There are substantial data in the literature documenting excellent protection for substances that have been treated with cyclodextrins [12 pain treatment agreement discount 2mg artane visa,164?166] pain management for dogs with osteosarcoma buy artane 2 mg visa. As aforementioned pain treatment centers of america little rock generic artane 2 mg fast delivery, the cyclodextrin?guest complex formed is very stable to evaporation pain treatment for scoliosis purchase cheap artane on line. Szente and Szejtli [166] reported only about a 5% loss of included volatiles after 2 years of storage at room temperature heel pain treatment webmd discount artane online visa. More important treating pain in dogs hips discount artane 2mg on line, however kingston hospital pain treatment center safe 2 mg artane, is the oxidative stabil ity of the included guest compounds pain treatment algorithm buy generic artane canada. Many reports have demonstrated that inclusion complexes are quite stable to oxidation [164,166]. As with all processes, there are limits to the application of cyclodextrin complexation in the formation of flavors [167], and these include the following: 1. There is a limited amount of flavor, which can be incorporated into a formulation (average 9%?14% by weight). The size and polarity of flavors to be complexed limit the usefulness of the process. Cyclodextrin can act as an artificial enzyme, sometimes enhancing the rate of hydrolysis of some ester-type flavor components. The water solubility of -cyclodextrin flavor complexes is generally much lower than that of spray-dried and other microencapsulated samples. For our purposes, nanotechnology deals with the capability to image, measure, model, control, and manipulate matter at dimensions roughly 1?100 nm, where novel interfacial phenomena introduce new functionalities [90]. Some nanoscale phenomena have been utilized in functional food and nutraceutical formulation, manufacturing, and processes. New concepts are being explored to improve the effectiveness and efficiency in the delivery of multiple bioactive compounds, which do not normally mix well, like water and lipid-soluble vitamins; now, they can be released con secutively. Nanoparticles may be defined as being submicrometer colloidal systems generally, but not necessarily, made of polymers (biodegradable or not). Depending upon the process in question, two different types of nanoparticles are available, nanospheres and nanocapsules. Nanocapsules comprise a membrane-wall structure with an aqueous or oily core containing the bioactive substance, where as nanospheres are matrix systems where the bioactive substance is dispersed throughout the particles [168]. Nanospheres prepared by encapsulation can enhance solubility; facilitate controlled release; improve bioavailability; and protect the stability of micronutrients and bioactive compounds during food processing, storage, and distribution. Encapsulated nanospheres can also lead to the development of new flavor-targeted delivery systems to improve food quality and functionality. Controlled release may eventually lead to in situ flavor and color modification of products [90]. In recent years, the role of nanotechnology in delivery systems for bioactives and specialty gradients has advanced considerably, but owing to better delivery of the active ingredients, toxicity related to possible overdosing issues must be adequately investigated. Various properties of active materi als may be changed/modified by encapsulation. For example, handling and flow properties can be improved by converting a liquid to a solid encapsulated form. The stability of functional ingredients and bioactives that are volatile or sensitive to heat, light, or oxidation can be protected, thereby extending their shelf life. Materials that are otherwise incom patible can be mixed and utilized together safely. Using food fortification as an example, microencapsu lation can mask the undesirable taste of some nutrients. Currently, there are several hundred types of microcapsules being utilized as food additives or as ingredients in functional food formulations throughout North America [12]. They can be employed as flavor modifiers, preser vation aids, and processing acids. In addition, they facilitate the development of a wide variety of textural effects in foods because of their interaction with other macro and micromolecules such as proteins, starches, pectins, and gums [170]. Unencapsulated food acids can react with food ingredients to produce many undesirable effects. These include decreased shelf life of citrus-flavored and starch-containing foods. Encapsulated food acids overcome these problems and others because they preclude oxidation and provide controlled release under specific conditions. Moreover, encapsulated acids reduce hygroscopicity and dusting, and provide a high degree of flowability without clumping. Encapsulation of acids in a time-release matrix is suggested as a means of avoiding undesirable reac tions of acidulants with other food ingredients. The matrix used for forming the encapsulating coat in the acid products is generally a partially hydrogenated vegetable oil, although maltodextrin and emulsifiers are also available for this purpose. The encapsulated acids can be released at the appropriate time in the Encapsulation, Stabilization, and Controlled Release of Food Ingredients and Bioactives 543 processing operation either by heating to the melting point of the coating material, by contact with water, or a combination of these methods. Fat encapsulation allows the acid to survive the blending process, giving a uniform dispersion within the meat formulation. Later, the encapsulated acid controls the drop in pH and prevents the meat from prematurely setting [13]. In a meat preparation, encapsulated acids need to be released after later processing stages such as cooking. Early release causes protein binding, and the final texture of the product can become brittle and deemed as unacceptable. Bacteria is added to meat emulsions and allowed to proliferate until a sufficient amount of lactic acid has been generated. However, such products often tend to have inconsistent flavor, color, and textural characteristics from batch to batch. Uncoated lactic and citric acids cannot be added to meat during cur ing because they react almost instantly with meat proteins, rendering them unsuitable for further processing. Contamination is especially troublesome when the meat processor uses fermented raw meat as the source of bacteria rather than frozen cultures. An encapsulated acid, which is formulated for delayed release under smokehouse temperatures, can be employed as an alternative to the cultures. Acidification by encapsulated acids can improve emulsification and protein binding of emulsified meat and poultry products and impart the tangy? flavor associated with fermented sausages without the com plicated use of lactic acid starter cultures. In effect, encapsulation permits addition of the acidulants prior to stuffing without premature denaturation/binding of meat. More than 35 years ago, encapsulated acids in a heat-rupturable inert vehicle such as ethylcellulose were developed [171]. The prepared encapsules were mixed with nitrite-treated comminuted meats, and upon thermal processing the encapsulated acid was released and brought about a lowering in the pH of the meat product and gave rise to rapid development and stabilization of the cured meat color. The more acidic conditions within the meat matrix assisted in the production of nitrous acid and dinitrogen trioxide from the exogenous sodium nitrite. The effect of encapsulated food acids on restructured pork from prerigor sow meat was studied by Cordray and Huffman [172]. Lactic acid can also be encapsulated by plating it onto a particle calcium lactate carrier and then encapsulating the carrier and acid with a molten edible lipid [173]. Encapsulation of sodium bicarbonate is particularly important in such products when high moisture/low pH fruits are mixed into a batter or dough, as it prevents premature leavening and undesirable color changes in the fruit [174]. Products commonly encapsulated for bakery applications include a variety of leavening system ingredients as well as vitamin C, acetic acid, lactic acid, potassium sorbate, sorbic acid, calcium propionate, and sodium chloride. Examples include stronger sidewalls, uniform crust 544 Handbook of Food Preservation, Second Edition color, and improved slicing, in addition to a stronger structure that supports the addition of other pro tein-rich ingredients (such as soybean flour, nonfat milk powder, and wheat germ). Because ascorbic acid degrades rapidly in the presence of water and oxygen, most of the acid is destroyed before it is needed. Encapsulation can delay the reactivity of ascorbic acid from the dough mixing stage to well into or after the proof stage. Encapsulated in an edible coating, ascorbic acid imparts some of the effect of an oxidizing agent when used alone in natural breads. In combination with bromate, it enables greater amounts of protein-rich ingredients to be utilized without disturbing the grain of the bread to any great extent [175]. Pan breads and flat breads are the most common applications for such an ingredient. For yeast-raised doughs, encapsulated salt, potassium sorbate, and sorbic acid are employed because they do not allow the pH to drop too early in the baking process and therefore the yeast can grow. Once baked, however, the mold-inhibiting properties of these ingredients are released in the dough and help to extend the shelf life of the finished product [13]. Seighman [176] developed a