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By: R. Jorn, M.B. B.CH. B.A.O., Ph.D.
Clinical Director, University of California, Irvine School of Medicine
Giardia lamblia infection presents with bloating kinds of allergy shots generic deltasone 5 mg with visa, flatulence allergy treatment in cats discount deltasone online visa, foul-smelling diarrhea allergy x amarillo purchase deltasone from india, and light-colored fatty stools allergy testing qml order deltasone on line. On microscopy, one observes teardrop-shaped trophozoites with a ventral sucking disc or cysts. A young man presenting with hemoptysis should raise a high index of suspicion for Goodpasture syndrome. This diagnosis is supported by his fatigue and hematuria (although typically renal symptoms follow pulmonary symptoms by weeks to months). As the disease progresses, one would expect a nephritic picture with hematuria, hypertension, and oliguria. The diagnosis of Goodpasture syndrome is confirmed by the renal biopsy, which on immunofluorescence staining shows a linear pattern of IgG deposition along the basement membrane. This could account for a nephritic picture, but immunofluorescence would show an absence of any immue deposition. Furthermore, if the patient had Wegener granulomatosis, one would expect to see a specific pattern of symptoms involving the sinuses, lungs, and kidneys. The cause can be idiopathic, due to an antigenic stimulus, or due to a systemic immune complex disorder. On immunofluorescence one would see lumpy or granular deposition of immune complexes in the glomerulus. It has been proposed that pauci-immune glomerulonephritis is mediated by T lymphocytes, which release cytokines and thereby recruit inflammatory cells. Release of intracellular potassium may lead to the development of significant arrhythmias and possibly death. Hepatomegaly is a nonspecific sign of many medical conditions but is not a typical consequence of rhabdomyolysis. Pain in a dermatomal distribution is characteristic of shingles and is unrelated to rhabdomyolysis. A shuffling gait may be seen in Parkinson disease and is unrelated to rhabdomyolysis. These defects are caused by the failure of the caudal portion of the neural tube to close. Children with these defects suffer from a varying degree of symptoms that usually include motor and sensory defects in the lower extremities and dysfunction of bowel and bladder control. Folate deficiency during the first four weeks of pregnancy has been implicated in causing neural tube defects. Drugs that increase the risk of neural tube defect include valproate and carbamazepine. Bilateral renal agenesis (Potter syndrome) is caused by disruption in the interaction between the ureteric bud and the metanephrogenic tissue. Because the fetus does not produce urine (which is a component of amniotic fluid), there is a smaller volume of amniotic fluid than normal. The smaller amount of protective fluid results in pulmonary hypoplasia, fetal compression with altered facies, and positioning defects of hands and feet. The ductus arteriosus is a connection between the pulmonary artery and the aorta that allows oxygenated blood from the placenta to bypass the fetal lungs and enter the systemic circulation. At birth, as the infant takes a breath, an increase in oxygen content causes a decrease in prostaglandins, resulting in closure of the connection. If the ductus arteriosus remains patent after birth, the baby can be given indomethacin to help stimulate the vessel to close. It is possible that this fetus inherited a recessive disorder such as cystic fibrosis, phenylketonuria, or sickle cell anemia. Nondisjunction during meiosis is the usual cause of trisomy 21, the genetic abnormality in Down syndrome. On clinical examination, typical absence seizures appear as brief staring spells with no warning or postictal phase. Children are not responsive during the seizure and are amnestic of what happened during the attack. Classically, a regular and symmetric 3-Hz spike is found on electroencephalography.
