Professor, University of Toledo College of Medicine
Malabsorption and maldigestion mainly result from a diffuse shortening of epithelial microvilli symptoms of flu order aricept 5mg otc, which is associated with loss of disaccharidase activity symptoms hypoglycemia purchase aricept 5mg without prescription. Activation of lymphocytes is secondary to Giardia-induced disruption of epithelial tight junctions medicine zanaflex cheap aricept online american express, which in turn increases permeability medicine woman cast discount aricept online mastercard. Loss of epithelial barrier function is a result of Giardia-induced enterocyte apoptosis. Direct physical injury by the parasite, release of parasite products such as lectins and enzymes and mucosal inflammation due to cytokine release have all been postulated [159,163]. Nevertheless, an increased intra-epithelial T-cell infiltrate is only occasionally demonstrated in small intestinal biopsies [164]. Trophozoites are detected in stool specimens, duodenal fluid, mucosal impression smears and biopsies. In biopsies, the parasites are usually demonstrated in clusters in the lumen, on or adjacent to the epithelial surface (Figure 20. A Giemsa preparation stains the organism well but, in normal or heavy infestation, special stains are usually not required. It is important not to mistake sickled red blood cells, often present in biopsy material, for the protozoa. Although varying degrees of villous atrophy, chronic inflammation in the lamina propria and modest intraepithelial lymphocytosis are all seen, it is important to emphasise that, in most cases (96% in one series), the duodenal mucosa appears normal [160]. Thus a search for the parasite should be undertaken in all duodenal biopsies in patients presenting with diarrhoea and malabsorption, whether or not the biopsies are morphologically normal [160]. Furthermore the protozoan may be detected in gastric, jejunal, ileal and colonic mucosa: these mucosae are also usually normal histologically. Outside these conditions, there is also strong positive association between giardiasis and gastric helicobacter infection [160]. Coccidiosis the gut coccidia are obligate intracellular protozoan parasites, four genera of which are human pathogens: Cryptosporidium, Cyclospora, Isospora and Sarcocystis. Cryptosporidiosis Cryptosporidium parvum is the only type of this genus known to infect humans [165], although a murine Cryptosporidium sp. The primary site of infection is the upper small bowel, although the disease is most often diagnosed microbiologically in stool samples. Infection occurs through the ingestion of oocysts, which excyst and infect intestinal epithelial cells. The later stages of parasite development are accompanied by apoptosis of host epithelial cells. In immunocompetent individuals, the disease is self-limiting, with Inflammatory disorders of the small intestine 331 (a) Figure 20. The small bowel mucosa shows strikingly variable changes which correlate with a highly variable clinical picture from minor symptoms, through a cholera-like acute enteritis, to chronic diarrhoea. The symptomatology and morphological changes also correlate with the oocyst concentration in the stool [169]. Extensive involvement of the small and large bowel with heavy oocyst load correlates with the most severe clinical features [171]. The pathogenesis of the enteritis remains poorly understood in both immunocompetent and immunocompromised individuals [172]. In histological sections the organism is recognised by its proximity to the epithelial surface, being attached to the microvillous border of the epithelial cells (Figures 20. Cryptosporidia become internalised within the cytoplasm by extension of the cytoplasm around them [173]. Probably the most useful stains are mucin stains, which help to differentiate the organisms from blobs of mucin, the most likely confounding histopathological feature. Notably, the cryptosporidia are of consistent size 332 Small intestine whereas mucin blobs are of varying sizes, serving to differentiate the two. Isosporiasis Isospora belli is an upper small bowel pathogen that is a relatively common cause of enteropathy in tropical countries. Unlike cryptosporidia, isospora organisms are internalised within the enterocyte cytoplasm and readily detected there by high power light microscopy and electron microscopy. It primarily involves the proximal small bowel and may be demonstrated in duodenal biopsies [178]. Heavy infection may cause inflammation and epithelial injury with villous blunting [179,180]. Sarcosporidiosis Sarcocystis hominis is the least common of the human coccidial small intestinal infections, in western countries at least [158]. Microsporidiosis Microsporidia are obligate, intracellular, spore-forming protozoa of uncertain phylogeny, generally considered Inflammatory disorders of the small intestine 333 closely related to other coccidioses [186]. The diagnosis formerly relied on electron microscopy, which reveals the phases of the life cycle: a proliferative phase known as merogony and a sporulating phase known as sporogony. The proliferative phase demonstrates small rounded organisms with one to six nuclei found within the cells as electron-lucent structures. The sporulating phase is characterised by electron-dense stacks of discs, which aggregate to form the polar tubule and later the spores. Septata intestinalis is characterised by numerous intracytoplasmic spores separated by granular material (hence the name Septata). Electron microscopic examination has been important for light microscopic diagnosis (Figure 20.