method for encapsulation of foodgrade phosphoric acid in a dispersion containing a film-forming agent (hydrogen octenylbutane dioate?amylodextrin) and a matrix-forming ingredient (modified and hydrolyzed starches). The dispersion is thermal processed and then extruded into cold aqueous alcohol to solidify the matrix-forming ingredients and allow the film-forming agent to harden to a vitreous structure. The vast majority of flavor compounds used are a liquid at room temperature, and con stituents of the flavors tend to show sensitivity toward air, light, irradiation, and elevated temperatures. Moreover, these flavor concentrates are generally oily and lipophilic materials, which can be difficult to work with. It is therefore necessary to employ a process to convert these flavor compounds to a more use able form. One of the purposes behind encapsulation in the food industry is the conversion of liquid fla vors to dry powders. Microencapsulated flavors provide the convenience of a solid form over a liquid one with reduced volatility and less oxidation [23,107,162]. Microencapsulation has become an attractive option to transform liquid food flavorings into stable and free-flowing powders, which are easier to han dle and incorporate into a dry food system. The flavor industry depends heavily on encapsulation as a means of providing solid flavor compounds that offer them protection until consumption. Flavoring agents and spices are encapsulated by a variety of processes and offer numerous advantages to food processors. Processes for flavor encapsulation and encapsulated flavorings prepared during the last 45 years are summarized in Table 22. Examples of commonly used encapsulated flavors are citrus oils, mint oils, onion and garlic oils, spice oleoresins, and whole spices. Citrus oils are very susceptible to oxidation due to sites of unsaturation in their mono and sesquiterpenoid structure. Oxidative deterioration results in the development of off flavors described as painty or turpentine-like. Encapsulated citrus oil, prepared by spray drying in a mal todextrin matrix, has a greater stability than unprotected oil [27]. Because flavors are often volatile materials, the stability of the dry microcapsules is an important con sideration. Many volatile liquids can be encapsu lated and subsequently dried to form free-flowing powders with minimal loss of activity during storage. For example, flavors encapsulated by inclusion complexation in -cyclodextrin were protected against volatilization and attack by oxidation [162,166]. Storage stability of flavors encapsulated in -cyclodextrin under nonstress? conditions at room temper ature showed that molecular encapsulation, in most cases, provides an almost perfect preservation of fla vors for up to 10 years [166] (Table 22. There has been a great expansion in the development of techniques to encapsulate flavors. Excellent reviews of microencapsulation technology as it applies to food flavors have been written [14,23,106,123,177,179,182]. It should be noted, however, that details pertaining to these techniques are difficult to obtain since they tend to be of a proprietary nature. Encapsulation of sweeteners?namely sugars and other nutritive or artificial sweeteners?reduces their hygroscopicity, improves their flowability, and prolongs their sweetness perception. Sugar, that has been encapsulated with fat and incorporated in a chewing gum, requires more shear and higher temperatures to release its sweetness than uncoated sugar, which dissolves more rapidly in the mouth. Patents awarded for the encapsulation of sweeteners emerged mainly during the 1980s, as the techni cal development of encapsulation allowed their commercial manufacture. It is the methyl ester of a dipeptide made from two amino acids, pheny lalanine and aspartic acid (aspartate). At high temperatures, aspartame degrades into the amino acids, aspartic acid and phenylalanine, which is accompanied by a loss in sweetness. This internationally marketed sweetener has now been encapsulated by many methods. Yang and coworkers developed a process for encapsulat ing aspartame in a film composed of high molecular weight polyvinyl acetate and a hydrophobic plasticizer (mono or diacylglycerol with fatty acid chains of 16?22 carbon atoms) [211,219,220]. By this process active ingredients, including soluble dietary fibers, flavoring agents, and drugs, can also be encapsulated. The product may be used to give chewing gum an extended shelf life, with highly controlled release of active ingredients [211]. A process developed by Cherukuri and coworkers can be used to produce a stable delivery system. It comprises a dipeptide or amino acid sweetener or flavorant or mixture thereof encapsulated in a mixture of fat and high melting point polyethylene wax [221?223]. Gas chromatographic analyses were employed to measure the retention of orange, synthetic pepper mint, and natural lemon flavors, which had been cocrystallized and then stored in polyethylene bags under ambient conditions. Results from oxidation studies [224] showed that peanut-butter flavored products had a very good shelf life, even after storage for an appreciable period of time. Some typical examples of products encapsulated by cocrystallization are listed in Table 22. Encapsulated colors are easier to handle and offer improved solubility, sta bility to oxidation, and control over stratification from dry blends. Synthetic colors, together with other food ingredients, can also be encapsulated to improve their stabilities [226]. The pigment in oil was solubilized in an aqueous solution containing 60% (w/w) corn syrup solids and 1% (w/w) polypeptone. The solubilized mixture so obtained was solidified by vacuum drying at 60?C and formed into granules by crusting and sieving. These granules containing ~12% pig ment-containing oil underwent virtually no discoloration during storage for 20 days at 60?C or when sub jected to irradiation from a fluorescent lamp. Dispersibility of the pigments in water was improved by their encapsulation in the protein?carbohydrate matrix [227]. Ciliberto and Kramer [228] developed an encapsulation process for producing granular water-soluble food ingredients, which otherwise deteriorated on exposure to the atmosphere (such as coloring agent). It was claimed that the resulting coated particles had a long shelf life and were still substantially instan taneously soluble in water. One possible way to protect lipid moieties against oxidative deterioration is via encapsulation. Early research in this area focused mainly on the production of encapsulated lipids for animal feed [199,230?232], but more recently, encapsulated high-fat powders or shortenings have been available in food formulations for human [233]. Because of the prohealth benefits of fish oils, encapsulated oils have been available in health food stores, pharmacies, and supermarkets for a number of years. It should be noted that fish oils are exceptionally sus ceptible to autoxidation and can form complex mixtures of high molecular weight oxidation prod ucts. Shukla and Perkins [239] reported that because of the unknown health effects of the oxidative polymeric materials and their high level in some encapsulated oils, caution should be exercised when ingesting fish oil capsules on a regular basis. The microencapsulated linoleic acid was not susceptible to oxidative deterio ration even though more effective encapsulating wall materials could have been used. Ono and Aoyama [104] reported that vacuum-dried rice brain oil embedded in granules containing corn syrup solids and pork polypeptone did not undergo much oxidation upon exposure to air at high temperature for a few weeks. These authors reported that the employment of microencapsulated sardine oil in fortified cookies did not affect their sensory quality. The authors reported that the microcapsules so obtained from the experiment were highly resistant to oxidative deterioration during long-term storage at various aws [242]. Shahidi and Wanasundara [243] spray dried an emulsion of seal blubber oil, which contained 21%?26% long chain omega-3 fatty acids, with either -cyclodextrin, corn syrup solids, or maltodextrins. They found -cyclodextrin to be the most effective entrapping agent as it prevented oxidative deterioration of the seal blubber oil. Because vitamins are such important nutritional and dietary factors, processed foods are often enriched or forti fied with them. Encapsulation also improves flow properties and reduces dusting when nutrients are added to dry mixes. Both fat and water-soluble vitamins may be encapsulated with a variety of coatings to provide many advantages. Hall and Pondell [246] developed a process to encapsulate vitamin or mineral parti cles. The coating matrix for this process is chiefly ethylcellulose together with propylene glycol monoester and acetylated monoglycerol. Vitamins and minerals can also be encapsulated in fat [247] or starch matrices [248]. Encapsulation, Stabilization, and Controlled Release of Food Ingredients and Bioactives 549 For encapsulation of water-soluble vitamins, ethylcellulose is useful because it is water insoluble, and coatings with increased thickness reduce the water permeability of the prepared capsules. A procedure for microencapsulating thiamine in an ethylcellulose coating to protect it from alkaline conditions experi enced in bakery products, and mask its undesirable bitter taste, has been successfully developed [249]. Riboflavin, thiamine, and niacin are partially destroyed during processing and cooking of pasta prod ucts. Studies on unprotected versus encapsulated thiamine, riboflavin, and niacin in cooked enriched spaghetti showed that concentrations of the three B vitamins tested were higher in cooked pasta that con tained encapsulated vitamins [250]. Lipid-soluble vitamins lose their activity due to isomerism, anhydrovitamin formation, oxidation, and photochemical reactions [162]. Losses of vitamins in fortified foods can be minimized if they are added as cyclodextrin complexes [162] or gelatine-encapsulated beadlets [251]. It was found that the stability of vitamin A in skim milk was substantially increased by its encapsulation in gelatine.
