By Y. Emet. Michigan Jewish Institute. 2019.
War 207 0 2 80 66 24 10 3 2 187 Other intentional injuries 12 1 0 3 3 1 1 1 0 10 130 | Global Burden of Disease and Risk Factors | Colin D order 25 mg sumatriptan amex muscle relaxants for tmj. Note: — an estimate of zero; the number zero in a cell indicates a non-zero estimate of less than 500 best 25mg sumatriptan muscle relaxant names. For East Asia and Pacific purchase sumatriptan 25 mg otc spasms nose, Europe and Central Asia order 25 mg sumatriptan mastercard muscle relaxant chlorzoxazone, and Latin America and the Caribbean regions, these figures include late effects of polio cases with onset prior to regional certification of polio eradication in 1994, 2000, and 2002, respectively. Does not include liver cancer and cirrhosis deaths resulting from chronic hepatitis virus infection. This cause category includes “Causes arising in the perinatal period” as defined in the International Classification of Diseases, principally low birthweight, prematurity, birth asphyxia, and birth trauma, and does not include all causes of deaths occurring in the perinatal period. The Burden of Disease and Mortality by Condition: Data, Methods, and Results for 2001 | 131 Table 3B. Communicable, maternal, perinatal, 2,470 535 35 83 153 160 137 135 86 1,324 and nutritional conditions A. Hookworm disease 0 — — 0 0 0 0 0 0 0 Other intestinal infections 1 0 0 0 0 0 0 0 0 0 Other infectious diseases 190 24 3 13 16 11 8 15 12 102 B. Birth asphyxia and birth trauma 158 83 — — — — — — — 83 Other perinatal conditions 152 78 0 — — — — — — 78 E. Iron-deficiency anemia 25 1 0 1 1 2 0 0 0 6 Other nutritional disorders 9 1 0 0 0 0 0 1 1 3 132 | Global Burden of Disease and Risk Factors | Colin D. Leukemia 76 3 5 10 4 7 6 5 2 42 Other malignant neoplasms 104 2 1 1 3 15 15 12 5 54 B. Mental retardation, lead-caused 0 0 0 0 0 0 0 0 0 0 Other neuropsychiatric disorders 50 1 1 2 2 4 5 7 4 26 F. Hearing loss, adult onset — — — — — — — — — — Other sense organ disorders 0 0 0 0 0 0 0 0 0 0 G. Inflammatory heart diseases 81 1 0 1 2 5 7 11 10 36 Other cardiovascular diseases 415 3 2 6 10 25 33 50 49 177 H. Asthma 56 1 1 3 5 8 5 5 2 28 Other respiratory diseases 189 5 1 2 3 8 16 27 32 96 134 | Global Burden of Disease and Risk Factors | Colin D. Appendicitis 6 0 0 0 0 1 0 1 0 3 Other digestive diseases 220 26 2 6 10 16 18 19 13 111 J. Benign prostatic hypertrophy 8 — — — 0 1 2 3 3 8 Other genitourinary system diseases 39 1 0 1 2 3 6 5 3 21 K. Low back pain 0 0 0 0 0 0 0 0 0 0 Other musculoskeletal disorders 15 0 0 0 0 1 1 1 1 5 M. Spina bifida 1 1 0 — — 0 0 — — 1 Other congenital anomalies 52 26 1 1 0 0 0 0 0 30 N. War 14 0 0 5 4 2 1 0 0 13 Other intentional injuries 3 0 0 1 1 0 0 0 0 2 136 | Global Burden of Disease and Risk Factors | Colin D. Note: — an estimate of zero; the number zero in a cell indicates a non-zero estimate of less than 500. These figures include late effects of polio cases with onset prior to regional certification of polio eradication in 1994. Does not include liver cancer and cirrhosis deaths resulting from chronic hepatitis virus infection. This cause category includes “Causes arising in the perinatal period” as defined in the International Classification of Diseases, principally low birthweight, prematurity, birth asphyxia, and birth trauma, and does not include all causes of deaths occurring in the perinatal period. The Burden of Disease and Mortality by Condition: Data, Methods, and Results for 2001 | 137 Table 3B. Communicable, maternal, perinatal, 326 70 4 15 40 42 21 13 7 211 and nutritional conditions A. Hookworm disease 0 — — — — 0 0 0 0 0 Other intestinal infections 0 0 — 0 — — — — 0 0 Other infectious diseases 15 2 0 1 2 1 1 1 0 9 B. Birth asphyxia and birth trauma 17 10 0 0 — 0 — — — 10 Other perinatal conditions 16 10 0 0 0 0 — 0 — 10 E. Iron-deficiency anemia 3 0 0 0 0 0 0 0 0 2 Other nutritional disorders 0 0 0 0 0 0 0 0 0 0 138 | Global Burden of Disease and Risk Factors | Colin D. Leukemia 27 0 1 2 2 3 3 3 1 15 Other malignant neoplasms 123 0 1 3 6 20 22 15 4 71 B. Mental retardation, lead-caused 1 0 0 0 0 0 0 0 0 0 Other neuropsychiatric disorders 17 1 1 2 1 2 1 1 0 10 F. Hearing loss, adult onset — — — — — — — — — — Other sense organ disorders 0 0 0 0 0 0 0 