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Co-Director, Chicago Medical School of Rosalind Franklin University of Medicine and Science

It characteristically reduces nitrates, ferments glucose and usually lactose, and is either motile (with peritrichate flagella) or non-motile. It gives a positive methyl red reaction and negative reactions with Voges-Proskauer, urease, phenylalanine deaminase, and citrate agents. Historically, some 80 variably heat-labile capsular (K) antigens also have been described (L, B, and A), not to mention the more recently appreciated numerous adherence, enterotoxin, cytotoxin, and invasiveness factors that may be gained or lost by a particular serotype, because they are characteristically encoded on transmissible genetic elements such as plasmids or bacteriophages. Consequently, this common inhabitant of the normal human intestinal tract becomes a pathogen when it houses one or more specific traits contributing to its colonization and virulence in the intestinal tract. Other traits such as O and H serogroup also may be important for certain enteropathogenic and enteroinvasive organisms. For reasons that remain obscure, only a few O serogroups tend to predominate in the normal human colon (O groups 1, 2, 4, 6, 7, 8, 18, 25, 45, 75, and 81) whereas others noted in Table 345-1 tend (albeit not absolutely) to be associated with specific virulence traits and thus different types of pathogenesis in the intestine. However, the attachment traits of animal strains are different from those that infect humans and likely substantially influence their epidemiology. A large waterborne outbreak of diarrhea at a popular national park was found to be caused by enterotoxigenic E. More recently, bloody, non-inflammatory diarrhea has been increasingly associated with enterohemorrhagic E. As with most diarrheal illnesses, the highest age-specific attack rates of enterotoxigenic E. Of potential immunologic significance is the continued occurrence of symptomatic infections with E. This is followed by an incubation period of 2 to 7 days, during which colonization of the involved part of the intestinal tract and toxin production, invasion or other disruption of cell function take place. The colonization fimbriae bind the organism to cell surface receptors in the upper small bowel where the enterotoxin is delivered to reduce normal absorption and cause net electrolyte and water secretion. Also like choleratoxin, the active subunit adenosine diphosphate ribosylates the regulatory subunit of adenylate cyclase to activate adenylate cyclase. The consequently increased chloride secretion and reduced sodium absorption combine to cause net isotonic electrolyte loss that must be replaced to prevent severe dehydration and hypotension and its potential consequences. Both the colonization traits and enterotoxin production are encoded on transmissible plasmids. Besides the complications of dehydration, the only significant pathologic change is depletion of mucus from intestinal goblet cells. As seen with shigellosis, a striking inflammatory response is seen, with sheets of polymorphonuclear leukocytes in the stool. The colon shows patchy, acute inflammation in the mucosa and submucosa with focal denuding of the surface epithelium but usually without deeper invasion or systemic spread. Nevertheless, they are well-established causes of infantile diarrhea and exhibit a remarkable array of chromosomal and plasmid-encoded traits that orchestrate their initial attachment and subsequent effacement of the brush border epithelium. There is also villus atrophy, mucosal thinning, inflammation in the lamina propria, and variable crypt cell hyperplasia. These morphologic changes are associated with a reduction in the mucosal brush border enzymes and may contribute to the impaired absorptive function and diarrhea. These organisms produce Shiga-like toxins that may be responsible for the characteristic colonic mucosal and hemorrhage, as well as the complication of hemolytic-uremic syndrome. Sigmoidoscopy usually reveals only moderately hyperemic mucosa, and barium enema may reveal a thumbprint pattern of submucosal edema in the ascending and transverse colon. Some patients have superficial ulceration with mild neutrophil infiltration in the edematous submucosa. This may range from mild to severe, cholera-like diarrhea that may be life threatening, especially in small children and elderly patients, who are particularly prone to suffer the most severe consequences of dehydration, undernutrition, and electrolyte imbalance (especially hypokalemia and acidosis). Characteristic symptoms include malaise, abdominal cramping, anorexia, and watery diarrhea, occasionally associated with nausea, vomiting, or low-grade fever. The illness is usually self-limited to 1 to 5 days and rarely extends beyond 10 days or 2 weeks. The persistence of impaired mucosal absorptive capacity for 1 to 3 weeks may further compound the cycle of malnutrition that complicates diarrheal illnesses in children in developing, tropical areas.