Drug-induced enteritis can be subdivided into two major types: ischaemic injury and inflammation symptoms just before giving birth discount aricept 10mg line. Ischaemic injury is frequently multifactorial medications when pregnant purchase aricept uk, one of the factors usually being some form of intrinsic vascular disease in which medicine reactions cheap aricept 10 mg with visa, when further factors are added treatment 3 cm ovarian cyst buy aricept pills in toronto, an ischaemic episode may result. The major categories include trauma to vessels after manipulation, vasoconstriction or obstruction, including vasculitis, pump failure or peripheral vasodilatation (see Chapter 22). Radio-embolisation with resin or glass micro-spheres loaded with radioactive isotopes, for instance, produced symptomatic gastroduodenal ulceration in 3. Potassium chloride tablets, gold and chemotherapeutic agents have also received some attention because of their effects on the small bowel mucosa. In the more distal small intestine, perforation, ulcers, stricturing and obscure bleeding are the most likely presentations [383,385]. Capsule endoscopy shows that erosions in areas other than the proximal and distal small bowel are also common. Loss of prostaglandin biosynthesis may be a promoting factor, as illustrated by reports from patients with chronic recurrent small intestinal ulcers, small bowel perforations and gastrointestinal blood loss. The drugs may injure the small intestine by contact irritant effects and the enterohepatic circulation seems to be a key effect. Increased mucosal permeability leads to protein loss whereas ulceration causes obscure haemorrhage, presenting as unexplained anaemia [391,392]. In this condition, which usually affects the ileum, but is also now increasingly recognised more proximally in the small intestine and the colon, patients present with subacute obstruction due to thin mucosa-lined septa that resemble a perforated diaphragm when seen en face (Figure 20. It is particularly important for surgeons to know of their existence (a) (b) Figure 20. Once other pathologies have been excluded, the diligent pathologist should seek an accurate drug history because many of these lesions are caused by drugs, especially non-steroidal anti-inflammatory drugs. Inflation of the unopened fresh specimen is important to display the lesions to best advantage. Diaphragms may be associated with ulcers but often the adjacent mucosa is entirely normal [393]. The pathogenesis of diaphragm disease appears to relate to superficial circumferential ulceration, followed by submucosal fibrosis and a high degree of mucosal restitution. Diaphragms show a close resemblance to the normal plicae circulares of the small bowel but have additional characteristic features. Immediately adjacent to the stenotic lumen there is mucosal attenuation and ulceration, often with features of mucosal prolapse in the form of fibromuscular proliferation in the lamina propria in the adjacent intact mucosa (Figure 20. There is a well-defined area of underlying submucosal fibrosis, which is more prominent in broadbased lesions (Figure 20. If suspected clinically, diaphragm disease can be diagnosed either radiologically and/or endoscopically and may be treated by enteroscopic means rather than having to resort to surgical resection. At higher power the insert demonstrates submucosal fibrosis at the tip and villous blunting. There is now some resemblance to the pattern of microscopy in the potassium-induced ulceration. Other drug-induced enteropathies Enteric-coated potassium supplements and hydrochlorthiazide are both associated with small intestinal ulceration and haemorrhage [397]. As a treatment for hyperkalaemia in uraemic patients, Kayexalate (sodium polystyrene sulphonate in sorbitol) may be given by mouth, via a nasogastric tube or by enema. Patients treated for rheumatoid arthritis with gold therapy occasionally develop an eosinophilic enterocolitis with diarrhoea and peripheral eosinophilia usually within 3 months of drug initiation [399,400]. Histopathologically, there is ulceration with diffuse inflammatory changes, including crypt abscesses. Given the rapid cell turnover of the small intestinal mucosa, it is not surprising that chemotherapeutic