By S. Sinikar. Carroll College, Helena, MT.

The Supreme Court concluded then that the circumstances dictate the necessary decision order rabeprazole 20 mg with mastercard, and that in this case order 10 mg rabeprazole visa, the Master should have sought medical attention beyond that which was available aboard the vessel. The case affirmed the historical duty of the ship owner and Master to provide proper medical treatment and attendance for a mariner taken ill or sustaining an injury in the service of the owner’s ship. The court in that case stated: “We cannot say that in every instance where a serious accident occurs the Master is bound to disregard every other consideration and put into the nearest port, though if the accident happened within a reasonable distance of such port, his duty to do so would be manifested. Each case must depend upon its own circumstances, having reverenced to the seriousness of the injury, the care that can be given the sailor on ship board, the proximity of an intermediate port, the consequences of delay to the interests of the ship owner, the direction of the wind and the probability of its continuing in the same direction, and the fact whether a surgeon is likely to be found with competent skill. With reference to putting into port, all that can be demanded of the Master is the exercise of reasonable judgment, and the ordinary acquaintance of a seaman with the geography and resources of the country. He is not absolutely bound to put into such port if their cargo be such as would be seriously injured by the delay. Even the claims of humanity must be weighed in a balance with the loss that would probably occur to the owners of the ship and cargo. A seafaring life is a dangerous one, accidents of this kind are peculiarly liable to occur, and the general principle of law that a person entering a dangerous employment is regarded as assuming the ordinary risks of such employment is peculiarly applicable to the case of seamen. If an incorrect decision is made, the most likely result will be a civil suit against the vessel owner by the injured or ill crew member, a suit which will not involve the vessel’s Master. However, it should be remembered that any decision made regarding deviation or even treatment of a crew member may be scrutinized by the U. Coast Guard against the vessel Master’s license for negligence or inattention to duty. A passenger is one who travels aboard a vessel by way of a contract, express or implied, for some payment of fare or other consideration to 22 the carrier. The standard of care for passengers and all other persons lawfully 23 aboard a vessel has been “reasonable care under the circumstances. Visitors are not passengers but have in fact boarded the vessel with the consent of the owner or operator of the vessel 24 and are thereby entitled to the same standard of care. If a passenger or visitor is injured, it is the duty of the Master to give such care as is reasonably practical given the facilities available on board. If a competent physician happens to be available and is consulted by the Master, following such advice will exonerate the 25 Master. Again, with seriously infirm passengers or crew members, it may be necessary to decide whether or not to deviate to a nonscheduled port to obtain medical attention. The court in Gamble listed a number of factors, which should be considered when assessing the reasonableness of the decision to deviate or not to deviate for the care of passengers. The court stated that: “It is generally established that a vessel is not required to deviate from its course in every instance in order to procure medical assistance for an injured passenger. The role of passengers aboard a vessel differs slightly from that of crewmember in that the passenger is more of a guest aboard the vessel rather than a functional member of the crew, thus courtesy and kindness afforded to them are consideration in respect to care. A stowaway is owed no greater duty than whatever constitutes “humane 26 treatment”. Though a stowaway will not succeed in a cause based on negligence, one could 22 The Vueltabajo, 163 Fed. It is clearly the duty of the Master to give assistance to strangers rescued at sea and this is one area in particular where the owner is not held accountable if the Master neglects this duty. The Master must, if he or she can do so without causing serious risk to vessel, crew, or passengers, render assistance to every person who is found at sea in danger of being lost: and if he or she fails to do so, shall, upon conviction, be liable to a penalty of not exceeding $1,000, or imprisonment for a term not 27 exceeding 2 years, or both. In one case, the court exonerated the vessel’s owner for its Master’s failure to 28 give aid to strangers. The court noted that the International Salvage Treaty of 1910, which specifically holds the Master liable for failure to give such aid, was adopted by the United States (which was an original signatory to the treaty, and passed by the Congress as 46 U. Although the Master was not involved in the Warshaeur case, the court, implied that the Master could be held civilly liable for damages for failure to give aid, as well as criminally liable under the statute. As a medical matter, humanitarian aid should be provided to such persons, protecting the vessel’s own crew appropriately from the possibility of unknown communicable diseases. The legal consequences and exposure to liability by rendering humanitarian aid are few. The taking aboard of shipwrecked or persons fleeing political oppression raises legal issues better dealt with after the successful rescue and rendering of aid to such distressed persons. The humanitarian care and safety of human life should be addressed first, and political or legal issues dealt with thereafter. Two other parties often allowed aboard ship who are not exactly the responsibility of the Master are longshoreman and scientific personnel. When a longshoreman is injured aboard a merchant vessel, the vessel is usually tied up at pier side. Responsibility is shifted in large part to the longshoreman’s hatch boss, ship foreman, or even to the vessel’s port captain and pier personnel. Of course if first aid can be rendered or aid given by personnel within the Master’s control, then such should be done immediately. This is because such personnel are usually employed by a separate institution, university, or company. Though not eligible for Jones Act protection, the general maritime law does protect scientific personnel, and claims for unseaworthiness can be brought. The application of law to oil rigs is dependent upon whether the rig is fixed or floating. A fixed rig is deemed an artificial island, and is not generally subject to the precepts of general maritime law, which is not to say a vessel servicing such a platform is not. An interesting legal situation may occur when a vessel’s Master is faced with a crewmember whom he suspects may be mentally ill or suffering from delirium tremens, and presents as a danger to himself or herself and perhaps to other crewmembers. Coast Guard has instituted licensing proceedings against Masters who failed to safeguard mentally infirm crewmembers. The necessity for placing the infirm crewmember under restraint, as well as the form and extent of restraint used, have been closely examined by the Coast Guard. Coast Guard was faced with a situation wherein a Master was charged for failure to adequately guard a mentally infirm crewmember. In that case, the crewmember had exhibited symptoms of mental infirmity and had actually jumped overboard at one point.