Syndromes

• Nausea, mood changes, worsening of migraines (mostly due to estrogens)
• Kidney problems
• Problems with personal hygiene
• Believed to be making too much thyroid hormone
• Hematoma (blood accumulating under the skin)
• Preschooler development
• Aspirin or NSAID use
• Irregular heartbeat
• Skin breakdown

Intravenous drug therapy should be given until clinical improvement is seen, which usually occurs in 2 to 4 days. Culture is the most sensitive diagnostic technique, but its absolute sensitivity is unknown; reasonable estimates are 80 to 90%. Quinolone antimicrobials (especially levofloxacin, trovafloxacin, and sparfloxacin) and the newer macrolide antimicrobials (clarithromycin and especially azithromycin) are more effective than erythromycin or doxycycline in experimental laboratory studies. The availability of newer and more active drugs makes such combination therapy less desirable. The symptoms clearing most rapidly are rigors, mental confusion, myalgia, anorexia, fatigue, and abdominal complaints. Fever may persist for a week after the initiation of therapy but starts a downward trend within a few days. Despite this clinical evidence of improvement, other findings may falsely imply disease progression, such as evidence of increased pulmonary consolidation on physical examination and on radiography. Patients with respiratory failure have a relatively poor prognosis and tend to have a much slower response to therapy. Streptococci colonize the skin and mucous membranes of animals, produce catalase, and may be aerobic, anaerobic, or facultative. On blood agar plates, streptococci may cause complete (beta), incomplete (alpha) or no hemolysis (gamma). The exhaustive work of Rebecca Lancefield has allowed hemolytic streptococci to be classified into types A through O based on acid-extractable carbohydrate antigens of cell wall material. The availability of rapid latex agglutination kits provides even small clinical laboratories with the means to identify streptococci according to Lancefield group. Modern schemes of classification of hemolytic and non-hemolytic streptococci use complex biochemical and genetic techniques. The concept of group A streptococcus as a pure human pathogen is supported by the observations that (1) natural group A streptococcus infection in animals is rare; (2) laboratory animals are not useful models of streptococcal pharyngitis, scarlet fever, erysipelas, rheumatic fever, or post-streptococcal glomerulonephritis; (3) the inoculum needed to cause infection in laboratory animals is orders of magnitude greater than that estimated to cause infection in humans; and (4) streptococci have developed highly sophisticated defensive molecules that bind, inactivate, or destroy human immune response molecules. All group A streptococcal infections have the highest incidence in children younger than 10 years. The asymptomatic prevalence is also higher (15 to 20%) in children than in adults (<5%). Age is not the only factor; crowded conditions in temperate climates during the winter months are also associated with epidemics of pharyngitis in school children, as well as in military recruits. Impetigo is most common in children aged 2 to 5 and may occur year-round in tropical areas but largely in the summer in temperate climates. Similarly, 90% of cases of scarlet fever occur in children 2 to 8 years old and, like pharyngitis, it is most common in temperate regions during winter. An experiment of nature in the Faeroe Islands (Denmark) suggested that susceptibility to scarlet fever is not dependent on young age per se. Briefly, scarlet fever had disappeared from that isolated island group for several decades until it was reintroduced by a visitor with unsuspected scarlet fever. An epidemic of scarlet fever ensued, with significant attack rates in all age groups, thus suggesting that other factors, such as the lack of protective antibody against scarlatina toxin or the introduction of a new strain, rather than age predisposed those individuals to clinical illness. In contrast to pharyngitis, impetigo, and scarlet fever, bacteremia has had the highest age-specific attack rate in the elderly and in neonates. However, between 1986 and 1988, the prevalence of bacteremia increased 800 to 1000% in adolescents and adults in western countries. Although some of this increase is attributable to intravenous drug abuse and puerperal sepsis, most of the increase is due to cases of streptococcal toxic shock syndrome, in which a defined portal of entry is not apparent in 50% of cases. Pharyngeal and cutaneous acquisition is by person-to-person spread via aerosolized microdroplets or by direct contact, respectively. Epidemics of pharyngitis and scarlet fever have also occurred after the consumption of contaminated, non-pasteurized milk or food. Epidemics of impetigo have been reported, particularly in tropical areas, in day care centers, and among underprivileged children.