0 0 0 G. Inflammatory heart diseases 67 0 0 2 7 11 8 7 5 40 Other cardiovascular diseases 383 1 0 4 14 20 30 44 50 162 H. Asthma 27 0 0 0 1 3 6 5 2 17 Other respiratory diseases 33 1 0 1 3 4 5 4 2 21 140 | Global Burden of Disease and Risk Factors | Colin D. Appendicitis 1 0 0 0 0 0 0 0 0 1 Other digestive diseases 77 1 0 2 7 10 9 8 3 41 J. Benign prostatic hypertrophy 3 — — 0 0 0 1 1 1 3 Other genitourinary system diseases 14 0 0 0 1 1 2 2 1 7 K. Low back pain 0 0 0 0 0 0 0 0 0 0 Other musculoskeletal disorders 3 0 0 0 0 0 0 0 0 1 M. Spina bifida 1 1 0 0 0 0 0 0 0 1 Other congenital anomalies 12 6 0 0 0 0 0 0 0 7 N. War 17 0 0 7 6 2 1 0 0 16 Other intentional injuries 1 0 0 0 0 0 0 — 0 0 142 | Global Burden of Disease and Risk Factors | Colin D. Note: — an estimate of zero; the number zero in a cell indicates a non-zero estimate of less than 500. These figures include late effects of polio cases with onset prior to regional certification of polio eradication in 2000. Does not include liver cancer and cirrhosis deaths resulting from chronic hepatitis virus infection. This cause category includes “Causes arising in the perinatal period” as defined in the International Classification of Diseases, principally low birthweight, prematurity, birth asphyxia, and birth trauma, and does not include all causes of deaths occurring in the perinatal period. The Burden of Disease and Mortality by Condition: Data, Methods, and Results for 2001 | 143 Table 3B. Communicable, maternal, perinatal, 716 177 8 26 50 37 24 31 38 390 and nutritional conditions A. Hookworm disease 0 — 0 — 0 0 — — — 0 Other intestinal infections 1 0 0 0 0 0 0 0 0 1 Other infectious diseases 87 13 2 4 6 6 5 6 6 48 B. Birth asphyxia and birth trauma 89 51 0 0 0 0 — — — 51 Other perinatal conditions 54 31 0 0 — — — — — 31 E. Iron-deficiency anemia 13 1 0 1 1 1 1 1 1 6 Other nutritional disorders 3 0 0 0 0 0 0 0 0 2 144 | Global Burden of Disease and Risk Factors | Colin D. Leukemia 22 1 2 2 1 2 1 2 1 12 Other malignant neoplasms 82 1 1 2 4 10 10 9 5 43 B. Mental retardation, lead-caused 0 0 0 0 0 0 0 0 0 0 Other neuropsychiatric disorders 23 2 1 2 2 2 2 2 1 13 F.
Because these thin-walled oocysts are easily ruptured order sumatriptan 50mg fast delivery spasms cerebral palsy, their sporozoites remain in the intestine purchase sumatriptan 50 mg fast delivery spasms left side abdomen, reinfecting the same host (Fayer and Ungar order sumatriptan 50 mg overnight delivery muscle relaxant robaxin, 1986) 25mg sumatriptan free shipping spasms in spanish. Cases of human cryptosporidiosis have been reported from more than 50 countries on 6 continents (Benenson, 1997). Occurrence in Man: The first two clinical cases of human cryptosporidiosis were identified in 1976 in two immunodeficient patients. Various surveys have indicated that the oocyst prevalence in feces ranges from 1% to 2% in Europe, 0. However, serologic evidence of past infections has shown positivity rates of 25% to 35% in industrial- ized countries and up to 65% in developing countries. Infection is much more common than the clinical disease and most frequently occurs in children under 2 years of age, contacts of infected individuals, livestock handlers, travelers to developing countries, homosexuals, and, especially, immuno- deficient individuals. Occurrence in Animals: Several species of Cryptosporidium infect both warm- and cold-blooded animals. In all the affected domestic species, very young unweaned animals are more susceptible to the infection and the disease than adults, and calves appear to be most susceptible. The first clinical case of cryptosporidiosis in animals was identified in a calf in 1971. Subsequently, the infection has been found in up to 80% of calves under 1 month of age and up to 62% of apparently healthy adult cattle. The Disease in Man: In individuals with healthy immune systems, cryp- tosporidiosis may be asymptomatic or may occur as a self-limiting disease. The ill- ness is characterized by profuse watery diarrhea that begins explosively one or two weeks after infection and generally lasts 8–20 days, often accompanied by abdomi- nal pain, nausea, vomiting, low-grade fever (under 39°C), and weight loss. In immunodeficient individuals, the symptoms are more severe and