Meydani M: Effect of functional food ingredients: vitamin E modulation of cardiovascular diseases and immune status in the elderly generic rabeprazole 20mg visa, Am J Clin Nutr 71(6 Suppl):1665S-8S buy rabeprazole 10mg overnight delivery, 2000. Brighthope I: Nutritional medicine tables, J Aust Coll Nutr Env Med 17:20-5, 1998. 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—Its presence and power, J Aust Coll Nutr Env Med 17:5-18, 1998. Meydani M, Meisler J: A closer look at vitamin E: can this antioxidant prevent chronic disease, Postgrad Med 102(2):199-207, 1997. Primack A: Complementary/Alternative therapies in the prevention and treatment of cancer. Vitamin K is a fat-soluble vitamin obtained from bacteria in the bowel and from dietary sources such as liver, leafy green vegetables, and milk. Die- tary vitamin K includes phylloquinone (vitamin K1) and menaquinone (vitamin K2). Vitamin K is a trace nutrient necessary for the synthesis of four plasma clotting factors, two anticlotting factors (protein C and protein S), and the synthesis of two bone proteins (osteocalcin and matrix Gla-protein). Vitamin K is not only involved in the synthesis of clotting factors but it also contributes to the synthesis of proteins that prevent clotting. Case series have reported reduced plasma concentrations of protein S in patients with arterial thromboses, and other studies have reported increased levels in patients with coronary heart disease. A prospective survey found a one standard deviation increase in free protein S was associated with a hazard risk of 1. Matrix Gla-protein also requires vitamin K for its synthesis in the smooth muscle cells of healthy vessel walls. In addition to its effect on coagulation and the vasculature, vitamin K1 has a potentially important role in cell signaling. Growing evidence suggests that most normal and tumor cells possess an active K1-dependent gamma-carboxylation mechanism necessary for the production of gamma-carboxyglutamic acid-containing proteins. Gamma-carboxyglutamic acid residues in proteins facilitate calcium- dependent protein/phospholipid interaction. These observations provide an explanation for the rigid control of vitamin K1 levels in the mammalian fetus and its minimal hepatic stores in the adult. Vitamin K2 is used in the treatment of osteoporosis, and laboratory studies suggest that vitamin K2 inhibits apoptotic cell death of osteoblasts and maintains the number of osteoblasts. A prospective study found low vitamin K intakes were associated with an increased incidence of hip fractures in eld- erly men and women; however, neither low vitamin K intake nor E4 allele status, postulated to affect vitamin K transport, was associated with low bone mineral density. Results of a preliminary study examining serum bone markers and ultrasound veloc- ity support the hypothesis that carboxylation of osteocalcin is related to bone quality. Weight for weight, kale, spinach, soybeans, broccoli, and cabbage are the best sources. One hundred grams of kale have 700 μg of vitamin K, compared with the 100 μg found in 100 g of cabbage. This can be pre- vented by an injection of vitamin K to enable them to synthesize coagulation factors while their intestine is being colonized by bacteria capable of vitamin K synthesis. One dose of vitamin K (1 mg imi) reduces clinical bleeding at 1 to 7 days, including bleeding after circumcision, and improves biochemical indices of coagulation status in neonates. A review of clinical trials concluded that vitamin K administered to women before the birth failed to significantly pre- vent periventricular hemorrhages in preterm infants. A multicenter, double- blind, placebo-controlled, randomized trial found low dose oral vitamin K more effective than placebo in restoring blood coagulation to the therapeu- tic range in overanticoagulated patients receiving warfarin. Results from a 24-month randomized, open study of osteo- porotic patients suggested that vitamin K2 (45 mg daily) effectively pre- vented the occurrence of new fractures, despite any increase in lumbar bone mineral density being detected. A randomized study of post- menopausal women found that daily supplementation with 80 μg vitamin K1 seemed necessary to reach premenopausal percentage carboxylated osteo- calcin levels. Furthermore, heparin inhibits lipoprotein-mediated carriage of vitamin K and possibly other lipids to bone and may explain heparin-induced osteoporosis. A constant dietary intake of vitamin K that meets current dietary recom- mendations of 65 to 80 μg/day is the most acceptable practice for patients on warfarin therapy. In addition to patients on warfarin being wary of green leafy vegetables and certain plant oils, they may also need to avoid prepared foods containing these plant oils, ranging from baked goods to margarine and salad dressings. In fact, it is possible that the population may be mildly deficient in vitamin K and in older adults, this may contribute to increased bone fracture risk, arterial cal- cification, and cardiovascular disease. Shirakawa Y, Shirahata A, Fukuda M: Differences in reactivity to vitamin K administration of the vitamin K-dependent procoagulant factors, protein C and S, and osteocalcin, Semin Thromb Hemost 26:119-262, 2000. Urayama S, Kawakami A, Nakashima T, et al: Effect of vitamin K2 on osteoblast apoptosis: vitamin K2 inhibits apoptotic cell death of human osteoblasts induced by Fas, proteasome inhibitor, etoposide, and starosporine, J Lab Clin Med 136: 181-93, 2000. Sakagami H, Satoh K, Hakeda Y, et al: Apoptosis-inducing activity of vitamin C and vitamin K, Cell Mol Biol 46:129-43, 2000. Sugiyama T, Kawai S: Carboxylation of osteocalcin may be related to bone quality: a possible mechanism of bone fracture prevention by vitamin K, J Bone Miner Metab 19:146-9, 2001. Brighthope I: Nutritional medicine tables, J Aust Coll Nutr Env Med 17:20-5, 1998. Shiraki M, Shiraki Y, Aoki C, et al: Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis, J