agents may cause enteropathy. Acute injury is induced by enhanced apoptotic activity, increased migration of crypt epithelial cells and reduced compensatory mitotic activity leading to a hypoplastic villous atrophy (Figure 20. Chemotherapy-induced enteropathy may be exacerbated by radiotherapy [404] although there is some evidence that vitamin A treatment may lessen the effects of methotrexate enteropathy [405]. The immunosuppressive drug mycophenolate mofetil can also damage the small bowel (as well as all other levels of the gastrointestinal tract). Colchicine toxicity, mainly in patients with renal failure, has been linked to increased numbers of metaphase mitoses, epithelial pseudo-stratification and loss of polarity, and an increase in the proliferation zone as demon- strated by Ki67 staining. In patients with therapeutic levels of colchicine, a villous atrophy/hyperplastic crypt pattern has been described in the jejunum. Mitotic arrest with numerous metaphase mitoses in crypt epithelium is also a characteristic feature of recent taxane chemotherapy. Villous atrophy in the ileum or small intestine with lymphocytic ileo-colitis has been reported with ticlodipine and Cyclo 3 Fort (a veinotonic) [407,408]. Finally, successful chemotherapeutic ablation of primary tumours of the small intestine, notably malignant lymphoma, can induce perforation of the intestine through the necrotic tumour and strictures can develop later [409]. Miscellaneous inflammatory conditions of the small intestine Numerous miscellaneous inflammatory conditions affect the small bowel. Two more general pathological phenomena not uncommonly presenting to the surgical pathologist and providing a taxing differential diagnosis, often requiring clinical, therapeutic and radiological correlation, are ulceration and/or perforation and tissue eosinophilia of the small intestine.
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Genus Streptococcus A large group of Gram-positive cocci distributed widely in humans and animals symptoms 0f yeast infectiion in women cheap aricept 5 mg on-line, mostly forming part of the normal flora medications names order aricept 10mg free shipping, but some species responsible for some major infections medications 7 discount aricept 5 mg with visa. The medically significant streptococci may be divided on the basis of either haemolysis on blood agar (complete haemolysis symptoms 3dpo purchase generic aricept pills, beta; partial haemolysis, alpha; no haemolysis, gamma) or by the presence or absence of a group-specific carbohydrate antigen. Non-suppurative sequelae (acute glomerulonephritis and rheumatic fever) are important complications of both skin and throat infections. In addition to this group-specific polysaccharide, type-specific M and T antigens can be detected for epidemiologic purposes. Pulsed-field gel electrophoresis and other molecular techniques are commonly used for epidemiologic analysis. Oral cephalosporin or vancomycin is an alternative for penicillin-allergic patients. Pathogenesis Treatment and prevention Further details Streptococcus Agalactiae (Group B Streptococci) Characteristics Laboratory identification Gram-positive cocci in chains. Biochemical tests include hippurate hydrolysis (positive), aesculin hydrolysis (negative). Group-specific carbohydrate and commercially available molecular tests for definitive identification. Babies acquire organism from colonized mother at birth or by contact spread between babies in nursery after birth. Screening pregnant women recommended; prophylactic antibiotics may be given to babies (especially premature) of carriers. Group D streptococci include the Streptococcus bovis group and organisms now classified in the genus Enterococcus (see below). Streptococcus Milleri Group Microaerophilic streptococci that often form small colonies (formerly termed Streptococcus milleri) and carry Lancefield Group A, C, F or G antigens. Susceptible to bile (bile solubility test) and Optochin (ethyl hydrocupreine hydrochloride; available in paper disks). They are antigenic and in the presence of specific antiserum appear to swell (quellung reaction). Pneumolysin may have a role as a virulence factor, but to date no known exotoxins. Penicillin remains the antibiotic