may include as many as 71 evacuations per day, with fluid loss of up to 25 liters (Ryan, 1994). Rather than being self-limiting, the disease may persist until the individual’s death. In such patients, the parasite has sometimes been found to invade the respiratory and biliary tracts (Clavel et al. The infection generally appears during the first three weeks of life and affects animals between 3 and 35 days of age. It is difficult to distinguish diarrhea caused by Cryptosporidium from diarrhea caused by other agents. Anderson (1982) reported that in calves aged 1–15 days from 47 herds, only 17 out of 51 were found to be excreting Cryptosporidium oocysts, although all had diarrhea. In horses, swine, and domestic carnivores, the disease has occasionally been reported in very young or immunodefi- cient animals (Barriga, 1997). Source of Infection and Mode of Transmission: The sources of infection for humans are other infected people and infected cattle. There is no solid evidence that other animals are an important source of human infection. These genotypes might represent different species, but unequivocal identification of Cryptosporidium species is difficult. Cross-trans- mission studies have demonstrated that parasites isolated from humans, goat kids, deer, lambs, and calves can infect and cause diarrhea in pigs, lambs, and calves, while they produce an asymptomatic infection in chickens, colts, and laboratory animals (Tzipori, 1983). Isolates from humans and calves have also been transmitted to kids, puppies, cats, mice, and calves (Current, 1983). Cryptosporidium species that infect birds do not infect mammals, and species that infect mammals rarely infect birds. The infection is transmitted through ingestion of foods and water contaminated with fecal matter from an infected individual, direct contact with infected feces, or ingestion of water from sources contaminated by effluents from sewerage systems or cattle farms. Children, childcare workers who change diapers, bed-ridden patients and their caregivers, people who work with cattle, and individuals who engage in anal sex have a high risk of being infected through direct contact with fecal matter. Diagnosis: Diarrhea from Cryptosporidium is hard to distinguish clinically from diarrheal illnesses due to other causes. They are therefore more easily detected by means of techniques involving concentration in sugar solutions, such as Sheather’s solution, and by phase contrast microscopy. Giemsa or methylene blue staining makes the oocysts more visible but also turns yeast contaminants the same color, making it impossible to distinguish them from the parasite. Ziehl-Neelsen stain, on the other hand, turns oocysts red but does not stain yeast. Auramine-rhodamine and safranine-methylene blue are also useful for distinguishing oocysts. A recently developed technique uses fluorescent monoclonal antibodies specific to Cryptosporidium to visualize the parasites in fecal or environmental specimens. The specificity of serologic diagnosis by means of immunofluorescence assay or enzyme-linked immunosorbent assay was initially dubious, but the tests have been refined and now show satisfactory levels of sensitivity and specificity. Although serologic diagnosis is useful for epidemiological studies, the antibodies may appear too late for clinical purposes in immunocompetent patients or may not appear in suf- ficient quantities in immunodeficient patients. Procedures for recovering and identifying Cryptosporidium in environmental waters are highly variable, inefficient, and time-consuming. The currently recom- mended practice involves passing large volumes of water through special filters, centrifuging the material trapped by the filters to concentrate it, purifying the con- centrate in a Percoll-sucrose gradient, staining with fluorescent antibodies, and, finally, examining the material microscopically. Control: For an individual, prevention of cryptosporidiosis consists of avoiding the ingestion of raw foods or water that may be contaminated with human or animal feces and avoiding contact with feces (Juraneck, 1995). Cooking high-risk foods and washing hands carefully before eating should also reduce the danger of infection. People should avoid immersion in water