly in terms of mobility and nutrition. Further contributory factors were the in- troduction of invasive and aggressive medical therapies, neglect of estab- lished methods of infection control and, of course, the ability of pathogens to make full use of their specific genetic variability to adapt to changing con- ditions. The upshot is that physicians in particular, as well as other medical professionals and staff, urgently require a basic knowledge of the pathogens involved and the genesis of infectious diseases if they are to respond effec- tively to this dynamism in the field of infectiology. Prokaryotic and Eukaryotic Microorganisms According to a proposal by Woese that has been gaining general acceptance in recent years, the world of living things is classified in the three domains bac- teria, archaea, and eucarya. In this system, each domain is subdivided into Kayser, Medical Microbiology © 2005 Thieme All rights reserved. This domain includes the kingdom of the heterotrophic eubacteria and includes all human pathogen bacteria. The other kingdoms, for instance that of the photosynthetic cyanobacteria, are notpathogenic. It is estimated that bacterial spe- cies on Earth number in the hundreds of thousands, of which only about 5500 have been discovered and described in detail. This domain includes forms that live under extreme environmental con- ditions, including thermophilic, hyperthermophilic, halophilic, and methanogenic microorganisms. The earlier term for the archaea was archaebacteria (ancient bac- teria), and they are indeed a kind of living fossil. Thermophilic archaea thrive mainly in warm, moist biotopes such as the hot springs at the top of geothermal vents. The hyperthermophilic archaea, a more recent discovery, live near deep-sea volcanic plumes at temperatures exceeding 1008C.

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The initial passage of meconium usually occurs within the first 24 hours of life clomid 50 mg with mastercard women's health subscription, but it may be delayed in normal premature infants without intestinal obstruc- tion buy clomid 50mg on line pregnancy week 8. Delayed passage of meconium is a frequent finding in patients with distal intestinal obstruction and is observed in 90% of infants with Hirschsprung’s disease cheap clomid 100mg on line women's health clinic spruce grove. The passage of meconium does not indicate that a complete intestinal obstruction is not present, since meconium formed in utero distal to an obstruction may be evacuated. The maternal ultrasound can provide important clues about the possible etiology of intestinal obstruction and should be reviewed when a neonate presents with signs or symptoms suggesting an intestinal obstruction. Amniotic fluid is normally swallowed by the fetus and absorbed from the gastrointestinal tract. Obstruction will impair intestinal absorption, leading to accumulation of amniotic fluid or polyhydramnios. As the length of intestine available for absorption decreases, the degree of polyhydramnios increases. Polyhydramnios more likely is observed in the fetus with a proximal obstruction, such as esophageal atresia without tracheoesophageal fistula or duodenal atresia, and not those with a distal obstruction, such as distal ileal or colonic atresia (Fig. The sonographic findings of a dilated proximal esophageal pouch and lack of fluid in the stomach suggests esophageal atresia. Prominent upper abdomen fluid collections representing the fluid-filled stomach and duodenum suggest obstruction at the level of the duodenum, as in the case presented. Dilated loops of bowel with increased peristal- sis may be observed in a fetus with distal intestinal obstructions, while 36. Yes No Attempt to pass orogastric tube Obtain abdominal film Able to pass tube into stomach? Meconium peritonitis No Perforation from: Yes Volvulus Ascites Imperforate anus Atresia Intraperitoneal mass Retroperitoneal mass Obtain abdominal film Meconium ileus Choledochal cyst Hydronephrosis Renal mass Low Calcifications? No Hydrometrocolpos Obtain contrast enema Yes Ovarian cyst Pyloric atresia Duodenal atresia Meconium peritonitis Ileal atresia Malrotation with volvulus Perforation from: Meconium ileus Jejunal atresia Volvulus Meconium plug syndrome Atresia Small l colon syndrome Meconium ileus Hirschsprung’s disease Colorectal atresia Algorithm 36. Burd Low obstruction Small bowel No polyhydramnios High obstruction Small bowel Normal-caliber polyhydramnios coion Figure 36. Calcifications can form when the peritoneal cavity is exposed to meconium, and their presence suggests an antenatal intestinal perforation. Morphologic abnormalities suggesting a chromosomal defect also may have been observed, prompting amniocentesis and chromosomal testing. Chro- mosomal defects are found in about 5% of infants with esophageal atresia (most frequently trisomy 18 and 21) and about 30% of infants with duodenal atresia (most commonly trisomy 21). Family and maternal history may provide additional insight into the cause of neonatal intestinal obstruction. Because a familial association has been reported for most causes, a family history of newborn or child- hood surgery for intestinal