of choice, but resistance is increasing rapidly, and susceptibility test results should be used to guide therapy. Most strains are susceptible to penicillin; however, moderate to high resistance has also been observed. Moderately resistant isolates may be treated with penicillin plus an aminoglycoside while highly resistant strains require a broad-spectrum cephalosporin or vancomycin. Genus Enterococcus (Faecal Streptococci) Formerly classified in the genus Streptococcus, with which they share many characteristics; there are more than 30 species of enterococci. Characteristics Laboratory identification Gram-positive cocci, cells often in pairs and chains; more ovate appearance than streptococci. Urinary tract infection; endocarditis; infrequent, but severe septicaemia after surgery and in the immunocompromised. Most infections thought to be endogenously acquired, but cross-infection may occur in hospitalized patients. Patients with known heart defects should be given prophylactic antibiotics to prevent endocarditis before dentistry or surgery on gut or urinary tract. Although cell wall structure has similarities to Mycobacterium and Nocardia, the short-chain mycolic acids present do not confer acid-fast staining. This and other pathogens within the genus need to be distinguished from commensal corynebacteria. Species identification is established on the basis of biochemical tests or species-specific sequencing. It is important to demonstrate toxigenicity to confirm diphtheria diagnosis, but non-toxigenic strains may also be associated with disease. Disease is due to production of diphtheria toxin controlled by the tox gene, which is integrated into the bacterial chromosome on a lysogenic phage. When concentration of exogenous inorganic iron (Fe3 +) is very low, exotoxin production is maximal; the selective advantage to the organism is unknown. The mode of action of the toxin is to block protein synthesis of the host cells by inactivating an elongation factor. Antitoxin neutralizes toxin, penicillin kills organisms; antibiotics have little effect since diffusion of toxin is not influenced by inhibition of organisms at local site. Immunization effective in prevention of diphtheria; in areas where immunization rates reach 85%, herd immunity sufficient to protect whole population. Circulating antibody after immunization neutralizes test dose of standardized toxin (Schick test). It produces two toxins, one of which is neutralized by diphtheria antitoxin, the other is similar to that produced by C. It is usually detected by its relative resistance to antibiotics other than glycopeptides such as vancomycin.
The latter autoantibodies are considered by many to be diagnostic of pernicious anaemia [303] treatment norovirus 5mg aricept. In a contested large study of white patients with pernicious anaemia [303] treatment varicose veins order 5mg aricept fast delivery, a trend was showed for gradual disappearance of parietal cell autoantibodies while intrinsic factor autoantibodies became more prevalent [303 medications zolpidem aricept 10mg cheap,309] medicine youtube generic aricept 5 mg mastercard. Clinical symptoms in early stages are nonspecific and no different from other forms of chronic gastritides. Once anaemia develops, symptoms resemble those seen in other anaemias (namely fatigue, pallor and shortness of breath). Late complications of vitamin B12 deficiency include neurological abnormalities such as peripheral neuropathy and subacute combined degeneration of the spinal cord [321,322]. Of note, in the presence of hypochlorhydria or achlorhydria, the absorption of non-haem iron is decreased, leading to concomitant iron deficiency anaemia. Autoimmune gastritis is a corpus-predominant gastritis with severe atrophy of the oxyntic mucosa (see Figure 11. Although most believe that the antrum is uninvolved, there is invariably some antral involvement [323], and this may represent an immune response aimed at the scattered parietal cells located within the junctional mucosa. The histopathological diagnosis in the early stages can be challenging, because biopsies reveal chronic inflammation only primarily in the gastric corpus with minimal atrophy and no metaplasia or endocrine cell hyperplasia [324]. In advanced