containing effluents from sewerage systems or cattle farms. Exposure to water temperatures of 25°C and 8°C for 4 weeks kills only 50% and 25% of oocysts, respectively (Barriga, 1997). Under favorable conditions, they are probably capable of surviving for several months in nature. Treatment of drinking water in well-run plants with good filters removes around 99. Genetic polymorphism among Cryptosporidium parvum isolates: Evidence of two distinct human transmission cycles. Etiology: Leishmaniasis is caused by flagellate protozoa of the family Trypanosomatidae, genus Leishmania. The flagellate forms of the parasite—oval amastigotes measuring 2 to 5 µm in diameter (see the chapter on Chagas’ Disease)—exist within macrophages of a definitive vertebrate host, including humans. Small flies of the family Phlebotomidae (genus Phlebotomus in the Old World and Lutzomyia in the Americas) ingest the parasites when they feed on the host’s blood. Once in the fly’s intestine, the amastigotes become promastigotes—extracellular forms with a flagel- lum emerging from the anterior end, which are fusiform and measure 14 to 20 µm long and 2 to 4 µm wide. In the insect, two promastigote forms can be observed: a wider, relatively immotile form that attaches to the wall of the intestine, and another, thinner, motile form that moves freely in the insect’s intestinal lumen and proboscis. Once inside the vertebrate, the promastigotes become amastigotes, invade the cutaneous macrophages, and multiply in a parasitophorous vacuole. These parasites are equipped with several adaptation mechanisms that enable them to overcome the lethal effects of macrophages and lysosomes on microorganisms (Antoine, 1995).
About half of the vitamin A activity is derived from animal and half from plant sources buy sumatriptan 50mg on-line xanax muscle relaxant dosage. Preformed vitamin A (retinol) is present in liver safe sumatriptan 25mg muscle relaxant drugs for neck pain, fatty fish purchase 50mg sumatriptan amex spasms eye, dairy products buy generic sumatriptan 50mg online spasms coronary artery, and fortified margarine. Inclusion of fortified dairy products in the diet may be a practical, sustain- able, and cost-effective approach for improving vitamin intake and status in the elderly. A proportion of dietary carotenoids are converted to retinol in the intes- tine and liver. However, recent studies have shown that the basis for describing vitamin A activity of carotenoids overestimates the bioavailability of provitamin A carotenoids and their bio- conversion to retinol (vitamin A). An intake of at least 3 mg vitamin A, along with 130 mg vitamin C and 67 mg vitamin E or more daily, is thought to possibly reduce the risk of cancer. Unlike vitamin A, β-carotene can reduce lipid peroxidation and modulate enzymatic activity of lipoxygenases. However, the immunologic impact of vitamin A is not solely attributable to its carotene precursor. Animal studies do suggest vitamin A and retinoids regulate epithelial cell differentiation and maintenance and inhibit tumor angiogenesis. Vitamin A decreases serum insulin-like growth factor-1, inhibits 5-α-reductase (the enzyme that catalyzes formation of dihydrotestosterone), and up-regulates transforming growth factor-β. Vitamin A has a number of other promising and interesting clinical appli- cations. Retinoids protect gastric mucosa against the ulcerogenic effects of indomethacin treatment without any inhibition of gastric acid secretion. There is a potential for therapeutic supplements of vitamin A in children with insulin-dependent diabetes mellitus to reduce or prevent atherogenic risk. A case-control study found children with poor metabolic control of their type 1 diabetes mellitus were at greater risk of atherosclerosis and relative vitamin A deficiency than those with good metabolic control of their ill- ness. With new, more effective, and less toxic retinoids being developed, there are great expectations for the use of these derivatives, alone or in combina- tion with other drugs. With new delivery systems being developed, it is hoped vitamin A may provide therapeutic solutions to conditions as diverse as benign proliferative skin diseases, such as psoriasis and skin cancer. The relative sever- ity of side