Ahlman H, Wangberg B, Jansson S, et al: Management of disseminated midgut carcinoid tumors. Describes an approach to cytoreduction with surgical resection and hepatic arterial embolectomy in a well-studied series. A selective review that presents the results of octreotide theraphy in 66 patients. New Nathalie Josso Gonads, genital ducts, and external genitalia become sexually dimorphic during fetal life, depending on the presence or absence of genetic and endocrine factors, nearly all of which actively impose maleness. Female differentiation usually requires no specific stimulus and occurs constitutively in the absence of male-determining factors. In contrast, female pseudohermaphroditism results from inappropriate exposure of female anlagen to masculinizing agents. The gonadal primordium is represented by the gonadal ridge, which is progressively colonized by extraembryonic primordial germ cells. Leydig cells differentiate at 8 weeks of gestation and increase until 12 to 14 weeks, when they begin to degenerate. At birth, very few remain in the interstitial tissue; the Leydig cell population reappears at puberty. After gonadal differentiation, the internal reproductive tract consists of two pairs of ducts: the wolffian ducts and the mullerian ducts. In males, mullerian duct regression begins at 8 weeks and is more or less complete at 10 to 12 weeks. The wolffian ducts develop into the vasa deferentia, epididymides, and seminal vesicles. Prostatic buds develop around the opening of the ducts at 10 to 11 weeks of gestation, and fusion of outgrowths of the urogenital sinus forms the prostatic utricle, the male equivalent of the vagina. At 10 weeks, elongation of the genital tubercle and fusion of the urethral folds over the urethral groove lead to formation of the penile urethra, whereas the genital swellings move posteriorly and fuse to form the scrotum. Male anatomic development is completed by 90 days of gestation, but penile growth occurs only between 20 weeks and term, at a time when, paradoxically, serum testosterone levels are declining. Slower than the testis to differentiate initially, the fetal ovary eventually reaches a more advanced stage of maturation. At 12 to 13 weeks, some oogonia located in the deepest layer of the cortex have entered the meiotic prophase. Female fetal sex differentiation is characterized by degeneration of the wolffian ducts at 10 weeks, whereas the mullerian ducts develop into fallopian tubes, uterus, and the upper part of the vagina. The vagina differentiates at the level of the mullerian tubercle, between the openings of the wolffian ducts where the prostatic utricle forms in males. Whereas in males the prostatic utricle opens just beneath the neck of the bladder, in females, the lower end of the vagina slides down the posterior wall of the urethra to acquire a separate opening on the body surface (see. Feminization of the external genitalia begins with formation of the dorsal commissure between the genital swellings, which in the female do not migrate posteriorly or fuse and give rise to the labia majora. Because the genital folds do not fuse, they become the labia minora, and the genital tubercle becomes the clitoris. In the female, all these steps are constitutive and occur in the absence of hormonal stimulation. Testicular differentiation is usually called sex determination because it determines whether testicular hormones, responsible for subsequent somatic sex differentiation, will be produced. The pseudoautosomal regions of the sex chromosomes enter into homologous recombination at meiosis, and it is essential that the testis-determining gene be situated in the non-recombining Y-specific region. Androgens are responsible for maintenance of the wolffian ducts and virilization of the urogenital sinus and external genitalia. Testosterone is produced from cholesterol by gonadotropin stimulation of fetal Leydig cells through the coordinated action of steroidogenic enzymes, most of which are also expressed in the adrenal gland. P-450 side-chain cleavage enzyme, which is responsible for the initial step in the steroidogenic pathway, is located at the inner mitochondrial membrane.