cases, the degree of inflammation may decrease, with loss of virtually all specialised glands of the upper stomach along with pseudo-pyloric, intestinal and/ or pancreatic metaplasia [253,324,325]. Immunohistochemical studies have demonstrated an absolute increase in T cells and, more notably, B lymphocytes and an increased IgG: IgA ratio of secreting plasma cells [326]. Interestingly, it has been noted that cross-reacting autoantibodies initiated by H. Notably, the prevalence of anti-canalicular and parietal cell antibodies increases significantly with the duration of H. In another study, 2 of 18 children with juvenile autoimmune thyroid disease had elevated parietal cell antibodies, hypergastrinaemia, and negative histology and serology for H. There is a report of a young woman with systemic lupus erythematosus and pernicious anaemia. Thus, it can be inferred that individuals with autoimmunity predisposition may develop spontaneous autoantibodies without H. We recommend taking four biopsies from the antrum and at least six from the body and fundus; these should be spaced equidistantly along the lesser and greater curvatures. If no endocrine tumours (carcinoids) or dysplastic lesions are discovered, screening at periodic intervals is not likely to be required [351]. One exception concerns patients with a history of gastric cancer in a first-degree relative; here we would be inclined to repeat the examinations, as above, every 5 years. In the rare event that a patient is found to have dysplasia, particularly high grade dysplasia, a second endoscopy and more biopsies should be performed to rule out coexisting carcinoma while, ideally, the lesion should be treated with endoscopic mucosal resection. With regard to microcarcinoidosis, follow-up studies of patients show that they tend not to grow, so that, at best, occasional endoscopy is required. Endoscopy and surveillance Severe gastric atrophy may be evident as thinning of the mucosa, with a paucity of the gastric folds at the greater curvature and prominent vessels [344]. If there is extensive intestinal metaplasia, the mucosa may acquire a silvery sheen. However, none of the endoscopic features is sufficiently specific to render the diagnosis without histological confirmation. Patients who develop pernicious anaemia also have a three- to fivefold increased risk for gastric cancer [348,349]. Juvenile forms of pernicious anaemia these rare conditions present in three forms [352]. One, occurring in later childhood and adolescence, is associated with gastric atrophy and appears to correspond to the adult type with an unusually early age of onset. Acid secretion is normal when vitamin B12 is given, although it may be reduced without it. The stomach in other types of megaloblastic anaemia Infestation with Diphyllobothrium latum occurs in Scandinavian countries, producing a megaloblastic anaemia. The gastric mucosa shows varying degrees of atrophic gastritis with superficial inflammation and zones of intestinal metaplasia [356]. Acute haemorrhagic gastritis is associated with multiple mucosal petechiae, acute erosions and ulcers. Acute gastritis may result from the ingestion of corrosives or drugs such as ferrous sulphate; milder forms are seen in patients with uraemia and in the early stages of H. Acute phlegmonous gastritis is a rare disease in which there is suppurative inflammation of the full thickness of the gastric wall. Phlegmonous and emphysematous gastritis Phlegmonous gastritis is an uncommon condition characterised by suppurative bacterial infection of the gastric wall. It primarily affects the submucosa but may spread to all layers of the stomach, resulting in necrosis and gangrene. The latter complication, when unassociated with thrombosis of the major vessels, has sometimes been designated acute necrotising gastritis [359]. Emphysematous gastritis is probably the same disease but associated with gas-forming bacterial organisms [360]. Both phlegmonous and emphysematous gastritis are rare and potentially life threatening [361]. Phlegmonous gastritis was more common in the preantibiotic era [362] but sporadic cases continue to occur and appear to be increasing. The presentation is usually with nausea, vomiting, and upper abdominal pain and tenderness.