effects varies widely between patients and, apart from skeletal and skin changes, most signs and symptoms disappear within 7 days. Hypervitaminosis A is sometimes associated with abnormalities of calcium metabolism and bone mineral status, and a recent study found a negative association between reported dietary vitamin A intake and bone mineral density. A prospective study with 18 years of fol- low-up suggested long-term intake of a diet high in retinol may promote the development of osteoporotic hip fractures in women. While large doses of vitamin K may impair absorption of vitamin A, hyper- vitaminosis A causes hypoprothrombinemia, which can be corrected with vitamin K. Vitamin E may enhance the therapeutic efficacy of vitamin A by protecting against the oxidative destruction of this vitamin. Zinc deficiency impairs vitamin A function, limiting the bioavailability of this vitamin. A random- ized, double-blind, placebo-controlled, intervention trial found combined zinc and vitamin A supplementation improved vitamin A nutriture in vita- min A-deficient children. Vitamin A deficiency also leads to drying of the conjunc- tiva and mucous membranes; a rough dry skin with follicular hyperkeratosis is common. A critical and constructive review of epidemiology and supplementation data regarding cardiovascular disease and cancer, Biofactors 7(1-2):113-74, 1998. Brighthope I: Nutritional medicine tables, J Aust Coll Nutr Env Med 17:20-5, 1998. Breuer-Katschinski B, Nemes K, Marr A, et al: Relation of serum antioxidant vitamins to the risk of colorectal adenoma, Digestion 63(1):43-8, 2001. Primack A: Complementary/alternative therapies in the prevention and treatment of cancer. Majewski S, Kutner A, Jablonska S: Vitamin D analogs in cutaneous malignancies, Curr Pharm Des 6(7):829-38, 2000. Mozsik G, Bodis B, Figler M, et al: Mechanisms of action of retinoids in gastrointestinal mucosal protection in animals, human healthy subjects and patients, Life Sci 69(25-26):3103-12, 2001. Ballew C, Galuska D, Gillespie C: High serum retinyl esters are not associated with reduced bone mineral density in the Third National Health And Nutrition Examination Survey, 1988-1994, J Bone Miner Res 16(12):2306-12, 2001. This water-soluble B vitamin is essential for converting carbohydrate into energy. It works synergistically with other vitamins of the B complex, particularly riboflavin (B2) and niacin (B3). Thiamin is required for synthesis of acetylcholine and is important for neural transmission. Thiamin is best taken with meals, since it is better absorbed in an acidic environment. Treatment in adults is 5 to 10 mg of vita- min B1 three times a day; in children, the dose is 10 mg/day. Severe thiamin deficiency may cause depression, memory problems, weakness, dyspnea, and tachycardia. Early signs of beriberi that are often missed include anorexia, constipation, muscle weakness, paresthesia, and pedal edema. Numbness and tingling attributable to peripheral neuropathy can be relieved by 10 mg vitamin B1 daily. In the heart, this results in impaired contrac- tile strength; in the blood vessels, this results in vasodilatation. The cardiac failure of wet beriberi results from a combination of reduced venous return and impaired cardiac muscle contractility compromising cardiac output. Persistent thiamin deficiency in dry beriberi may cause Korsakoff’s psychosis and Wernicke’s encephalopa- thy. Acute Wernicke-Korsakoff syndrome, a form of amnesia caused by brain damage occurring in long-term alcoholics, is normally reversible with thi- amin but may proceed to profound dementia. Lasix increases urinary excretion of thiamin, and supplementation with 200 mg of thiamin daily may benefit cardiac failure patients on this drug. Brighthope I: Nutritional medicine tables, J Aust Coll Nutr Env Med 17:20-5, 1998. Riboflavin is a water-soluble vitamin of the B group that is important in energy metabolism. Since riboflavin is sensitive to light, it is lost when milk is stored in glass bot- tles, hence the trend to opaque containers. In these forms, riboflavin acts as a catalyst for redox reactions in a large number of energy- producing pathways, including oxidation of glucose, certain amino acids, and fatty acids. It is also involved in the conversion of pyridoxine to its active co-enzyme and is required for tryptophan metabolism. The usual therapeutic dose range is 12 to 200 mg/day; rarely 5000 mg/day is required.