obstruction should be sought, and the cause should be determined, if possible. Family members with disorders and anomalies outside of the gastrointestinal tract also may suggest an eti- ology of neonatal intestinal obstruction. Almost half of neonates with small left colon syndrome are infants of diabetic mothers. Physical Examination A complete examination is mandatory for all neonates with suspected intestinal obstruction. Particular attention should be focused on the abdominal examination, on the perineal inspection, and on identifying other anomalies, including features suggesting a chromosomal disor- der. In the case presented at the beginning of the chapter, the presence of trisomy 21 provides indirect evidence supporting the diagnosis of duodenal atresia. Although difficult to observe in most cases, gastroduodenal or high jejunal obstruction may result in epigastric distention with a scaphoid lower abdomen, as described in the case presented. As discussed pre- viously, mechanically ventilated neonates with esophageal atresia and 36. Neonatal Intestinal Obstruction 651 a tracheoesophageal fistula also may exhibit abdominal distention. The abdomen should be examined for tenderness and masses, and the inguinal region should be inspected for hernia. The main features to evaluate are the general perineal appear- ance and anal position and patency. The anal canal normally is posi- tioned about halfway between the coccyx and base of the scrotum in males or the vestibule in females, and it is within a perineal depression surrounded by slightly pigmented skin. Variations from this standard suggest that a variant of imperforate anus may be present. Neonates with a short distance from the distal colon to the perineum (low imper- forate anus) may have a perineal depression with pigmentation without a patent anal canal. With observation during the first 24 hours of life, meconium eventually may pass through a rectoperineal fistula and be seen exiting on the perineum anterior to the normal anal posi- tion or at midline raphe of the scrotum or penis in males or vestibule in females. Because meconium may be seen exiting on the perineum in patients with low imperforate anus, the examination should be per- formed carefully, since a normal anal canal may be confused by inex- perienced observers with a low imperforate anus with a rectoperineal fistula. Neonates with a long distance from the distal colon to the per- ineum (high imperforate anus) have more remarkable perineal find- ings, including the absence of an anal opening, absence of a perineal depression (“flat bottom”), and lack of pigmented skin. Additional screening maneuvers may be used to supplement the physical examination. To screen for esophageal atresia, a tube gently is passed through the mouth into the esophagus. In term infants with esophageal atresia, passage of the tube usually stops at about 10cm (Fig. If the tube successfully passes into the stomach, the gastric Pass 10-Fr tube through mouth Tube 10cm Dilated esophageal pouch Fistula Trachea Figure 36. Aspiration of more than 10 to 15cc of bilious material suggests an intestinal obstruction and provides further support for pursuing additional workup for the cause.

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Patients must have taken ≥80% of the scheduled doses in order to be considered compliant with the study protocol buy 50 mg clomid mastercard menstruation ovulation period. Superinfections were considered microbiological failures and were assessed separately 25mg clomid fast delivery women's health center elk grove ca. Patients with indwelling catheters were to have had blood cultures (2 sets from 2 different sites) obtained simultaneously with the catheterized urine specimen at the time of study enrollment buy clomid 25mg on line women's health questions answered. If 2 or more pathogens grew from the baseline urine culture, all isolates were considered contaminants (i. If the method of obtaining a specimen for urine culture was switched between the baseline and the Test-of-Cure visit (e. Clinical Reviewer’s Comment: The applicant noted that because there were very few patients who switched the urine collection technique between the baseline and the Test-of-Cure visit (e. This approach is acceptable to the reviewer, since there were less than 10 patients affected. All pertinent laboratory tests or procedures that reflected the course of the infectious disease were also assessed. Absence of or reduction of signs and symptoms was used to assess clinical response. In the event that the patient failed study drug therapy and was prescribed alternative antimicrobial therapy, continued clinical evaluation of the patient focused on their response to the alternative antimicrobial therapy at a subsequent visit. An indeterminate designation at Test-of-Cure invalidated the patient for efficacy evaluation. The clinical outcome was determined to be failure as soon as there was one assessment of failure at any time point. Clinical Reviewer’s Comment: The protocol included a definition for an overall clinical assessment of efficacy, which was to be a combination of the Test-of-Cure clinical response and the long-term follow-up