Individual structural proteins associate into subunits allergy testing price generic deltasone 10mg fast delivery, which associate into protomers allergy quinine discount deltasone express, capsomeres (distinguishable in electron micrographs) allergy medicine nasal congestion cheap deltasone 40 mg with visa, and finally allergy medicine claritin deltasone 40mg without a prescription, a recognizable procapsid or capsid (Figure 36-5). For some viruses, the capsid forms around the genome; for others the capsid forms as an empty shell (procapsid) to be filled by the genome. The simplest viral structures that can be built stepwise are symmetric and include helical and icosahedral structures. Helical structures appear as rods, whereas the icosahedron is an approximation of a sphere assembled from symmetric subunits (Figure 36-6). Nonsymmetric capsids are complex forms and are associated with certain bacterial viruses (phages). Poxviridae Herpesviridae Adenoviridae Hepadnaviridae Polyoma- and papillomaviridae Parvoviridae 85-140 100-150 20-25 1. Louis encephalitis virus, West Nile virus, hepatitis C virus Norwalk virus, calicivirus Rhinoviruses, poliovirus, echoviruses, coxsackievirus, hepatitis A virus Delta agent *The size of the type is indicative of the relative size of the virus. Individual proteins associate into subunits, which associate into protomers, capsomeres, and an empty procapsid. During assembly, the genome may fill the capsid through the holes in the herpesvirus, polyomavirus, and papillomavirus capsomeres. Simple icosahedrons are used by small viruses such as the picornaviruses and parvoviruses. The icosahedron is made of 12 capsomeres, each with fivefold symmetry (pentamer or penton). For the picornaviruses, every pentamer is made up of five protomers, each of which is composed of three subunits of four separate proteins (see Figure 36-5). X-ray crystallography and image analysis of cryoelectron microscopy have defined the structure of the picornavirus capsid to the molecular level. These studies have depicted a canyon-like cleft, which is a "docking site" to bind to the receptor on the surface of the target cell (see Figure 46-2). Larger capsid virions are constructed by inserting structurally distinct capsomeres between the pentons at the vertices. This extends the icosahedron and is called an icosadeltahedron, and its size is determined by the number of hexons inserted along the edges and within the surfaces between the pentons. The adenovirus capsid is composed of 252 capsomeres, with 12 pentons and 240 hexons. The reoviruses have an icosahedral double capsid with fiber-like proteins partially extended from each vertex. Under mild acidic conditions, the hemagglutinin folds over to bring the virion envelope and cellular membrane together and exposes a hydrophobic sequence to promote fusion. Cellular proteins are rarely found in the viral envelope, even though the envelope is obtained from cellular membranes. Most enveloped viruses are round or pleomorphic (see Figures 36-2 and 36-3 for the complete listing of enveloped viruses). Two exceptions are the poxvirus, which has a complex internal and a bricklike external structure, and the rhabdovirus, which is bullet shaped. Most viral glycoproteins have asparagine-linked (Nlinked) carbohydrates and extend through the envelope and away from the surface of the virion. This causes the envelope to adhere tightly and conform (shrink-wrap) to an icosahedral structure discernible by cryoelectron microscopy. These enzymes are required to initiate virus replication, and their association with the genome ensures their delivery into the cell. Matrix proteins lining the inside of the envelope facilitate the assembly of the ribonucleocapsid into the virion. The herpesvirus envelope is a baglike structure that encloses the icosadeltahedral nucleocapsid (see Figure 43-1). Depending on the specific herpesvirus, the envelope may contain as many as 11 glycoproteins. The poxviruses are enveloped viruses with large, complex, bricklike shapes (see Figure 44-1). Enveloped viruses may also enter by steps 2 and 3 and assemble and exit from the cell by steps 8 and 9. The antiviral drugs for susceptible steps in viral replication are listed in magenta. Each infected cell may produce as many as 100,000 particles; however, only 1% to 10% of these particles may be infectious.