Managing breastfeeding problems 4-23 What should you do if an infant refuses the breast? Sometimes the mother may have too much milk and the milk may fow too fast causing the infant to choke or gag when feeding phantom pain treatment buy artane cheap online. Only ofer one breast per feed and only when the infant appears hungry and the milk supply will setle with time pain treatment center university of rochester generic artane 2 mg on-line. A normal pain research and treatment journal impact factor 2mg artane with mastercard, full breast feels tense and heavy pain medication for pancreatitis in dogs order artane with amex, but is not painful and is relieved by feeding who cancer pain treatment guidelines purchase artane discount. Breasts that are swollen midsouth pain treatment center reviews order 2 mg artane fast delivery, tender pain treatment center of franklin tennessee buy cheap artane 2 mg line, hard pain treatment in multiple myeloma artane 2mg free shipping, lumpy and painful are caused by either engorgement or mastitis. Usually both breasts are swollen, hard and painful but the mother does not feel ill. Engorged breast are common if the infant does not feed correctly, if the mother does not room-in and if the mother does not demand feed. Placing ice onto the breasts between feeds will help to reduce the swelling and a warm shower relieves the discomfort, while a mild analgesic like paracetamol (Panado) is helpful. Mastitis is an infammation of the breast due to blocked milk ducts and seepage of milk into the surrounding tissues. Because of the pain of a breast abscess, feeding may have to be stopped on that breast for a few days. Nipples should not be painful, even in the frst few days, if the infant is correctly latched to the breast. Make sure that the infant has all of the nipple and most of the areola in the mouth when feeding. Cracked nipples are very painful and should be prevented by correctly latching the infant to the breast and avoiding engorged breasts. Usually with correct latching to the breast the mother will feel no pain and the crack will heal within a day. Complementary feeds decrease the time the infant spends on the breast and, thereby, reduce the production of breast milk. However, expressing milk into a sterile container for the missed feed would be preferable. Frozen milk should be thawed slowly by placing the container in warm (not hot) water. Alternatively, formula can be given while the mother is away at work and then breastfeeds given when she is home. Tere is no evidence that antituberculous drugs or antiviral drugs that cross in the breast milk are dangerous to the infant. Avoid breastfeeding for 24 hours afer radioactive iodine is given to treat thyrotoxicosis. If a mother is unable to breastfeed because she is separated from her infant, she should express her milk, manually or with a breast pump, for the infant. However, the mother should be encouraged to continue to express her breast milk to increase her milk production. They are very similar and, therefore, the milk available at the local clinic or the cheapest milk should be bought. One of the great dangers of formula feeds is to make the mixture too strong or too weak. Formula-fed infants may be ofered a few clear feeds daily if the weather is very hot. The greatest advantage of cup feeding is that a cup can be easily cleaned with soap and water. A cup also dries easily, especially if placed in the sun which helps to sterilise the cup. Mothers who do not breastfeed should be shown how to cup feed correctly before they are discharged home afer delivery. Additional iron and vitamin supplements may, however, be of beneft in poor communities when iron drops 0. In some areas with very little fluoride in the drinking water, supplementary fluoride drops can be given to reduce the risk of dental caries. Even if the mother can only breastfeed for a few weeks or months, this will be of beneft to both her and her infant. This practice is particularly important in poor communities as breast milk provides the infant with a good source of protein. To become registered as a Baby Friendly Hospital all the Ten steps to successful breastfeeding? have to be implemented. Have a writen breastfeeding policy that is frequently communicated to all the health-care staf. Train all the health-care staf in the skills needed to implement successful breastfeeding. Do not give newborn infants formula or water feeds unless this is indicated for medical reasons. Allow mothers and their infants to remain together all the time from delivery to discharge. Promote the formation of breastfeeding support groups and refer mothers to these groups on discharge from hospital or clinic. Tere are social and cultural barriers to formula feeding in many poor communities. The mother should be able to prepare feeds hygienically and be able to clean the botles, teats and cups. Women who decide to formula feed must be taught how to prepare and give formula correctly. Yes, many mothers are able to breastfeed successfully even if they did not breastfeed their previous children. The commonest cause of failure to breastfeed successfully is that mothers are not managed correctly and not fully informed about the advantages and method of breastfeeding. This decision should be made during pregnancy and preferably before the infant is born. With prevention of breast engorgement and careful atention to latching the infant correctly, cracked nipples should not occur. If the infant is unable to latch correctly due to swelling of the areola and breast, the nipple can be damaged by the infant sucking incorrectly. Demand feeding whenever the infant is hungry helps prevent engorged breasts which can lead to cracked nipples. Like most other antibiotics, fucloxacillin will cross into the breast milk in small quantities only. She can still breastfeed in the morning before going to work and again when she gets home. She can also breastfeed throughout the weekend and express her breast milk at work to be stored and fed by cup during the next day. She is discharged from the clinic 6 hours afer delivery without any clear instructions. Fresh cows milk, evaporated milk or skimmed milk are not suitable for small infants. This is particularly important in poor communities where gastroenteritis is common. The botle and teat must be cleaned and sterilised by boiling or standing in a disinfecting agent (Milton or half diluted Jik). To decide which group an infant falls into, the history must be reviewed and the infant examined. Infants that do not have all of the above features are either high-risk infants or sick infants. A high-risk infant is an infant that appears well but has a much greater chance than most infants of developing a clinical problem, such as hypothermia, hypoglycaemia, apnoea, infection, etc. An infant that appears well but has any of the following features should be regarded as high risk and, therefore, likely to develop a problem during the newborn period: 1. It is essential to identify the clinical problem that the infant is at risk of developing, so that the problem can be anticipated. It is important to anticipate problems in high-risk infants so that steps can be taken to prevent these problems occurring. The infant may previously have been well or may previously have been identifed as a high-risk infant. The recognition of a sick infant is one of the most important clinical skills that nurses and doctors must learn. Infants that have a congenital abnormality but are otherwise well are ofen grouped together with sick infants when management is planned. Handling a sick infant, such as changing the nappy, may precipitate an apnoeic atack or bradycardia. The infant should be handled and moved as litle as possible when observations are made. Look for any other abnormal signs that are present, such as vomiting, loose stools, etc. The type and volume of the fuid intake (both oral feeds and intravenous fuids) are recorded. In severely ill infants the urine is collected in a urine bag or urethral catheter so that the volume of the urine passed can be measured. The content of the urine (protein, blood and glucose) is determined with a reagent strip. The blood pressure should be recorded in severely ill infants in level 2 or 3 nurseries. It is very important that the observations be carefully recorded on an observation chart together with the time of the observations. A chart that is specially designed for the recording of observations on newborn infants should be used. The observation chart must have columns for the recording of the vital signs and other important observations. Shock is the failure of the circulation to provide an adequate blood supply to the tissues. A cuf is placed around the upper arm to measure the blood pressure (mean, systolic and diastolic) in the brachial artery. The normal range increases with the birth weight and gestational age of the infant. A false reading may be obtained if the infant is cold, as this may also cause poor perfusion of the skin. Correcting the poor peripheral circulation by giving intravenous resuscitation fuids, such as normal saline, fresh frozen