clinical response. In the analysis, the overall clinical assessment of efficacy was not used by the applicant, since for analysis purposes; clinical response at follow-up encompassed all the components of the planned overall clinical response assessment of efficacy. Responses were graded according to the following: Cure: resolution of signs and symptoms related to the current infection and not requiring further antibiotic therapy; Failure: persistent fever or flank pain or insufficient reduction in severity of the signs and symptoms of infection to qualify as resolution, requiring a modification of the antibacterial therapeutic regimen; Indeterminate: patients in whom a clinical assessment was not possible for various reasons, including early withdrawal due to adverse events, protocol violations, etc. The definition of arthropathy was generally considered as any condition affecting a joint or periarticular tissue where there is historical and/or physical evidence for structural damage and/or functional limitation that may have been temporary or permanent. This definition was seen as broad and inclusive of such phenomena as bursitis, enthesitis and tendonitis. The musculoskeletal safety assessments were carried out primarily through objective evaluations of joint appearance, structure and function (i. Patients with any pretreatment baseline musculoskeletal exam abnormalities were excluded from the study. Infants and children with spina bifida with total or near total paralysis of the lower extremities (i. Subjective complaints spontaneously volunteered by both patients and by their parents or caregivers, especially those attributable to the musculoskeletal system, were carefully recorded and followed up with additional objective clinical assessments regardless of the period on-study (i. For shoulders, knees, hips and ankles/feet, the motions tested were the following with the patient ranges of motion recorded: • shoulders: extension, flexion, abduction, internal and external rotation; • hips: extension, flexion, adduction, abduction, internal and external rotation; • knees: extension and flexion; • ankles/feet: plantar flexion, dorsiflexion. All joint examinations were performed by an examiner skilled in the evaluation of joint function/appearance; preferably the same individual in order to minimize inter-rater variability. Gait was evaluated in both the stance and swing phases with any abnormalities noted. A training video on physical therapy evaluations was provided by the applicant to all sites to ensure that all patients were examined using the same instructions. Neurological system adverse events were to be captured for up to 1­ year post-therapy. Urine was analyzed for semiquantitative and microscopic examination for appearance, specific gravity, occult blood, protein, pH, ketones, glucose, red blood cells, crystals, bacteria, epithelial cells, white blood cells, and casts. A urinary leukocyte count (cell count by hemocytometer or the sediment examination 3 method) was performed. Patients were then examined on Day 2 to 5 during therapy, with additional on- therapy visits every 2 to 5 days during an extended treatment course. The patient was evaluated again at the Day +5 to +9 post-therapy (Test-of-Cure) visit and the Day +28 to +42 follow-up (first follow-up) visit. Interim telephone calls were conducted at the 6- and 9-month time points to assess musculoskeletal and neurological safety. Joint and gait assessment was done prior to initiation of study drug treatment to exclude patients with pre-existing abnormalities and to establish a baseline values. If qualified personnel were not available at the time of initial patient presentation, the patient’s pretherapy gait/joint examination could be conducted from 48 hours prior to initiation of study drug therapy up to 24 hours after receipt of the first dose of study drug. In cases where bacteremia was suspected, two different sets of blood cultures were also to be drawn. Patients having a protracted treatment course (14 -21 days) were to have weekly safety laboratory collection. The following procedures were performed during the on-therapy visits: • Vital signs including blood pressure, heart rate and temperature were obtained; • An assessment of pyuria was done and a urine culture was obtained, with appropriate susceptibility testing of potential pathogens; • A complete gait/joint examination was performed; • Adverse event data were collected; • Blood and urine samples for safety laboratory assessments were obtained; • Repeat blood cultures were to be drawn from patients having positive blood cultures at the pre-therapy visit; • Blood samples (1-2 mL) were to be drawn for measurement of ciprofloxacin serum concentrations. Clinical and bacteriological evaluation (urine culture and quantitative measurement of pyuria) were obtained and adverse event data were collected at each of these time points. In addition, a thorough safety assessment, including gait/joint examinations and safety laboratory assessments were performed. All procedures except for safety labs were to be repeated at the first follow- up visit (Day +28 to +42).

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