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Because the choice of which chromosome to inactivate is random allergy symptoms gatorade purchase deltasone 5 mg on-line, half of the pre-B cells in a carrier female will have inactivated the chromosome with the wild-type btk allergy shots alcohol order cheap deltasone line. This means they can express only the defective btk gene allergy symptoms but no allergies purchase deltasone 10 mg free shipping, and cannot develop further allergy medicine makes my heart race 40mg deltasone otc. Therefore, in the carrier, mature B cells always have the nondefective X chromosome active. This is in sharp contrast to all other cell types, which have the nondefective X chromosome active in only half of the B cells. Nonrandom X chromosome inactivation in a particular cell lineage is a clear indication that the product of the X-linked gene is required for the development of cells of that lineage. It is also sometimes possible to identify the stage at which the gene product is required, by detecting the point in development at which X-chromosome inactivation develops bias. Immunoglobulin levels in newborn infants fall to low levels around 6 months of age. Newborn babies have high levels of IgG, transported across the placenta from the mother during gestation. After birth, the production of IgM starts almost immediately; the production of IgG, however, does not begin for about 6 months, during which time the total level of IgG falls as the maternally acquired IgG is catabolized. Thus, IgG levels are low from about the age of 3 months to 1 year, which can lead to susceptibility to disease. The commonest humoral immune defect is the transient deficiency in immunoglobulin production that occurs in the first 6 12 months of life. The newborn infant has initial antibody levels comparable to those of the mother, because of the transplacental transport of maternal IgG (see Chapter 9). As the transferred IgG is catabolized, antibody levels gradually decrease until the infant begins to produce useful amounts of its own IgG at about 6 months of age. Thus, IgG levels are quite low between the ages of 3 months and 1 year and active IgG antibody responses are poor. In some infants this can lead to a period of heightened susceptibility to infection. This is especially true for premature babies, who begin with lower levels of maternal IgG and also reach immune competence later after birth. The most common inherited form of immunoglobulin deficiency is selective IgA deficiency, which is seen in about 1 person in 800. Although no obvious disease susceptibility is associated with selective IgA defects, they are commoner in people with chronic lung disease than in the general population. However, effective host defense against a subset of extracellular pyogenic bacteria, including staphylococci and streptococci, requires opsonization of these bacteria with specific antibody. These infections can be suppressed with antibiotics and periodic infusions of human immunoglobulin collected from a large pool of donors. As there are antibodies against many pathogens in this pooled immunoglobulin, it serves as a fairly successful shield against infection. Patients with X-linked hyper IgM syndrome have normal B- and T-cell development and high serum levels of IgM but make very limited IgM antibody responses against T-cell dependent antigens and produce immunoglobulin isotypes other than IgM and IgD only in trace amounts. For example, they are susceptible to infection with the opportunistic lung pathogen Pneumocystis carinii, which is normally killed by activated macrophages. Patients with X-linked hyper IgM syndrome are unable to activate their B cells fully. Lymphoid tissues in patients with hyper IgM syndrome are devoid of germinal centers (top panel), unlike a normal lymph node (bottom panel). B-cell activation by T cells is required both for isotype switching and for the formation of germinal centers, where extensive B-cell proliferation takes place. Thus, inherited immunodeficiencies can either lead us to new genes or help us to determine the roles of known genes in normal immune system function. Not surprisingly, the spectrum of infections associated with complement deficiencies overlaps substantially with that seen in patients with deficiencies in antibody production. Defects in the activation of C3, and in C3 itself, are associated with a wide range of pyogenic infections, emphasizing the important role of C3 as an opsonin, promoting the phagocytosis of bacteria. In contrast, defects in the membrane-attack components of complement (C5 C9) have more limited effects and result exclusively in susceptibility to Neisseria species. This indicates that host defense against these bacteria, which are capable of intracellular survival, is mediated by extracellular lysis by the membrane-attack complex of complement. This compares with a risk of 1/200 in the same population to a person with inherited deficiency of one of the membrane-attack complex proteins a 10,000-fold increase in risk compared to a person with normal complement activity.