Bone Miner Res 15:515-21, 2000. The leaves and bark of this shrub are a popular remedy for minimizing bruising and reducing painful swelling. It has traditionally been used to treat hemorrhoids, varicose veins, bruises, and minor skin damage. Witch hazel is available over-the-counter and is used as an astringent for relief of minor skin or anorectal irritation. A number of the tannins are potent inhibitors of 5-lipoxygenase and consequently leukotriene production. It is also used to treat mild skin inflammation5 and may be included in suntan lotions. A double-blind, randomized trial lasting 14 days in patients with moderately severe atopic eczema found cream with 5. On the other hand, a study using healthy volunteers found the antiinflammatory action of aftersun lotion with 10% hamamelis superior to a number of other aftersun formulations. Although no significant side effects are anticipated, ingestion of witch hazel may cause gastric irrita- tion in susceptible individuals.

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Currently cheap rabeprazole 20mg online, African trypanosomiasis in man is endemic in 36 African countries south of the Sahara; the two forms of the disease together pose a risk for approximately 50 million people; and about 25 buy generic rabeprazole 20mg,000 new cases are being reported annually, with the likelihood that not all cases were being notified (Bales, 1991; Kusoe, 1993). Gambiense trypanosomiasis, which is chronic, tends to occur in epidemics, whereas rhodesiense trypanosomiasis, which has a more acute course, occurs spo- radically, and gives rise to far fewer epidemics. The latter infection is endemic among livestock-raising tribes in eastern Africa and frequently affects hunters, fish- ermen, and travelers. Overall incidence is rather low because the people avoid areas infested by the vector. The Disease in Man: The human disease usually has three phases: the primary lesion, parasitemia, and invasion of the central nervous system. Two or three days after the bite of an infected fly, a painful inflammation (chancre) appears at the inoc- ulation site, and it disappears after two to three weeks (McGovern et al. From the chancre site, the trypanosomes invade the bloodstream, and the patient suffers from irregular and intermittent fever, mirroring the waves of parasitemia. Other signs during this acute period are painless adenopathies, especially in the posterior cervical lymph nodes, as well as edema of the eyelids and joints. The most common symptoms of the acute phase are cepha- lalgia, insomnia, arthralgia, weight loss, and generalized erythema and pruritus, par- ticularly in the sternal region. In later stages of the disease, the symptomatology is related to the affected organ. Invasion of the central nervous system is common, and a large variety of psychological, motor, and sensory perturbations may be seen. Following the meningitis that develops early in the course of the infection, a rupture occurs in the choroid plexus which allows the parasites to invade sites in the brain. The result is encephalitis, consisting of generalized inflammation with perivascular infiltrations of B and T lymphocytes, plasmocytes, and macrophages. The blood- brain barrier becomes permeable, and this condition may give rise to vasogenic cere- bral edema. Astrocytes and microglia are activated, and, together with immune cells, they begin to produce cytokines, which also contribute to progression of the disease (Pentreath et al. There is irritability, paresthesia, and insomnia, and later on, cerebral edema can cause severe headaches and edema of the optic papillae. There can also be neurologic manifestations such as epileptic seizures, chorea, psychotic episodes, euphoria, somnolence, lethargy, and coma. Weeks or months may elapse between the first and second phase, and months or years may elapse between the second and third phase. Rhodesiense trypanosomiasis has a more acute course and its phases are less marked; death may come within a few months, in contrast to patients with T. Both forms of African trypanosomiasis severely alter the patient’s immune sys- tem. The main characteristics are synthesis of large amounts of gamma globulin, autoantibody formation, and immunodeficiency (Vincendeau et al. Some parasites, however, manage to express another of the more than 1,000 genes coded for this antigen and are covered with a different glycoprotein, thereby initiating a new wave of parasitemia. The succession of new antigens is a powerful stimu- lus for the immune response, which participates in both the defense and the pathol- ogy of the disease. Although there is epidemiologic evidence of protective immunity in gambiense trypanosomiasis (Khonde et al. In terms of immunopathology, there is no evidence that high gamma globulin levels or an abun- dance of immune complexes play an important role in pathology of the human dis- ease. Nevertheless, there is experimental evidence suggesting that autoantibodies to components of the central nervous system, such as anti-galactocerebrosides and tryptophan anti-analogous antibodies, may play a part in the development of encephalitis (Hunter et al. The Disease in Animals: Infections caused by African trypanosomes in animals have a variety of local names, but they are most often referred to as nagana. It causes an important disease in camels, equines, cats, dogs, and small ruminants. The dis- ease is chronic and occasionally fatal in cattle; it is rarely fatal in swine. The primary symptoms in animals are lymphadenopathy, intermittent fever, anemia, and progressive emaciation (Urquhart, 1980). Depending on the species, the age of the host, and the parasite load, the dis- ease may be acute or chronic. Trypanosomiasis in animals has played a role in configuring African societies: awareness of the parasite’s fatal effect on horses protected the original inhabitants from foreign invasions, while its effect on cattle has