plasma, stabilised human serum or Haemaccel. It is ofen very difcult to recognise a ft in a newborn infant as infants usually do not have a typical grand mal ft (generalised extension followed by jerking movements) as seen in older children and adults. Hypoxia, especially neonatal encephalopathy (hypoxic ischaemic encephalopathy) due to severe intrapartum hypoxia) 2. Do not keep paraldehyde in a plastic syringe for more than 2 minutes as it may react with the plastic. Unfortunately there is no standard method yet of treating hypoxic brain damage once it has already occurred. All infants that have had a ft should be transferred to a level 2 or 3 nursery for further investigation and management. Normally acid and alkali are present in equal amount in the body and are therefore in balance. It is due to the accumulation of lactic acid which is formed during hypoxia, septicaemia, dehydration and shock when the cells of the body do not receive enough oxygen. If the cells receive too litle oxygen, some energy can still be produced by converting a lot of glucose into lactic acid (anaerobic metabolism). The increased production of lactic acid lowers the pH, resulting in a metabolic acidosis. This type of acidosis is caused by the accumulation of carbon dioxide in the blood during respiratory distress and apnoea. Acidosis, therefore, is diagnosed by measuring the pH of a sample of arterial blood. The pH, the base defcit and carbon dioxide concentration are determined with a blood gas analyser which also calculates the base defcit. The correct amount of 4% sodium bicarbonate that should be given can be calculated from the base defcit. Case study 1 A preterm infant of 1500 g has a normal Apgar score and appears healthy afer delivery. The infant should be classifed as high risk as the infant, although appearing well, is preterm and low birth weight. Case study 2 A two day old term infant becomes lethargic and develops abdominal distension. The heart rate is 180 beats per minute, the respiration and temperature are normal and the infant is peripherally cyanosed. By giving 10 to 20 ml of normal saline (or fresh frozen plasma, stabilised human serum or Haemaccel) per kilogram by intravenous infusion over 10 to 20 minutes. The septicaemia, which has caused the shock, must also be treated with parenteral antibiotics. Case study 3 A term infant is delivered by caesarean section afer a diagnosis of fetal distress is made. Afer resuscitation the infant appears lethargic and at 2 hours has a generalised ft. Nasogastric feeds are stopped, an antibiotic is prescribed and an intravenous infusion is started. Writing good clinical notes Good clinical notes, which form the patient record, should be accurate, brief and easy to read. The management consists of the nursing care, the observations needed, the medical treatment, and the management of the parents. Although most of the information is given, these notes are not systematic and, therefore, they are difcult to understand. It is very useful in a nursery where infants may need ongoing care for days or weeks. The respiratory distress has improved slightly but the infant has developed a mild conjunctivitis. The problem of neonatal asphyxia has been removed from the problem list, as it has resolved and no longer has any efect on the infant, while the new problem of conjunctivitis has been added to the list. A list of the commonly used abbreviations in your nursery should be drawn up and displayed in the nursery. Usually a new page is started each day, most commonly in the morning when the day staf take over duty from the night staf. The type of intravenous fuid given, together with the time it was started, the time it was completed and the volume received, must also be carefully recorded. The type of oral or tube feed to be given, together with the volume and frequency of feeds, must be clearly writen on the intake chart. Some forms of fuid loss, such as in the stools and from the lungs and skin, cannot be measured easily and therefore are not routinely recorded. Urine has to be collected in a urine bag, aspirated via a catheter and measured with a plastic syringe if an accurate record of urine output is to be kept. This is ofen difcult, especially in a female infant, as the urine tends to leak out of the bag. Terefore, an accurate record of the volume of urine passed is only kept when there is a clinical indication. Oliguria in a newborn infant is defned as a urine output of less than 1 ml/kg/hour. Loose stools may contain a lot of fuid and, therefore, must be recorded carefully. The concentration of the various constituents of body fuid varies between these diferent areas. Water and all the constituents of body fuid are continually being lost in the urine, stool and sweat, and, therefore, need to be replaced. The fluid requirements per day increase from 60 ml/kg on day 1 to 150 ml/kg on day 5. To prevent dehydration, the kidneys of the newborn infant, therefore, produce litle urine during this period. Infants weighing less than 1500 g need 75 ml/kg on both the frst and second days of life. Infants under a radiant warmer need an extra 25 ml/kg a day to replace the additional fuid lost through their skin. Some preterm infants need between 150 and 180 ml/kg afer day 5 before they obtain enough energy for growth. Weighing the infant daily is the best method of assessing whether enough fuid is being given. If an infant looses more than 10% of their birth weight, then the daily fuid intake must be increased. Instead of increasing the volume of the feeds, however, extra energy can be added to the milk by giving 1 ml Liprocil (medium-chained triglyceride oil giving 38 kJ) before each feed. Resuscitation fuid is used to resuscitate an infant that is shocked due to hypoxia, septicaemia, blood loss or severe dehydration. Haemaccel The choice of fuid depends on which fuid is available and the cause of shock. Resuscitation fuid is given 10?20 ml/kg over 10?20 minutes until normal perfusion and blood pressure are achieved.
The main function of endoplasmic space through intercellular junctions or junctional complexes reticulum is the manufacture of protein pain treatment for ra 2 mg artane amex. Morphologically pain treatment during pregnancy generic artane 2 mg fast delivery, visible under electron microscope and are of 4 types there are 2 forms of endoplasmic reticulum: rough (or (Fig gallbladder pain treatment home remedies purchase artane 2mg without prescription. These are tight its outer surface is rough or granular due to attached junctions situated just below the luminal margin of adjacent i) fibrillar structural proteins (collagen neuropathic pain treatment guidelines iasp buy generic artane online, elastin); 25 ii) adhesion proteins (fibronectin pain solutions treatment center hiram cheap artane 2mg with visa, laminin pain sacroiliac joint treatment purchase artane 2 mg, fibrillin pain treatment center west plains mo buy cheap artane 2mg on-line, osteonectin pain treatment center northside hospital buy genuine artane, tenacin); and iii) molecules of proteoglycans and glycosaminoglycans (heparan sulphate, chondroitin sulphate, dermatan sulphate, keratan sulphate, hyaluronic acid). The examples of occluding lectins or lectin-like protein molecules which bind to zones are seen in renal tubular epithelial cells, intestinal glycoproteins and glycolipids on the cell surface. Their major epithelium, and vascular endothelium in the brain role is in movement of leucocytes and platelets and develop constituting blood-brain barrier. They have a major role plates present focally between the adjacent epithelial cells, in recognition and binding of immunocompetent cells. The last group of adhesion molecules is a break cells between plasma membrane and the basement away from immunoglobulin superfamily. Pits or holes are present with each other is by release of peptides and other molecules in the regions of gap junctions so that these regions are acting as paracrine function. Their main role is in activation Molecular Interactions between Cells of immune system. Mitosis is molecules consisting of proteins, glycoproteins or controlled by genes which encode for release of specific lipoproteins and may be located on the outer cell membrane, proteins molecules that promote or inhibit the process of inside the cell, or may be trans-membranous. Mitosis-promoting protein molecules are synthesised by the cell itself depending upon molecules are cyclins A, B and E. The cell receptors take part in activation of synthesis and secretion cycle is the phase between two consecutive divisions of various hormones. The activated receptor for ion exchange such (gap 1) phase, S (synthesis) phase, G2 (gap 2) phase, and M as for sodium, potassium and calcium and certain peptide (mitotic) phase. M phase is the stage in which process of mitosis to form two daughter cells is completed. Each chromosome divides into 2 chromatids proteins) and ubiquitin (so named due to its universal presence which are held together by centromere. These are a variety of intracellular carrier proteins of the nucleus and the nuclear membrane disintegrates. They normally perform the role of chaperones the two centrioles forming spindle, while the chromosomes (house-keeping) i. The centromeres divide and each set of folding, disaggregation of protein-protein complexes and separated chromosomes moves towards the opposite poles transport of proteins into various intracellular organelles of the spindle. The daughter cells may continue to remain in the tissue necrosis in ischaemic reperfusion injury in myocardial cell cycle and divide further, or may go out of the cell cycle infarcts. In addition, they