In Asia trusted 25 mg sumatriptan spasms jerking limbs, infections with the human liver ﬂuke Clonorchis sinensis are acquired by eating ﬁsh infected with the metacer- Parasitic infections affecting the liver carial stage cheap sumatriptan 25mg fast delivery ql spasms. Juvenile ﬂukes released in the intestine move up An inﬂammatory response to the eggs of the bile duct and attach to the duct epithelium buy sumatriptan 25 mg on-line spasms down there, feeding on Schistosoma mansoni results in severe liver the cells and blood and tissue ﬂuids purchase sumatriptan 25mg mastercard spasms left side under rib cage. In heavy infections there damage is a pronounced inflammatory response, and proliferation Liver pathology in parasitic infections is most severe in S. There only a relatively short time in the liver before moving to the may be an association with cholangiocarcinoma, but there is mesenteric vessels, eggs released by the females can be swept little evidence for this in humans. These include species of Opisthorchis (in Asia these trapped eggs is the primary cause of the complex and Eastern Europe) and the common liver ﬂuke Fasciola hep- changes that result in hepatomegaly, ﬁbrosis and the forma- atica. Other parasitic Whereas schistosomiasis is widespread in tropical and sub- infections associated with liver pathology are malaria, leishma- tropical regions, other parasitic infections affecting the liver niasis, extraintestinal amebiasis, hydatid disease and ascariasis. In the related Schistosoma haematobium infection, a similar process occurs in the wall of the bladder. Despite its name an amebic liver abscess Mycobacterial infection requires specific antituberculous does not consist of pus therapy (see Chapter 30), while actinomycosis responds well E. However, the term ‘amebic liver abscess’ is not strictly accu- rate because the lesion formed in the liver consists of necrotic Summary liver tissue rather than pus. True liver abscesses – walled-off lesions containing organisms and dead or dying polymorphs The length and complexity of the gastrointestinal tract is (pus) – are frequently polymicrobial, containing a mixed ﬂora matched by the variety of microorganisms that can be of aerobic and anaerobic bacteria (Fig. Lesions caused acquired by this route, causing damage locally or invading to by Echinococcus granulosus in hydatid disease can become sec- cause disseminated disease. The source of infection may of morbidity and mortality in malnourished populations in be local to the lesion or another body site, but is usually the developing world and will only be combatted successfully undiagnosed. Broad spectrum antimicrobial therapy is when there are adequate public health measures. Biliary tract infections Certain infections such as typhoid are initiated in the gas- Infection is a common complication of trointestinal tract, but cause systemic disease, while hepatitis biliary tract disease A is acquired and excreted by the intestinal route. The Although infection is not often the primary cause of disease remaining members of the hepatitis ‘alphabet’ are also dealt in the biliary tract, it is a common complication. Infections result not only from the inges- patients with gallstones obstructing the biliary system tion of pathogens from an external source, but also from the develop infective complications caused by organisms from the normal ﬂora of the gastrointestinal tract if there are acciden- normal gastrointestinal flora such as enterobacteria and tal or manmade breaches of the mucosa as microorganisms anaerobes. Local infection can result in cholangitis and sub- can then ‘escape’ and cause intra-abdominal sepsis. Removing the underly- ing obstruction in the biliary tree is a prerequisite to success- ful therapy. Antibacterial therapy is usually broad-spectrum, covering both aerobes and anaerobes. Peritonitis and intra-abdominal sepsis The peritoneal cavity is normally sterile, but is in constant danger of becoming contaminated by bacteria discharged through perforations in the gut wall arising from trauma (accidental or surgical) or infection. The