prevented ranchers from taking advantage of 7 million km2 of pastureland to raise high-yield European cattle. Another form of trypanosomiasis that occurs both in Africa and outside the conti- nent is caused by T. It is transmitted by tabanid flies and is especially path- ogenic for camels, equines, and dogs. Because the infection is pro- longed and includes intervals between febrile attacks during which the patient feels relatively well, affected individuals may move about and propagate the infection in new areas where the vectors exist. The success of control programs aimed exclusively at eliminat- ing the human parasite would indicate that animal reservoirs are not important in gambiense trypanosomiasis. Nevertheless, the presence of animal reservoirs could account for maintenance of the T. These species belong to the palpalis,or riverine, group of flies, which inhabit dense vegetation along the shores of rivers and lakes. Human infection occurs almost always in the vicinity of watercourses or places where water pools in rural settings; tourists are rarely affected. The male and female tsetse flies are biological vectors, but they can transmit the infection mechan- ically during epidemics, when there are many patients with parasitemia. In addition, according to some reports, con- genital transmission can occur in man. By contrast, in the case of rhodesiense trypanosomiasis, lower animals, especially cattle, play an important role as reservoirs. These animals are responsible for persistence of the parasite in areas that have not been inhabited by humans for years. These species belong to the morsitans group of flies, which inhabit savannahs and forested areas and prefer to feed on cattle and wild animals.

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Infections are acquired by consumption of contami- nated food buy cheap rabeprazole 10mg online, especially poultry buy rabeprazole 10mg overnight delivery, milk or water. Recent studies have shown an association between infection and consumption of milk from bottles with tops that have been 260 Gastrointestinal Tract Infections The clinical presentation is indistinguishable from diarrhea Cholera flourishes in communities with caused by salmonellae although the disease may have a longer inadequate clean drinking water and sewage incubation period and a longer duration. The 1990s have witnessed the seventh pandemic of cholera spreading into Latin America, and the disease remains Cultures for campylobacter should be set up endemic in South East Asia and parts of Africa and South routinely in every investigation of a diarrheal America. Asymptomatic human carriers are tant to note that the media and conditions for growth differ believed to be a major reservoir. Growth is often contaminated food; shellfish grown in fresh and estuarine somewhat slow compared with that of the Enterobacteria, waters have also been implicated. Direct person to person but a presumptive identification should be available within spread is thought to be uncommon. Cases still occur in developed countries, but high campylobacter diarrhea standards of hygiene mean that secondary spread should Erythromycin is the antibiotic of choice for cases of diarrheal not occur. Over the past 20 years there have been 66 cases disease that are severe enough to warrant treatment. Serotype O1 is the most important and is further divided into two biotypes: classical and El Tor (Fig. The El Cholera Tor biotype, named after the quarantine camp where it was Cholera is an acute infection of the gastrointestinal tract first isolated from pilgrims returning from Mecca, differs caused by the comma-shaped Gram-negative bacterium V. The disease has a long history charac- causes only a mild diarrhea and has a higher ratio of carriers terized by epidemics and pandemics. The El introduction of the bacterium by sailors arriving from Tor biotype, which was responsible for the seventh pandemic, Europe, and in 1849 Snow published his historic essay On has now spread throughout the world and has largely dis- the Mode of Communication of Cholera. The originated from the El Tor O1 biotype when the latter methods are given in the Appendix. This provided the recipient strain with a selective advantage in a region where a large part of the population is immune to O1 strains. The symptoms of cholera are caused by an enterotoxin sensitive to stomach acid large dose needed to cause The symptoms of cholera are entirely due to the produc- disease unless patient tion of an enterotoxin in the gastrointestinal tract (see achlorhydric or taking antacids Chapter 12). However, the organism requires additional virulence factors to enable it to survive the host defenses and adhere to the intestinal mucosa. The severe watery non-bloody diarrhea is known as production of mucinase rice water stool because of its appearance (Fig. It is this specific receptors fluid loss and the consequent electrolyte imbalance that results in marked dehydration, metabolic acidosis (loss of massive loss of fluid bicarbonate), hypokalemia (potassium loss) and hypovolemic and electrolytes (no damage to toxin production shock resulting in cardiac failure. Untreated, the mortality enterocytes; no blood or from cholera is 40–60%; rapidly instituted fluid and elec- white blood cells in stool) trolyte replacement reduces the mortality to less than 1%. When associated with severe malnutrition it may precipitate complications such as the protein deficiency syndrome ‘kwashiorkor’. Shigellae appear to be able to initiate infection from a small infective dose (10–100 organisms) and there- fore spread is easy in situations where sanitation or personal Fig. Shigella diarrhea is usually watery at first, but later contains mucus and blood Prompt rehydration with fluids and Shigellae attach to, and invade, the mucosal epithelium of electrolytes is central to the treatment of the distal ileum and colon, causing inflammation and ulcera- cholera tion (Fig. However, they rarely invade through the Oral or intravenous rehydration may be used. Enterotoxin is produced, but not necessary, but tetracycline may be given as some evidence its role in pathogenesis is uncertain since toxin-negative indicates that this reduces the time of excretion of V. There have, how- The main features of shigella infection are summarized in ever, been reports of tetracycline-resistant V. Lower abdominal cramps can be As with other diarrheal disease, a clean drinking water severe. The disease is usually self-limiting, but dehydration supply and adequate sewage disposal are fundamental to the can occur, especially in the young and elderly. As there is no animal reservoir, it can be associated with malnutrition (see above). However, carriage in humans, albeit for only a few weeks, Antibiotics should only be given for severe occurs in 1–20% of previously infected patients making erad- shigella diarrhea ication difficult to achieve. I Shigellosis Symptoms of Shigella infection range from mild to severe depending upon the infecting species Shigellosis is also known as bacillary dysentery (in contrast to amebic dysentery; see below) because in its more severe M E form it is characterized by an invasive infection of the mucosa Fig. Histology of the colon showing disrupted of the large intestine causing inflammation and resulting in epithelium covered by pseudomembrane and interstitial the presence of pus and blood in the diarrheal stool. Mucin glands have discharged their contents and the However, symptoms range from mild to severe depending goblet cells are empty. Two Gram-positive species are important causes of tions are most often food-associated, whereas cholera is diarrheal disease, particularly in association with spore-con- more often waterborne and shigellosis is usually spread by taminated food. The mechanism of after the consumption of contaminated meat by people pathogenesis is still unclear. Most strains associated with who are unaccustomed to a high protein diet and do not infection are hemolytic due to production of a heat-stable have sufficient intestinal trypsin to destroy the toxin. It is cytotoxin and have been shown to invade intestinal cells (in traditionally associated with the orgiastic pig feasts contrast to V. The clinical features of infection are summarized in The clinical features of the common type of infection are Figure 20. As the special media for cultivating vibrios are The organism is an anaerobe and grows readily on routine not used routinely, the request form accompanying the laboratory media. Enterotoxin production can be demon- specimen must provide adequate information about the strated by a latex agglutination method. Yersinia enterocolitica is a member of the Enterobacteriaceae and is a cause of food-associated infec- tion, particularly in colder parts of the world. The reason for this geographic distribution is unknown, but it has been speculated that it is because the organism prefers to grow at temperatures of 22–25°C. The organism survives and multiplies, albeit more slowly, at refrigeration temperatures (4°C) and has been implicated in outbreaks of infection associated with contaminated milk as well as other foods. The mechanism of pathogenesis is unknown, but the clinical features of the disease result from invasion of the terminal ileum, necrosis in Peyer’s patches and an associ- ated inflammation of the mesenteric lymph nodes (Fig.

The measles epidemic in Figure 4 lasted for about nine months generic 10 mg rabeprazole free shipping, but because the latent period for influenza is only one to three days and the infectious period is only two to three days rabeprazole 20mg sale, an influenza epidemic can sweep through a city in less than six weeks. To prove the theorem, observe that the solution paths i(t)+s(t) − [ln s(t)]/σ = io + so − [ln so]/σ in Figure 2 are found from the quotient differential equation di/ds = −1+1/(σs). The equilibrium points along the s axis are neutrally unstable for s>1/σ and are neutrally stable for s<1/σ. One classic approximation derived in [18] is that for small io and so slightly greater than smax =1/σ, the difference smax − s(∞) is about equal to so − smax, so the final susceptible fraction is about as far below the susceptible fraction smax (the s value where the infective fraction is a maximum) as the initial susceptible fraction was above it (see Figure 2). Observe that the threshold result here involves the initial replacement number σso and does not involve the basic reproduction number R0. Here the contact number σ remains equal to the basic reproduction number R0 for all time, because no new classes of susceptibles or infectives occur after the invasion. For this model the threshold quantity is given by R0 = σ = β/(γ + µ), which is the contact rate β times the average death-adjusted infectious period 1/(γ + µ). Ifσ ≤ 1 or io =0, then solution paths starting in T approach the disease-free equilibrium given by s =1and i =0. Ifσ>1, then all solution paths with io > 0 approach the endemic equilibrium given by se =1/σ and ie = µ(σ − 1)/β. If R0 = σ ≤ 1, then the replacement number σs is less than 1 when io > 0, so that the infec- tives decrease to zero. Although the speeds of movement along the paths are not apparent from Figure 5, the infective fraction decreases rapidly to very near zero, and then over 100 or more years, the recovered people slowly die off and the birth process slowly increases the susceptibles, until eventually everyone is susceptible at the disease-free equilibrium with s = 1 and i =0. IfR0 = σ>1, io is small, and so is large with σso > 1, then s(t) decreases and i(t) increases up to a peak and then decreases, just as it would for an epidemic (compare Figure 6 with Fig- ure 2). However, after the infective fraction has decreased to a low level, the slow processes of the deaths of recovered people and the births of new susceptibles grad- ually (over about 10 or 20 years) increase