have also been shown to have a into resting phase, called G0 phase. This is another related stress protein which has as under: ubiquitous presence in human body cells. Ubiquitin has been found to be Reparative stimulation of mitosis occurs when a tissue is involved in a variety of human degenerative diseases, injured. Premitotic phases are the G1, S and G2 phase while M (mitotic) phase is accomplished in 4 sequential stages: prophase, metaphase, anaphase, and telophase. On completion of cell division, two daughter cells are formed which may continue to remain in the cell cycle or go out of it in resting phase (interphase), the G0 phase. The cells may be broadly injured by two major ways: In a given situation, more than one of the above etiologic A. The acquired causes of disease comprise vast essentially require oxygen to generate energy and perform majority of common diseases afflicting mankind. Deficiency of oxygen or hypoxia results underlying agent, the acquired causes of cell injury can be in failure to carry out these activities by the cells. Chemical agents and drugs by reduced supply of blood to cells due to interruption i. Physical agents in causation of anything that causes harm to the patient, there are some disease are as under: diseases as well as deaths attributed to iatrogenic causes mechanical trauma. An ever increasing list of the etiology of diseases, there still remain many diseases for chemical agents and drugs may cause cell injury. For example, most examples include the following: common form of hypertension (90%) is idiopathic (or chemical poisons such as cyanide, arsenic, mercury; essential) hypertension. Similarly, exact etiology of many strong acids and alkalis; cancers is still incompletely known. However, infections caused by bacteria, rickettsiae, viruses, fungi, in general, the following principles apply in pathogenesis of protozoa, metazoa, and other parasites. A deficiency or an muscle can withstand hypoxic injury for long-time while excess of nutrients may result in nutritional imbalances. Morphologic consequences: All forms of biochemical ability of the cells to undergo replication and repair, and changes underlying cell injury are expressed in terms of ultimately lead to cell death culminating in death of the morphologic changes. Patho genesis of hypoxic and ischaemic cell injury is, therefore, membrane transport, protein synthesis, lipid synthesis and 29 described in detail below followed by brief discussion on phospholipid metabolism). Although underlying intracellular mechanisms and is generated from glucose/glycogen in the absence of ultrastructural changes involved in reversible and oxygen). If the ischaemia or hypoxia is accumulation of metabolic waste products in the cells. These biochemical anaerobic glycolytic pathway for the requirement of energy changes have effects on the ultrastructural components of. Damage to plasma membrane pumps: Hydropic Excess intracellular calcium collects in the mitochondria swelling and other membrane changes. Morphologically, mitochondrial interferes in generation of phospholipids from the cellular changes are vacuoles in the mitochondria and deposits of fatty acids which are required for continuous repair of amorphous calcium salts in the mitochondrial matrix. Damage operating for regulation of sodium and calcium as under: to membrane function in general, and plasma membrane in i) Failure of sodium-potassium pump. As a result of sustained ischaemia, there at the plasma membrane allows active transport of sodium is increased cytosolic influx of calcium in the cell. Besides, results in intracellular accumulation of sodium and diffusion there is also decreased replacement-synthesis of membrane of potassium out of cell. The normal cytoskeleton of the cell (microfilaments, microtubules ii) Failure of calcium pump. Membrane damage causes and intermediate filaments) which anchors the cell disturbance in the calcium ion exchange across the cell membrane is damaged due to degradation by activated membrane. The damage is seen in the form of loss of microvilli, nucleoproteins are damaged by the activated lysosomal intramembranous particles and focal projections of the enzymes such as proteases and endonucleases. Myelin figures may be seen lying in the damage to the nucleus can be in three forms: cytoplasm or present outside the cell, these are derived from i) Pyknosis: Condensation and clumping of nucleus which membranes (plasma or organellar) enclosing water and becomes dark basophilic. Lysosomal hydrolytic enzymes: Lysosomal damage, cell reticulum and Golgi apparatus swell up. The lysosomal membranes are detached from granular endoplasmic reticulum and damaged and result in escape of lysosomal hydrolytic polysomes are degraded to monosomes, thus dispersing enzymes. These enzymes are activated due to lack of oxygen ribosomes in the cytoplasm and inactivating their function. These hydrolytic enzymes include: Similar reduced protein synthesis occurs in Golgi apparatus. Persistence of ischaemia or masses of phospholipids called myelin figures which are either hypoxia results in irreversible damage to the structure and phagocytosed by macrophages or there may be formation of function of the cell (cell death). Two essential phenomena always estimation of which may be used as clinical parameters of distinguish irreversible from reversible cell injury (Fig. While cell damage from oxygen deprivation by above Ischaemia-Reperfusion Injury and mechanisms develops slowly, taking several minutes to Free Radical-Mediated Cell Injury hours, the cell injury is accentuated after restoration of blood Depending upon the duration of ischaemia/hypoxia, supply and subsequent events termed ischaemic-reperfusion restoration of blood flow may result in the following injury and liberation of toxic free radicals, discussed below. Generation of reactive oxygen radicals (superoxide, H2O2, Enzyme Disease hydroxyl radicals). Amylase Acute pancreatitis molecular forms as reactive oxygen radicals or reactive Sialadenitis oxygen species can be most devastating for the cells. When the period of with hydrogen atom (H) and in the process forms water ischaemia is of short duration, reperfusion with resupply of (H2O). This reaction of O2 to H2O involves four electron oxygen restores the structural and functional state of the donation? in four steps involving transfer of one electron at injured cell i. These for longer duration, then rather than restoration of structure are generated within mitochondrial inner membrane where and function of the cell, reperfusion paradoxically cytochrome oxidase catalyses the O2 to H2O reaction. This is termed intermediate molecules of partially reduced species of oxygen ischaemia-reperfusion injury. Cell death in such cases is not attributed to these are generated from enzymatic and non-enzymatic formation of activated oxygen species. But instead, on reaction as under: reperfusion there is further marked intracellular excess of 1. Superoxide (O?2): Superoxide anion O?2 may be generated sodium and calcium ions due to persistent cell membrane by direct auto-oxidation of O2 during mitochondrial electron damage. Alternatively, O?2 is produced the underlying mechanism of reperfusion injury and free enzymatically by xanthine oxidase and cytochrome P450 in radical mediated injury is complex but following three main the mitochondria or cytosol. Oxygen-derived free radicals cause of H O with ferrous (Fe++) ions; the latter process is termed 2 2 cell injury by oxidation of protein macromolecules of the cells, as Fenton reaction. In addition to superoxide, H2O2 of cytosolic neutral proteases and cell destruction. This results in cell injury; it may also cause malignant transformation of i) Release of superoxide free radical in Fenton reaction (see below). Free radicals are formed iv) Chemical carcinogenesis in physiologic as well as pathologic processes. Basically, v) Hyperoxia (toxicity due to oxygen therapy) oxygen radicals are unstable and are destroyed spon vi) Cellular aging taneously. The ix) Destruction of tumour cells net effect of free radical injury in physiologic and disease x) Atherosclerosis. These However, if not degraded, then free radicals are highly substances include the following: destructive to the cell since they have electron-free residue Vitamins E, A and C (ascorbic acid) and thus bind to all molecules of the cell; this is termed Sulfhydryl-containing compounds. Incoming activated neutrophils utilise oxygen radicals?lipid hydroperoxy radicals and lipid hypo quickly (oxygen burst) and release a lot of oxygen free radicals. Pathogenesis of Chemical Injury Chemicals induce cell injury by one of the two mechanisms: by direct cytotoxicity, or by conversion of chemical into reactive metabolites. Some chemicals combine with components of the cell and produce direct cytotoxicity without requiring metabolic activation. Depending upon the severity of cell injury, degree of damage and residual effects on cells and tissues are variable. In general, morphologic changes in various forms of cell injury can be classified as shown in Table 3. However, now it is realised that this poisoning, the greatest damage occurs to cells of the alimen term does not provide any information on the nature of tary tract where it is absorbed and kidney where it is excreted. Other examples of directly cytotoxic chemicals include Following morphologic forms of reversible cell injury are chemotherapeutic agents used in treatment of cancer, toxic included under this heading: heavy metals such as mercury, lead and iron. Mucoid change cells in this group of chemicals may not be the same cell that metabolised the toxin. This