outcome of peri- toneal contamination depends upon the volume of the inocu- lum (1 ml of gut contents contains many millions of microorganisms), and the ability of the local defenses to wall off and destroy the microorganisms. Peritonitis is usually caused by Bacteroides fragilis mixed with facultative anaerobes Fig. Mycobacterium tuberculosis and Actinomyces can Edematous bowel also cause intraperitoneal infection (Fig. Suitable regimens include a combination of gen- tamicin (for the aerobic Gram-negative rods), ampicillin (for Summary 285 • Diarrheal disease is a major cause of morbidity cause antibiotic-associated diarrhea. A wide • Viral gastroenteritis causes appalling morbidity range of diverse microbes cause infections of the and mortality, especially in young children in gastrointestinal tract. The chief culprits are the symptom, ranges from mild and self-limiting to rotaviruses, which are speciﬁc to humans, severe with consequent dehydration and death. The number of organisms ingested • Ingestion of food or water contaminated with and their virulence attributes are critical factors S. These pathogens invade the gut mucosa and • Microbiologic diagnosis is usually impossible are ingested by, and survive in, macrophages. Other less common causes therapy is required and speciﬁc prevention is include Cl. Important worms cause disease by multiplication in the gut and are Ascaris, Trichuris and the hookworms. Transmission is prevented by good • Parasitic infections involving the liver include hygiene, clean drinking water and hygienic infections by S. Other parasitic infections with enterotoxin, which acts on the gastrointestinal important liver pathology include malaria, mucosal cells. In contrast, Shigella invades the leishmaniasis, extraintestinal amebiasis, mucosa, causing ulceration and bloody diarrhea, hydatid disease and ascariasis. Removal of the bacterium by cause mixed infections, which may extend to combination treatment with antibiotics and produce liver abscesses and septicemia. The gut (usually due to antibiotic treatment) allows presentation is acute and infection can be fatal. What is the most likely diagnosis and what is he feels nauseated, and does not feel like eating, the differential diagnosis of a viral hepatitis in and he has developed right-sided abdominal this setting? Why was ice-cream involved and where did gastroenteritis were reported from Minnesota, the bacteria come from? What actions would you have recommended in caused an estimated total of 2000 cases of illness the ice-cream plant? What would be your immediate management pediatric unit with a two-day history of fever, of this baby? On examination she is unwell, mildly dehydrated, and febrile with a temperature of 38°C. Most nations with a developed understanding of health inequalities accept that health systems sometimes need to take account of differences between population groups in order to achieve fairer outcomes. There is no logical reason why gender differences in health outcome should not be treated in the same way. If this is so obvious, why do our authors - from countries as culturally varied and geographically distant from each other as Malaysia and Denmark, New Zealand and Canada – report similar diffculties in persuading governments to pay particular attention to the health of men? One reason is the one we have just considered - the idea that the problem lies with men them- selves. This may lead to the regrettable political view that it is up to men to change, not services. This is a fallacious argument that fails to acknowledge men’s poorer health as the inequality that it is. Furthermore, as our authors report, cultural pressures and social expectations make help-seeking very diffcult for men all over the world. Some may argue that would be desirable - but the only realistic view to take is that change on that scale is not going to happen in the foreseeable future. Politicians and clinicians may have simply become so used to men dying sooner than women that they have ceased to wonder why it happens. This perception may be reinforced by the fact that – as we have seen – there are some potential biological explanations for some of the differences.
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