the susceptible fraction until σs(t) is large enough that another smaller epidemic occurs. This process of alternating rapid epi- demics and slow regeneration of susceptibles continues as the paths approach the en- demic equilibrium given in the theorem. At this endemic equilibrium the replacement number σse is 1, which is plausible since if the replacement number were greater than or less than 1, the infective fraction i(t) would be increasing or decreasing, respectively. Notice that the ie coordinate of the endemic equilibrium is negative for σ<1, coincides with the disease-free equilibrium value of zero at σ = 1, and becomes positive for σ>1. This equilibrium given by se =1/σ and ie = µ(σ − 1)/β is unstable for σ<1 and is locally asymptotically stable for σ>1, while the disease-free equilibrium given by s = 1 and i =0is locally stable for σ<1 and unstable for σ>1. Thus these two equilibria exchange stabilities as the endemic equilibrium moves through the disease-free equilibrium when σ = 1 and becomes a distinct, epidemiologically feasible, locally asymptotically stable equilibrium when σ>1. The following interpretation of the results in the theorem and paragraph above is one reason why the basic reproduction number R0 has become widely used in the epidemiology literature. If the basic reproduction number R0 (which is always equal to the contact number σ when the entire population is susceptible) is less than 1, then the disease-free equilibrium is locally asymptotically stable and the disease cannot “invade” the population. But if R0 > 1, then the disease-free equilibrium is unstable with a repulsive direction into the positive si quadrant, so the disease can “invade” in the sense that any path starting with a small positive io moves into the positive si quadrant where the disease persists. The latter condition is used to obtain expressions for R0 in age-structured models in sections 5 and 6. This unrealistically short average lifetime has been chosen so that the endemic equilibrium is clearly above the horizontal axis and the spiraling into the endemic equilibrium can be seen. They unrealistically assume that the population is uniform and homoge- neously mixing, whereas it is known that mixing depends on many factors including age (children usually have more adequate contacts per day than adults). Moreover, different geographic and social-economic groups have different contact rates. By using data on the susceptible fractions so and s∞ at the beginning and end of epidemics, this formula can be used to estimate contact numbers for specific diseases [100]. Using blood samples from freshmen at Yale University [75], the fractions susceptible to rubella at the beginning and end of the freshman year were found to be 0. For the 1957 “Asian Flu” (H2N2 type A strain of influenza) in Melbourne, Australia, the fractions so = 1 and s∞ =0. This approach is somewhat naive, because the average seropositivity in a population decreases to zero as the initial passive immunity declines and then increases as people age and are exposed to infectives. The incidence rate at the endemic equilibrium is βiese, so that βie is the incidence rate constant, which with exponential waiting time implies that the average age of infection (the mean waiting time in S) is A =1/βie =1/[µ(σ − 1)]. Data on average ages of infection and average lifetimes in developed countries have been used to estimate basic reproduction numbers R0 for some viral diseases. These estimates of R0 are about 16 for measles, 11 for varicella (chickenpox), 12 for mumps, 7 for rubella, and 5 for poliomyelitis and smallpox [12, p. Because disease-acquired immunity is only temporary for bacterial diseases such as pertussis (whooping cough) and diphtheria, the formula R0 = σ =1+L/A cannot be used to estimate R0 for these diseases (see section 8 for estimates of R0 and σ for pertussis). Herd immunity occurs for a disease if enough people have disease-acquired or vaccination-acquired immunity, so that the introduction of one infective into the pop- ulation does not cause an invasion of the disease. Intuitively, if the contact number is σ, so that the typical infective has adequate contacts with σ people during the infectious period, then the replacement number σs must be less than 1 so that the disease does not spread. This means that s must be less than 1/σ, so the immune fraction r must satisfy r>1 − 1/σ =1− 1/R0. Using the estimates above for R0, the minimum immune fractions for herd im- munity are 0. Although these values give only crude, ballpark estimates for the vaccination-acquired immunity level in a community required for herd immunity, they are useful for comparing diseases. For example, these numbers suggest that it should be easier to achieve herd immunity for poliomyelitis and smallpox than for measles, mumps, and rubella. This conclusion is justified by the actual effectiveness of vaccina- tion programs in reducing, locally eliminating, and eradicating these diseases (eradi- cation means elimination throughout the world). The information in the next section verifies that smallpox has been eradicated worldwide and polio should be eradicated worldwide within a few years, while the diseases of rubella and measles still persist at low levels in the United States and at higher levels in many other countries. For centuries the process of variolation with material from smallpox pustules was used in Africa, China, and India before arriving in Europe and the Americas in the 18th century. Edward Jenner, an English country doctor, observed over 25 years that milkmaids who had been infected with cowpox did not get smallpox. In 1796 he started vaccinating people with cowpox to protect them against smallpox [168]. Two years later, the findings of the first vaccine trials were published, and by the early 1800s, the smallpox vaccine was widely available. Smallpox vaccination was used in many countries in the 19th century, but smallpox remained endemic.