is the commonest and earliest form of cell 3 bolising P enzyme system in the liver cells. The common causes include 450 produces profound liver cell injury by free radical generation. Reversible cell injury Retrogressive changes Injuries caused by mechanical force are of medicolegal (older term: degenerations) significance. Irreversible cell injury Cell death?necrosis by changes in atmospheric pressure. Programmed cell death Apoptosis by accidental or therapeutic exposure is of importance in 4. Residual effects of Subcellular alterations treatment of persons with malignant tumours as well as may cell injury have carcinogenic influences (Chapter 8). Deranged cell metabolism Intracellular accumulation Killing of cells by ionising radiation is the result of direct of lipid, protein, carbohydrate formation of hydroxyl radicals from radiolysis of water 6. Intracellular hyaline is 35 such as bacterial toxins, chemicals, poisons, burns, high fever, mainly seen in epithelial cells. A few examples are as follows: intravenous administration of hypertonic glucose or saline 1. This results in intracellular accumulation of muscle loses its fibrillar staining and becomes glassy and sodium and escape of potassium. In addition, influx of filaments in the hepatocytes in alcoholic liver cell injury. Nuclear or cytoplasmic hyaline inclusions seen in some reversible change upon removal of the injurious agent. Grossly, the affected in the rough endoplasmic reticulum of the plasma cells organ such as kidney, liver, pancreas, or heart muscle is (Fig. Extracellular hyaline is seen Microscopically, it is characterised by the following in connective tissues. Hyaline arteriolosclerosis in renal vessels in hypertension distended cisternae of the endoplasmic reticulum. Corpora amylacea are rounded masses of concentric hya line laminae seen in the prostate in the elderly, in the brain Hyaline Change and in the spinal cord in old age, and in old infarcts of the lung. Hyaline is a descriptive histologic term for glassy, homogeneous, Mucoid Change eosinophilic appearance of material in haematoxylin and Mucus secreted by mucous glands is a combination of eosin-stained sections and does not refer to any specific proteins complexed with mucopolysaccharides. Though fibrin and amyloid have hyaline appear glycoprotein, is its chief constituent. Mucin is normally ance, they have distinctive features and staining reactions produced by epithelial cells of mucous membranes and and can be distinguished from non-specific hyaline material. The tubular epithelial cells are distended with cytoplasmic vacuoles while the interstitial vasculature is compressed. The cytoplasm shows pink homogeneous globular material due to accumulated immunoglobulins. The centres of whorls of smooth muscle and connective tissue show pink homogeneous hyaline material (connective tissue hyaline). These occur at the level of cytoskeleton, lysosomes, of cell injury in mitochondria may be seen in the following 37 endoplasmic reticulum and mitochondria: conditions: 1. Megamitochondria consisting of skeleton may show the following morphologic abnormalities: unusually big mitochondria are seen in alcoholic liver disease and nutritional deficiency conditions. Their In Chediak-Higashi syndrome characterised by poor number increases in hypertrophy and decreases in atrophy. This phenomenon was previously referred to as infiltration, implying thereby that something unusual iii) Accumulation of intermediate filaments: Various classes has infiltrated the cell from outside which is not always the of intermediate filaments (cytokeratin, desmin, vimentin, case. Intracellular accumulation of the substance in mild glial fibrillary acidic protein, and neurofilament) may degree causes reversible cell injury while more severe damage accumulate in the cytosol. Lysosomes contain powerful ii) Accumulation of abnormal substances produced as a result hydrolytic enzymes. Heterophagy and autophagy are the two of abnormal metabolism due to lack of some enzymes. Some indigestible exogenous degeneration and fatty infiltration because fatty change neither particles such as carbon or endogenous substances such as necessarily involves degeneration nor infiltration. The lipofuscin may persist in the lysosomes of the cells for a long deposit is in the cytosol and represents an absolute increase time as residual bodies. As discussed in Chapter 10, a group of but may occur in other non-fatty tissues like the heart, skeletal lysosomal storage diseases due to hereditary deficiency of muscle, kidneys (lipoid nephrosis or minimum change enzymes may result in abnormal collection of metabolites in disease) and other organs. Hypertrophy of smooth endoplasmic Liver is the commonest site for accumulation of fat because reticulum of liver cells as an adaptive change may occur in it plays central role in fat metabolism. Mitochondrial injury and reversible, or severe producing irreversible cell injury plays an important role in cell injury. Fatty change in the liver may result from one From diet as chylomicrons (containing triglycerides and of the two types of causes: phospholipids) and as free fatty acids; and 1. Conditions with excess fat (hyperlipidameia), exceeding the From adipose tissue as free fatty acids. Most of free fatty acid is esterified to triglycerides by the these causes are listed below: action of? Conditions with excess fat: changed into cholesterol, phospholipids and ketone bodies. Decreased conversion of fatty acids into ketone bodies ether, aflatoxins and other poisons) resulting in increased esterification of fatty acids to viii) Drug-induced liver cell injury. Mechanism of fatty liver depends upon in decreased formation of lipoprotein from triglycerides. Block in the excretion of lipoprotein from the liver into transport and metabolism. But in the case of liver cell injury by chronic Lipids as free acids enter the liver cell from either of the alcoholism, many factors are implicated which includes: following 2 sources: increased lipolysis; increased free fatty acid synthesis; decreased triglyceride utilisation; decreased fatty acid oxidation to ketone bodies; and block in lipoprotein excretion. Grossly, the liver in fatty change is enlarged with a tense, glistening capsule and rounded margins. The cut surface bulges slightly and is pale-yellow to yellow and is greasy to touch (Fig. Microscopically, characteristic feature is the presence of numerous lipid vacuoles in the cytoplasm of hepatocytes. Fat in H & E stained section prepared by paraffin embedding technique appear non-staining vauloes because it is dissolved in alcohol (Fig. Stromal Fatty Infiltration this form of lipid accumulation is quite different from fatty change just described. Stromal fatty infiltration is the deposition of mature adipose cells in the stromal connective tissue in contrast to intracellular deposition of fat in the parenchymal cells in fatty change. Thus, heart can be the site for intramyocardial fatty change as well as epicardial (stromal) fatty infiltration. The presence of mature adipose cells in the stroma generally does not produce any dysfunction.
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It is recommended monthly nine while additional data are gathered on artesunate during the rainy season for chemoprophylaxis in regions safety arizona pain treatment center reviews purchase artane overnight. Artemisinins-Artemisinin (qinghaosu) is a sesquiter? effective for both the treatment and chemoprophylaxis of pene lactone endoperoxide leg pain treatment youtube discount artane 2 mg free shipping, the active component of an falciparum malaria treatment of acute pain guidelines purchase artane 2mg without a prescription, and it is approved for both indications herbal medicine that has been used for various indications in the United States (Table 35-4) pain medication for dogs after dental surgery artane 2mg with amex. Unlike sized to increase solubility and improve antimalarial ef? most other antimalarials pain treatment for rheumatoid arthritis cheap artane on line, Malarone provides activity cacy pain medication for shingles discount artane 2 mg otc. The most important of these analogs are artesunate davis pain treatment center statesville nc purchase 2 mg artane otc, against both erythrocytic and hepatic stage parasites pain joint treatment order on line artane. It has an advantage over mefo? Artemisinins act very rapidly against al erythrocytic? quine and doxycycline in requiring shorter durations of stage human malaria parasites. Ofconcern, delayed clearance treatment before and after the period at risk for malaria of parasites and some clinical failures have been seen afer transmission, due to activity against liver-stage parasites. It treatment with artesunate in parts of Southeast Asia, herald? should be taken with food. Adverse effects Artemisinins are playing an increasing role in the treat? include abdominal pain, nausea, vomiting, diarrhea, head? ment of malaria, including multidrug-resistant P fa lci? ache, and rash, and these are more common with the parum malaria. Reversible elevations in half-lives, recrudescence rates are unacceptably high after liver enzymes have been reported. The safety of atova? short-course therapy, leading to use in conjunction with quone in pregnancy is unknown. None of the antibiotics should be used as plus lumefantrine (Coartem), each of which is available as single agents for the treatment of malaria due to their slow a coformulated product. Doxycycline is also a standard chemo? Southeast Asia, but recent studies have shown declining prophylactic drug, especially for use in areas of Southeast efficacy in Cambodia. Doxycycline