Other species of Haemophilus that have been associated with clinical disease include H allergy forecast brenham tx purchase cheap deltasone on line. Although both are present in blood-containing media allergy shots maintenance buy deltasone 5 mg with amex, sheep blood agar (the most commonly used blood agar in the United States) must be heated to destroy the inhibitors of V factor allergy symptoms dizzy buy 5mg deltasone. This is a heterogeneous collection of organisms responsible for virtually all types of infections that would be seen in a clinical practice allergy symptoms worse in morning 10mg deltasone with mastercard. Escherichia coli-peritonitis; part of intestinal flora that is introduced into the peritoneum following bowel perforation. Klebsiella pneumoniae-pneumonia; colonize the oropharynx; aspiration of oral secretions. Proteus mirabilis-urinary tract infection; introduced into the urethra by migration from the colon, then passed into the bladder where the organisms can replicate. Salmonella-gastroenteritis, part of fecal flora of chickens; Escherichia coli 0157-gastroenteritis, part of fecal flora of cattle; Yersinia pestis-plague, colonizes rodents and is spread to humans by a flea bite. More than 50 genera and hundreds of species and subspecies have been described (Table 25-1). These genera have been classified based on biochemical properties, antigenic structure, and molecular analysis of their genomes Table 25-1 Important Enterobacteriaceae Organism Historical Derivation Escherichia coli Salmonella enterica Salmonella Typhi Salmonella Paratyphi Salmonella Choleraesuis Salmonella Typhimurium Salmonella Enteritidis Shigella dysenteriae Shigella flexneri Shigella boydii Shigella sonnei Yersinia pestis Yersinia enterocolitica Yersinia pseudotuberculosis Klebsiella pneumoniae Klebsiella oxytoca escherichia, named after Escherich; coli, of the colon salmonella, named after Salmon; enteron, gut; pertaining to the gut typhi, of typhoid; disease is typhoid fever paratyphi, of a typhoid-like infection cholera, cholera; sus, hog; cholera of a hog typhi, of typhoid; murium, of mice; typhimurium, typhoid of mice enteris, gut; idis, inflammation shigella, named after Shiga; dysenteriae, dysentery flexneri, named after Flexner boydii, named after Boyd sonnei, named after Sonne yersinia, named after Yersin; pestis, plague enterocolitica, pertaining to the intestine and colon tuberculum, a small swelling; pseudotuberculosis, false swelling klebsiella, named after Klebs; pneumoniae, inflammation of the lungs oxus, acid; tokos, producing; acidproducing (refers to biochemical properties) proteus, a god able to change himself into different shapes; mirabilis, surprising; refers to pleomorphic colony forms citrus, lemon; bacter, a rod; citrateutilizing rod; freundii, named after Freund koseri, named after Koser enteron, intestine; bacter, a small rod; aeros, air; genes, producing; small gas-producing intestinal rod cloacae, of a sewer; originally isolated in sewage serratia, named after Serrati; marcescens, becoming weak, fading away; originally believed not virulent by gene sequencing and protein composition by mass spectrometry. Despite the complexity of this family, most human infections are caused by relatively few genera and species (Box 25-1). Enterobacteriaceae are ubiquitous organisms found worldwide in soil, water, and vegetation and are part of the normal intestinal flora of most animals, including humans. A third group of Enterobacteriaceae exists-those normally commensal organisms that become pathogenic when they acquire virulence genes present on plasmids, bacteriophages, or pathogenicity islands. All members can grow rapidly, aerobically and anaerobically (facultative anaerobes), on a variety of nonselective. The Enterobacteriaceae have simple nutritional requirements, ferment glucose, reduce nitrate, and are catalase positive and oxidase negative. The absence of cytochrome oxidase activity is an important characteristic because it can be measured rapidly with a simple test and is used to distinguish the Enterobacteriaceae from many other fermentative and nonfermentative gramnegative rods. The appearance of the bacteria on culture media has been used to differentiate common members of the Enterobacteriaceae. Resistance to bile salts in some selective media has also been used to separate enteric pathogens. In this way, use of culture media that assess lactose fermentation and resistance to bile salts is a rapid screening test for enteric pathogens that would be otherwise difficult to detect in diarrheal stool specimens, where many different organisms may be present. Some Enterobacteriaceae such as Klebsiella are also characteristically mucoid (wet, heaped, viscous colonies with prominent capsules, whereas a loose-fitting, diffusible slime layer surrounds other strains. The epidemiologic (serologic) classification of the Enterobacteriaceae is based on three major groups of antigens: somatic O polysaccharides, K antigens in the capsule (type-specific polysaccharides), and H proteins in the bacterial flagella. Strain-specific O antigens are present in each genus and species, although cross-reactions between closely related genera are common. The K antigens are not commonly used for strain typing but are important because they may interfere with detection of the O antigens. Detection of these various antigens has important clinical significance beyond epidemiologic investigations-some pathogenic species of bacteria are associated with specific O and H serotypes. Many Enterobacteriaceae also possess fimbriae (also referred to as pili), which have been subdivided into two general classes: chromosomally mediated common fimbriae and plasmidencoded sex pili. The common fimbriae are important for the ability of bacteria to adhere to specific host cell receptors, whereas the sex or conjugative pili facilitate genetic transfer between bacteria. Pathogenesis and Immunity Numerous virulence factors have been identified in the members of the family Enterobacteriaceae. Some are common to all genera (Box 25-2), and others are unique to specific virulent strains. Endotoxin Endotoxin is a virulence factor shared among aerobic and some anaerobic gram-negative bacteria. Many of the systemic manifestations of gram-negative bacterial infections are initiated by endotoxin: activation of complement, release of cytokines, leukocytosis, thrombocytopenia, disseminated intravascular coagulation, fever, decreased peripheral circulation, shock, and death.