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Environmental investigation should be undertaken to identify system failures in vaccine distribution purchase rabeprazole 10 mg without a prescription. These may represent a failure of the ‘cold-chain’ to keep the vaccine within a defined temperature range 10 mg rabeprazole with mastercard. Environmental investigation of specific outbreak types: summary The following table summarises the typical components of environmental investigation of specific outbreak types. Laboratory investigation Laboratory techniques for identifying and quantifying organisms and toxins have always had an important role in disease outbreak investigation, mainly for identifying or confirming links between suspected contaminated substances and human illness. Recent developments in laboratory techniques mean that laboratory sciences can greatly improve the sensitivity of outbreak detection by identifying clusters of cases with a common source. As this manual is primarily directed towards personnel involved in responding to outbreaks in the field, this chapter does not attempt to describe laboratory testing processes in detail. Instead, the emphasis has been placed on the interface between laboratory investigation and field outbreak investigation personnel. Table 9 indicates the precise role of laboratory investigation in different types of outbreaks. The earlier in the episode such investigations are done the more useful the results would be. Further characterisation of the organism by a reference laboratory is usually necessary for an epidemiological investigation. Table 9: Role of laboratory investigation in different outbreak types Outbreak type Role of laboratory investigation Common event Laboratory investigation has an important role in the overall investigation of common event outbreaks. Laboratory investigation is important in confirming diagnoses, indicating possible sources and testing environmental specimens. This includes testing of clinical specimens from humans and animals as well as from food, water and the environment Common site Laboratory investigation of common site outbreaks contributes to the identification of links between cases, confirming diagnoses, indicating sources and testing specimens Dispersed Laboratory investigation of dispersed outbreaks has a particularly important role in identifying links between dispersed cases, as well as eventual testing of sources, once identified Community-wide Laboratory investigation of community-wide outbreaks is important in identifying links between cases Institutional Laboratory investigation has an important role in the overall investigation of institutional outbreaks. Laboratory involvement: overview of potential roles and services Laboratory scientists make a number of significant contributions to disease outbreak management. Provision of general microbiological and toxicological advice Advising on the range of plausible organisms and toxins involved in an outbreak to help focus the epidemiological and environmental components of the investigation. Outbreak identification On-going surveillance of notifiable and non-notifiable organisms, thereby providing an early warning about emerging groups of cases potentially with a common source. Outbreak description and investigation Identification or confirmation of the pathogen or toxin causing illness. Consult the laboratory early Contact the laboratory as soon as the need for outbreak investigation is suspected. Identify a contact person and deputy for on-going consultation, so that continuity throughout the outbreak investigation and response is maintained. Initial discussions should include defining the laboratory’s contribution, and should extend to inviting a laboratory representative to join the outbreak team. At this time, investigators should request the laboratory to save any relevant specimens from diagnostic testing work (before they are thrown out) and/or to refer these for additional testing. Establish appropriate laboratory testing With the guidance of the laboratory, decide what pathogens or toxins should be tested for and by what method(s), and therefore what type(s) of specimens are required. When assessing quantity, it may be more feasible in some investigations to test a selected sample of cases rather than everyone. It is a good idea to have an estimate of the turnaround time for testing and when results will become available. Timely follow-up of these results and their interpretation by the laboratory is important, and it may be necessary to discuss additional testing. Specimen collection, storage and transport Make plans for specimen collection, storage, transport, receipt and testing as clearly and as early as possible. These plans should be detailed – what, how, who, where, when – and co-ordinated with all involved. The laboratory should always be consulted about specific requirements, including transport and temperature. Equipment such as special containers and processing reagents may need to be organised, especially if chemical toxin testing is planned. Collection Specimen collection kits should be already assembled in preparation for an outbreak, as part of the outbreak plan. They should be portable and have equipment for a range of situations and specimens. General Sterile spoons, spatulas and gloves Method for surface sterilisation (e. Food, water and environmental specimens Containers for food, water and environmental specimens Sterile plastic bags or unopened containers for food, fluids and environmental material (e. Collection of clinical specimens Where specimens are collected from people, informed consent in writing must be obtained. This includes adequate explanation of the reasons for testing, the process involved and clear instructions for any self-collection (e. For serological testing, paired sera are commonly needed; therefore a second (convalescent) specimen may be required some four-to-six weeks after the first (acute) specimen. Identification details written on specimens and laboratory request forms must be legible and as comprehensive as possible. Providing additional information about the case and investigation on the request form is also important as it assists those performing the tests. For example, for diarrhoeal specimens the suspect food source, incubation period, symptoms and a history of recent overseas travel should be recorded. Adequate precautions must be taken when collecting clinical specimens to protect the collector from the transmission of hazardous agents. These include standard precautions such as wearing gloves, gowns and masks where appropriate, and taking necessary care during collection of the specimens themselves. Storage and transport After collection, the two key aims of storage and transport are to keep the specimens viable and to minimise contamination. For transportation outside of the laboratory environment, an overnight courier or faster means should be employed, using chiller pads and insulated containers to keep the specimens cool. These instructions could include (for faecal specimens): collect the faecal sample in the pottle supplied wash hands place pottle in the supplied biohazard bag place bag in a cool area out of direct sunlight while awaiting collection. Background Organism typing refers to a variety of processes that describe detailed characteristics of microorganisms of the same species, thereby allowing further subdivision into different organism types or subtypes.