side effects include In studies of severe malaria, intramuscular artemether gastrointestinal symptoms, candida! The drug should be taken while upright with a venous artesunate was superior to intravenous quinine in large amount of water to avoid esophageal irritation. Halofantrine and lumefantrine-Halofantrine, a are counseled on the prevention of malaria, it is imperative phenanthrene-methanol related to quinine, is effective to emphasize measures to prevent mosquito bites (insect against erythrocytic stages of all four human malaria spe? repellents, insecticides, and bed nets), since parasites are cies, but it is rarely used due to toxicity concerns. Chemoprophylaxis is available only as a fxed-dose combination with artemether recommended for all travelers from nonendemic regions to (Coartem or Riamet). Oral absorption is highly variable endemic areas, although risks vary greatly for different and improved when the drug is taken with food. Use of locations, and some tropical areas entail no risk; specifc Coartem with a fatty meal is recommended. Coartem is well tolerated; side effects the Caribbean and Central America west of the Panama include headache, dizziness, loss of appetite, gastrointesti? Canal), mefoquine or Malarone for most other malarious nal symptoms, and palpitations. Prevention to changing resistance patterns and increasing experience Malaria is transmitted by night-biting anopheline mosqui? with new drugs. Bed nets, in particular nets treated with permethrin priate for travelers to not use chemoprophylaxis but to insecticides, are heavily promoted as inexpensive means of carry supplies of drugs with them in case a febrile illness antimalarial protection, and improvement in mortality rates develops and medical attention is unavailable. Travelers to remote areas should consider carrying effective therapy (see text) for use if a febrile illness develops, and they cannot reach medical attention quickly. Malarone or mefloquine is currently recommended for other malarious areas except for border areas ofThailand, where doxycycline is recommended. Diagnosis and treatment of Plasmodium vivax ment practice in developing world populations due to the malaria. Delayed hemolysis after treatment with paren? sulfadoxine-pyrimethamine, provided once during both teral artesunate in African children with severe malaria-a the second and third trimesters, has improved pregnancy double-center prospective study. With increasing resistance the preventive infants and children in Africa: final results of a phase 3, indi? efficacy of sulfadoxine-pyrimethamine is likely falling, and vidually randomised, controlled trial. Dihydroartemisinin-piperaquine failure associ? ated with a triple mutant including kelch13 C580Yin Cambo? Sahel sub-region ofWest Africa, the policy is to administer dia: an observational cohort study. Malaria in pregnancy also increases the likelihood of poor pregnancy outcomes, with increased prematurity, low birth weight, and mortality. General Considerations Admission for non-falciparum malaria is only war? Babesiosis is an uncommon intraerythrocytic infection ranted if specific problems that require hospital man? caused mainly by two Babesia species and transmitted by agement are present. In the United States, hundreds of cases of Patients with falciparum malaria are generally admitted babesiosis have been reported, and infection is caused by because the disease can progress rapidly to severe illness; Babesia microti, which also infects wild mammals. Most exceptions may be made with individuals who are from babesiosis in the United States occurs in the coastal malaria-endemic areas, and thus expected to have a northeast, with some cases also in the upper midwest, degree of immunity, who are without evidence of severe following the geographic range ofthe vectorIxodes scapu? disease, and who are judged able to return promptly for laris, and Lyme disease and anaplasmosis, which are medical attention if their disease progresses. Spread ofartemisinin resistance in Plasmodium other Babesia-like organisms have been reported from fa lciparum malaria. Standard therapy for mild to moderate disease is a Serosurveys suggest that asymptomatic infections are 7-day course of atovaquone (750 mg orally every 12 hours) common in endemic areas. With B microti infections, plus azithromycin (600 mg orally once daily), which is symptoms appear 1 to severalweeks after a tick bite; para? equally effective and better tolerated than the alternative sitemia is evident after 2-4 weeks. Patients usually do not regimen, a 7-day course of quinine (650 mg orally three recall the tick bite. The typical fu-like illness develops times daily) plus clindamycin (600 mg orally three times gradually and is characterized by fever, fatigue, headache, daily). Other findings may include nau? plus clindamycin, and this regimen is recommended for sea, vomiting, abdominal pain, sore throat, depression, severe disease. Exchange transfusion has been used suc? emotional lability, anemia, thrombocytopenia, and sple? cessfully in severely ill asplenic patients and those with nomegaly. Severe complications are most likely to occur in older persons or in those who have had splenectomy. These infections progress rapidly with high fever, severe hemolytic anemia, jaundice, hemoglobinuria, and acute kidney injury, with death rates over 40%. Laboratory Findings gondii or identification of tachyzoites in tissue or Identifcation of the intraerythrocytic parasite on body fluids. Giemsa-stained blood smears establishes the diagnosis Primary infection (Figure 35-6). An indirect Congenital infection immunofuorescent antibody test for B microti is available. Reactivation leads to encephalitis, retinochoroidi? tis, pneumonitis, myocarditis. General Considerations T gondii, an obligate intracellular protozoan, is found worldwide in humans and in many species of mammals and birds. Humans are infected after ingestion of cysts in raw or undercooked meat, ingestion of oocysts in food or water contaminated by cats, transplacental transmission of trophozoites or, rarely, direct inoculation of trophozoites via blood trans? fusion or organ transplantation. It has decreased in the United States to 20-30% or less, but it is much higher in other countries in both the developed and developing worlds, where it may. Symptoms and Signs litis usually presents subacutely, with fever, headache, altered the clinical manifestations of toxoplasmosis may be mental status, fo cal neurologic fndings, and other evidence grouped into four syndromes. Chorioretinitis presents with ocular pain and After ingestion, T gondii infection progresses from the alterations in vision. Pneumonitis presents with fever, cough, gastrointestinal tract to lymphatics, and then dissemina? and dyspnea. About recipients of solid organ or bone marrow transplants due to 10-20% are symptomatic after an incubation period of reactivation or, more rarely, transmission of infection. Acute infections in immunocompetent persons tivation also can occur in those with hematologic malignan? typically present as mild, febrile illnesses that resemble cies or treated with immunosuppressive drugs. Nontender cervical or diffse primary or reactivated disease in those with immunodefi? lymphadenopathy may persist for weeks to months. Rare severe manifestations are pneumoni? tis, meningoencephalitis, hepatitis, myocarditis, polymyo? B. Symptoms may fuctuate, but most patients recover spontaneously within at most a few 1. The demonstration of tachyzoites indicates acute a result of infection, which may be syptomatic or asymp? infection; cysts may represent either acute or chronic infec? tomatic, in a nonimmune woman during pregnancy. With lymphadenopathy due to toxoplasmosis, exami? infection follows maternal infection in 30-50% of cases, but nation of lymph nodes usually does not show organisms. Serologic diagnosis-Multiple serologic methods are spontaneous abortion, stillbirths, or severe neonatal disease, used, including the Sabin-Feldman dye test, enzyme-linked including neurologic manifestations. Retinochoroiditis and other sight-threatening within 1-2 weeks of infection, and usually persist for life. Systemic fndings include fever or IgM antibodies peak earlier than IgG and decline more hypothermia, jaundice, vomiting, diarrhea, hepatospleno? rapidly, although they may persist for years. Infections later compromised individuals in whom reactivation is sus? in pregnancy less commonly lead to major fetal problems. The most common late presentation of congenital toxoplasmosis is retinochoroiditis. During pregnancy and in newborns-Conversion from a negative to positive serologic test or rising titers are sug? 3. Retinochoroiditis-This manifestation of congenital gestive of acute infection, but tests are not routinely per? toxoplasmosis presents weeks to years after congenital formed during pregnancy. Retino? screened, negative IgG and IgM assays exclude active infec? choroiditis also is seen in persons who acquire infection tion, but indicate the risk of infection during the preg? early in life, and these patients more often present with nancy. Disease presents highly suggestive of chronic infection, with no risk of with pain, photophobia, and visual changes, usually with? congenital disease unless the mother is severely immuno? out systemic symptoms. A positive IgM test is concerning for new improve, but visual defects may persist. In newborns, positive IgM Immunodeficient patients who are asymptomatic but have or IgA antibody tests are indicative of congenital infection, a positive IgG serologic test should receive long-term although the diagnosis is not ruled