Additional protein and energy should be provided during phase 3 for repletion and synthesis of new tissue. Refeeding can be harmful and even cause death because of impaired organ function and depleted nutrient stores from previous starvation. The adverse consequences caused by initiating feeding too aggressively are known as the "refeeding syndrome" and usually occur within the first 5 days. Refeeding syndrome complications include fluid overload, electrolyte imbalances, glucose intolerance, cardiac arrhythmias, and diarrhea. Severely malnourished patients are at increased risk for fluid retention and congestive heart failure after nutritional therapy because of compromised cardiac and renal function. The ability to excrete sodium is impaired, so even normal amounts of dietary sodium intake can be excessive. In addition, carbohydrates increase the concentration of circulating insulin, which stimulates sodium and water reabsorption by the renal tubule. The presence of heart failure requires discontinuation of feeding until the cardiac status is stabilized. Carbohydrate refeeding stimulates insulin release and intracellular uptake of phosphate, which is used for protein synthesis and glucose metabolism. Therefore, plasma phosphorus concentrations can sometimes fall precipitously to below 1 mg/dL after initiating nutritional therapy if adequate phosphate is not given. Severe hypophosphatemia, which is associated with muscle weakness, paresthesias, seizures, coma, cardiopulmonary decompensation, and death, has occurred in severely malnourished patients after receiving enteral or parenteral nutritional therapy. Nonetheless, serum potassium and magnesium concentrations may remain normal or nearly normal during starvation because of their release from tissue and bone stores. During refeeding, increases in protein synthesis, body cell mass, and glycogen stores require generous intake of potassium and magnesium. In addition, hyperinsulinemia during refeeding increases cellular uptake of potassium 1152 and can cause a rapid decline in extracellular concentrations. Malnourished patients are predisposed to hypoglycemia because of decreased hepatic glucose production. Therefore, providing enteral or parenteral carbohydrate can cause hyperglycemia, glucosuria, dehydration, and hyperosmolar coma. Sudden death from ventricular arrhythmias can occur during the first week of refeeding in severely malnourished patients and has been reported in conjunction with severe hypophosphatemia. Alterations in gastrointestinal tract function limit the ability of the gastrointestinal tract to digest and absorb food. Mild diarrhea after initiating oral/enteral feeding usually resolves and is not clinically important if fluid and electrolyte homeostasis can be maintained. However, in some severely malnourished patients, oral feeding is associated with severe diarrhea and death. Therefore, aggressive fluid and electrolyte replacement and a search for enteric pathogens should be considered in patients with prolonged or severe diarrhea. Excellent review of the pathophysiology, clinical findings, and management of malnutrition in children. Reviews nutritional assessment and management of severely malnourished adult patients and basic principles of nutritional metabolism. Comprehensive book that carefully discusses all major aspects of protein-energy malnutrition in children in underdeveloped countries. The most well known and well characterized of the eating disorders are anorexia nervosa and bulimia nervosa. The hallmark of anorexia nervosa is the pursuit of thinness in the presence of severe emaciation. The defining features of bulimia nervosa are a cycle of binge eating followed by inappropriate compensatory behavior to avoid weight gain. Although anorexia nervosa has long been recognized and well described, the etiology of the disorder is not well understood. Societal influences promoting an unrealistically thin body size and a cultural environment that associates slimness with happiness and success have been implicated in the development of anorexia nervosa. Genetic vulnerabilities also appear to play a role in the development of anorexia nervosa. Concordance rates for anorexia nervosa are higher in monozygotic than dizygotic twins. Furthermore, the prevalence of anorexia nervosa, as well as mood disorders, is higher in first-degree relatives of affected individuals than in the general population, thus suggesting genetic aggregation.