A glossary of terms that explains what terms • manifestations; mean; you should refer to this throughout each • complications; module buy rabeprazole 10mg on line. Some words or terms may be found in • risk factors / age groups affected; more than one module 20 mg rabeprazole overnight delivery. Stated learning outcomes, indicating what you • methods of treatment; should achieve on satisfactory completion at the • prevention of spread; end of each module. Key words, that is, words or terms of particular • contact tracing; relevance to an individual module. The main body of the text, containing theory • rehabilitation; and factual content; the same paragraph headings • prevention strategies; and are used throughout the manual where appropriate. Learning activities, to be carried out when and infectious diseases; and indicated in the text; a workbook is provided separately for this. Revision points: these indicate that you should workbook is designed to assist you to complete stop and note some points or answer a question. The summary of key points is a reiteration of is a blank space under an activity, this should be the most important messages to absorb and used for notes. It is sources whenever possible; only the main sources recommended that in order to get the most benefit used for each module are included in the from the manual, you should not refer to this until bibliography. Further information Theory versus practical learning composition The manual is designed to be self-contained. The The manual content contains most of the theory number of other sources of information in the required to provide a firm basis of knowledge on bibliography of each module has been kept to a infections and infectious disease. The purpose of minimum; those which have been cited are the revision points is to test your knowledge on particularly useful. Try to manual is only as up-to-date as the date of respond to the revision points without referring to publication; to obtain the most up-to-date the text in the first instance, then compare your information available, visit the websites mentioned response to the information in the manual. The learning activities are intended to be more Assessment of revision points practical and are related to nursing or midwifery You can test this yourself by comparing your practice incorporating wider aspects relevant to the response to the information in the manual text. For example, you may be asked to visit a laboratory, carry out an audit in your place of work or produce a leaflet to give to patients. The learning activities are designed to further develop your knowledge and are also practical and useful. Depending on your area of practice, some learning activities will be more useful than others. Assessment of learning activities It is indicated within the text of each module when you should carry out a particular learning activity. Infection control is especially important within healthcare settings, where the risk of infection to patients is greatly increased. Good infection control techniques adopted during patient care can assist greatly in preventing or reducing avoidable History of infection control Infection control measures help hospital-acquired infections. In the 14th century, the Venetians quarantined ships arriving at their port in order to contain diseases There are important public health issues in the prevention and control such as plague. In the 19th of infection, including the general health and nutritional status of the century, Semmelweiss, a Viennese obstetrician, realized that infection public, and their living conditions, such as housing, water and sanitation was passed to patients on the hands of healthcare workers. These influence the level of infectious disease in the community, showed conclusively that infection could be greatly reduced by hand which in turn affects the level of infection of those both in and outside washing. In addition, in the 19th century separate facilities for of hospitals, thus affecting the burden on healthcare facilities. Local infection control policy manuals should be produced within Basic infection control measures individual settings in order to give guidance to staff on the are essential in everyday practice today. The introduction of antibiotics in Hospital-acquired the 1940s saw a decrease in basic measures, such as cleaning, in (nosocomial) infections everyday hospital practice, which Hospital-acquired infections, or nosocomial infections, are infections that previously had been the only defence measure for patients were not present or incubating on admission of a patient to hospital. People thought These infections can be readily diagnosed in patients who have appeared that the microorganisms that had caused many deaths had been free of signs and symptoms of infection on admission and have then gone beaten. Unfortunately it was soon discovered that these micro- on to develop infection – for example, a surgical wound exuding pus. In addition, they were These infections can cause unnecessary suffering for the patient and also able to inactivate antibiotics by developing chemicals that rendered create unnecessary costs for the health facility. Page 4 Module 1 Microbiology To begin to understand why we must undertake infection control measures we must first consider aspects of microbiology. Microbiology is broadly described as the study of bacteria, fungi, protozoa, viruses, and helminths. In studying these groups of organisms, including their are small microorganisms of simple primitive form. Bacteria many subgroups and families, we can learn how: can commonly be found living • they live within us; within our bodies and in our environment, for example in • they live in our environment; animals, soil and water. For examples of common agents so small that they are microorganisms found in healthcare settings, see Appendix 1. Knowledge of Fungi are simple plants that are parasitic on other plants and this cycle is essential in order to understand how infection can occur. A few can cause fatal All precautions and measures taken in order to prevent and control disease and illness in animals and humans. Helminths are large parasites - worms, which can be a major cause of morbidity in some countries. The cycle of infection Infectious agent Bacteria Fungi Viruses Protozoa Susceptible host Helminths Neonates Reservoir Diabetics People Immunosuppression Equipment Cardiopulmonary Water disease Elderly Portal of entry Broken skin Portal of exit Mucous membrane Excretions Gastrointestinal tract Secretions Resipratory tract Droplets Urinary tract Skin contact Means of transmission Bloodborne Airborne Droplet Common vehicle Vectorborne Portals of entry are the same as the portals of (Note: certain organisms can be transmitted through more exit and are either natural or artificial. Examples of organisms that can be spread by all of these routes are found in Appendix Means of transmission: 1). The main concerns in healthcare settings are the Reservoir: where microorganisms can be found. Airborne: through inhalation of small particles that remain sinks or washbowls, bedpans, surfaces) suspended in the air for long periods of time and can be widely 2. Droplet transmission differs as the particles are larger and therefore do not remain suspended Susceptible host: Factors that affect the body’s natural ability in the air. Spread is therefore through close contact with infected to fight infection include: persons who may be sneezing, coughing, talking, or undergoing 1. Common vehicle: through food, water, drugs, blood or Portals of exit are required for microorganisms to be other solutions transmitted from human sources. Vectorborne: usually through arthropods such as healthcare settings include: intravenous lines, urinary catheters, mosquitoes and ticks but cockroaches, ants and flies can also wound sites, open skin lesions, invasive devices, the respiratory transmit infection.