out by a negative test. Positive IgG assays may represent transfer ofmaternal anti? bodies without infection of the infant. In immunocompetent individuals-Individuals with a combination ofpyrimethamine (200 mg loading dose, then suggestive clinical syndrome should be tested for IgG and 50-75 mg [1 mg/kg] orally once daily) plus sulfadiazine IgM antibodies. Pyrimethamine side show characteristic morphology, with or without effects include headache and gastrointestinal symptoms. Even with folinic acid therapy, bone marrow suppression may occur; platelet and white blood cell counts should be 5. A first-line alternative is sistent with toxoplasmic encephalitis warrants imaging of clindamycin (600 mg orally four times daily) replacing the brain. Standard therapy for positive IgG serologic test and no recent antitoxoplasma or acute toxoplasmosis during pregnancy is spiramycin (1 g antiviral therapy, the predictive value of a typical imaging orally three times daily until delivery) to decrease the risk study is about 80%. The differential diagnosis also includes placenta, so when fetal infection is documented or for tuberculoma, bacterial brain abscess, fungal abscess, and acute infections late in pregnancy (which commonly lead carcinoma. Definitive diagnosis requires brain biopsy and search for organisms and typical histology. Prevention examination shows vitreous infammatory reaction, white Prevention of primary infection centers on avoidance of retinal lesions, and pigmented scars. Diagnosis of other undercooked meat or contact with material contaminated clinical entities in immunocompromised individuals is by cat feces, particularly for seronegative pregnant women generally based on histology. Treatment cleaning of hands and surfaces is needed after contact with raw meat or areas contaminated by cats. Approach to Treatment cat feces can remain infective for a year or more, but fresh Therapy is generally not necessary in immunocompetent oocysts are not infective for 48 hours. However, litter boxes should be changed daily and soaked in boiling for severe, persistent, or visceral disease, treatment for water for 5 minutes, gloves should be worn when garden? 2-4 weeks may be considered. Treatment is appropriate for ing, fruits and vegetables should be thoroughly washed, primary infection during pregnancy because the risk of and ingestion of dried meat should be avoided. For retinochoroiditis, most episodes are self? antibodies is conducted in some countries but not the limited, and opinions vary on indications for treatment. Pregnant women should ideally have their Treatment is often advocated for episodes with decreases in serum examined for IgG and IgM antibody, and those with visual acuity, multiple or large lesions, macular lesions, negative titers should adhere to the prevention measures signifcant inflammation, or persistence for over a month. Seronegative women who continue to Immunocompromised patients with active infection must have environmental exposure should undergo repeat sero? be treated. For those with transient immunodeficiency, logic screening several times during pregnancy. Trans? laxis to prevent primary or reactivated infection is war? mission occurs through ingestion of cysts from fecally con? ranted. Urban outbreaks have three times weekly), used for protection against Pneumo? occurred because of common-source water contamination. Intestinal amebiasis-In most infected persons, the organism lives as a commensal, and the carrier is without symptoms. Toxoplasma prophylaxis in haematopoietic cell within a week of infection, although an incubation period transplant recipients: a review of the literature and recom? of 2-4 weeks is more common, with gradual onset of mendations. Neglected parasitic infections in the United States: of remission and recurrence may last days to weeks or lon? toxoplasmosis. Severe presentations are more common in young children, pregnant women, those who are mal? nourished, and those receiving corticosteroids. Thus, in endemic regions, corticosteroids should not be started for presumed infammatory bowel disease without first ruling. Positive serologic tests with colitis or hepatic More chronic complications of intestinal amebiasis include abscess, but these may represent prior infections. Localized granulomatous lesions (amebomas) can pres? abdominal pain, with potential progression to ent after either dysentery or chronic intestinal infection. Hepatic abscess with fever, hepatomegaly, and hemorrhage and may suggest intestinal carcinoma. Extraintestinal amebiasis-The most common extrain? testinal manifestation is amebic liver abscess. Patients present with the acute or gradual onset of abdominal pain, fever, an the Entamoeba complex contains three morphologically enlarged and tender liver, anorexia, and weight loss. Diar? identical species: Entamoeba dispar and Entamoeba mosh? rhea is present in a small number of patients. Physical kovskii, which are avirulent, and Entamoeba histolytica, examination may show intercostal tenderness. Abscesses which may be an avirulent intestinal commensal or lead to are most commonly single and in the right lobe of the liver, serious disease. Without prompt nal wall, resulting in diarrhea, and with severe involve? treatment, amebic abscesses may rupture into the pleural, ment, dysentery or extraintestinal disease, most commonly peritoneal, or pericardia! Of the estimated 500 million persons worldwide infected with Entamoeba, most are infected with E dispar Laboratory studies with intestinal amebiasis show leukocy? and an estimated 10% with E histolytica. The prevalence of tosis and hematochezia, with fecal leukocytes not present E moshkovskii is unknown. With extraintestinal amebiasis, leukocytosis ly tica infections is estimated at 100,000 per year. Diagnostic Testing leading to peritonitis from amebas or other (pyogenic or echinococcal) organisms. Stool evaluation for organ? most commonly single, but more than one may be present. Multiple serologic assays are available; these tests are fairly sensitive, although sensitivity. Treatment is lower (-70% in colitis) early in illness, and they cannot Treatment of amebiasis generally entails the use of metroni? distinguish recent and old disease, as they remain positive dazole or tinidazole to eradicate tissue trophozoites and a for years after infection. A commercially available stool luminal amebicide to eradicate intestinal cysts (Table 35-6). Colonoscopy of uncleansed bowel typi? E disparcolonization is likely, and treatment is not indicated. Effective luminal agents are diloxanide ing friable mucosa, resembling infammatory bowel dis? furoate (500 mg orally three times daily with meals for ease (Figure 35-7). Examination of fresh ulcer exudate for 10 days), iodoquinol (diiodohydroxyquin; 650 mg orally motile trophozoites and for E histolytica antigen may yield three times daily for 21 days), and paromomycin (30 mg/kg a diagnosis. Side effects associated with luminal agents bodies are almost always positive, except very early in the are fatulence with diloxanide froate, mild diarrhea with infection. Thus, a negative test in a suspicious case should iodoquinol, and gastrointestinal symptoms with paromomy? be repeated in about a week. Relative contraindications are thyoid disease for iodo? can be used to test serum, with good sensitivity if used quinol and kidney disease for iodoquinol or paromomycin. Examination of stools for Treatment of intestinal amebiasis requires metronida? organisms or antigen is frequently negative; the antigen test zole (750 mg orally three times daily for 10 days) or tinida? is positive in -40% of cases. As imaging studies cannot zole (2 g orally once daily for 3 days for mild disease and distinguish amebic and pyogenic abscesses, when a diagno? 5 days for serious disease) plus a luminal agent (Table 35-6). Metronidazole often induces transient nausea, Detection of organisms in the aspirate is uncommon, but vomiting, epigastric discomfort, headache, or a metallic detection ofE histolytica antigen is very sensitive and diag? taste. The same toxicities and con? cerns probably apply for tinidazole, although it appears to be better tolerated. Fluid and electrolyte replacement is also important for patients with signifcant diarrhea. Surgical management of acute complications of intestinal amebiasis is best avoided whenever possible. Successful therapy of severe amebic colitis may be followed by postdysenteric colitis, with continued diarrhea without persistent infec? tion; this syndrome generally resolves in weeks to months. Alternatives for the treatment of intestinal amebiasis are tetracycline (250-500 mg orally four times daily for 10 days) plus chloroquine (500 mg orally daily for 7 days). Emetine or dehydroemetine, which are not available in the United States, can be given subcutaneously or intramuscularly in a dose of 1-1. Gross pathology showing intestinal are effective but cardiotoxic with a narrow therapeutic range ulcers dueto amebiasis. Outbreaks of diarrhea secondary to contaminated human feces; adequate cooking of food; protection of food water or food. Diagnosis mostly by identifing organisms in spe? cysts are resistant to standard concentrations of chlorine), cially stained stool specimens. These infec? of highly active antiretroviral therapy, particularly with tions occur worldwide, particularly in the tropics and in advanced immunosuppression. Theyare causes of endemic variable, but patients commonly have chronic diarrhea childhood gastroenteritis (particularly in malnourished with frequent foul smelling stools, malabsorption, and children in developing countries); institutional and com? weight loss.
