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By Z. Ugo. Cypress College. 2019.

Venom-induced coagulopathy and thrombocytopenia may recur anytime up to 14 days after the last dose of antivenom [30] 2.5mg tadalafil otc, and fatal intracranial bleeding and other cases of major delayed bleeding have been reported [31 tadalafil 20 mg visa,32] buy tadalafil 10 mg line. If on follow-up there is evidence of clinically significant bleeding cheap 10 mg tadalafil amex, if the laboratory coagulopathy 3 is worsening or severe (i. The major reasons for poor outcomes in pit viper envenomation are delay in presentation, inadequate fluid resuscitation, inappropriate use of vasopressors, and delay in administration or inadequate dosing of antivenom [35]. The incidence of upper-extremity functional disability after pit viper envenomation is at least 32% [36], and may be higher when careful, objective functional measurements are obtained [37]. Coral Snake Envenomation There are fewer than 100 coral snake bites reported in the United States each year [38]. Owing to their much less effective venom-delivery mechanism (small fangs fixed in an upright position on the anterior maxillae), only approximately 40% of coral snake bites result in envenomation [1,40], although it has been estimated that one large coral snake is capable of delivering enough venom to kill four to five humans [41]. In the United States, it appears that the severity of envenomation tends to be greatest with the eastern coral snake (M. Low-molecular-weight polypeptides in the venom are capable of inducing nondepolarizing, postsynaptic blockade at neuromuscular junctions [43]. There are few local findings at the bite site, and the onset of systemic symptoms may be delayed for many hours [40,44]. Fang marks may be small and difficult to detect [45], with variable pain and little swelling at the site [44]. The patient may experience local paresthesias that may radiate proximally and be associated with muscle fasciculations [44]. Bulbar-type paralysis can occur as early as 90 minutes after the bite and progress to peripheral paralysis [1]. Findings may include extraocular muscle paresis, ptosis, pinpoint pupils, dysphagia, dysphonia, slurred speech, and laryngeal spasm [40,44]. Death from coral snake envenomation has been reported because of respiratory failure or cardiovascular collapse [1]. In areas where coral snakes coexist with harmless coral snake mimics, such as milk snakes (Lampropeltis spp), it is helpful if the color pattern of the offending snake can be reliably obtained or, better yet, if the victim can produce a digital photo of the offending reptile. The differential diagnosis of coral snake envenomation is usually limited to bites by other brightly colored, nonvenomous snakes. In the harmless coral snake mimics, the red and yellow bands are separated by black bands, and the bands do not completely encircle the body. In Australia, where all native venomous snakes are elapid relatives of the coral snake, a potentially beneficial first-aid intervention is use of a pressure-immobilization wrap. In this technique, the entire bitten extremity is firmly wrapped with an elastic or crepe bandage and splinted [48]. The wrap is applied snuggly—as tightly as for a sprained ankle [48]—and it is important that the extremity be kept as immobile as possible and the patient carried to medical care [49]. One small animal study has demonstrated apparent benefit of the technique in prolonging survival following coral snake venom injection [50]. As with pit viper bites, attention is initially directed to the patient’s airway, breathing, and circulatory status. Impending respiratory failure is suggested by cyanosis, trismus, laryngeal or pharyngeal spasm, increased salivation, or any sign of cranial nerve paralysis [44]. Once the airway and respiratory status are addressed, a more complete physical examination is performed. Antivenom Therapy As with most venomous snakebites, definitive management of significant Micrurus bites should center on the use of appropriate antivenom. Administer antivenom to any patient clearly bitten by an eastern coral snake (Micrurus fulvius) specimen, even in the absence of signs or symptoms, because once signs or symptoms appear, it may be difficult to reverse or halt their progression [40,44]. There is no antivenom for the Sonoran coral snake (Micruroides euryxanthus), but the venom of this snake is much less toxic, and there have been no reported deaths after its bite [1,46]. Airway protection and ventilatory support may be required for days following Micrurus bites [44], but with modern intensive care, the prognosis should be good. Wound Care The wounds from a coral snake bite should be washed with a germicidal solution and tetanus prophylaxis updated as necessary. Disposition and Outcome All patients with potential coral snake bites should be admitted to an intensive care unit for at least 24 hours for close monitoring regardless of symptoms or antivenom requirement [51]. Exotic (Imported) Snake Envenomation Exotic venomous snakes are commonly kept in zoos, museums, and sometimes by private individuals in “underground zoos. If a patient has been bitten by an exotic venomous snake, every effort should be made to definitively identify the reptile. The treating physician should then call a regional poison control center for assistance (1-800-222-1222). These centers have access to a national listing of available sources of exotic antivenoms in stock in the United States. Antivenoms tend to be quite specific for the species against which they protect, and should be used only if there is clear evidence of their efficacy against the offending species. Sound supportive care, combined with an appropriate antivenom when available, should offer the best chances of an optimal outcome. Widow Spider Envenomation Of five known species of widow spider in the United States, the black widows (Latrodectus mactans, L. The female black widow is dark black and oval shaped, with a characteristic, typically hourglass-shaped, ventral red, orange, or yellow marking on the abdomen. Widow spiders are found in all of the 48 contiguous states and Hawaii [53], and are responsible for most of the exceedingly rare spider-related deaths in North America. Only the female is dangerous to humans; the male, a nondescript and much smaller brown spider, is incapable of delivering a bite through human skin. The most deleterious venom component is alpha-latrotoxin, a potent neurotoxin that acts primarily at the neuromuscular junction [54]. The venom initially stimulates the release of neurotransmitters (acetylcholine, epinephrine, and norepinephrine) and then blocks neurotransmission by depleting synaptic vesicles [55,56]. Clinical Manifestations The widow spider’s bite may be unnoticed by the patient or may be felt as a sharp sting [55]. The bite site may be visible, with tiny fang marks approximately 1 mm apart, and the area may be slightly warm and blanched with a surrounding erythematous, indurated zone [58]. It begins at the bite site as a dull ache and spreads first to local muscle groups and then to larger regional muscle groups of the abdomen, back, chest, pelvis, and lower extremities. In patients at risk, the hypertension can lead to cerebrovascular accidents, exacerbation of congestive heart failure, and myocardial ischemia [55]. Cardiac dysrhythmias and priapism have been reported, and there are extremely rare cases of myocarditis [58,63]. Associated signs or symptoms include diaphoresis (local or diffuse; possibly asymmetrical), fever, headache, nausea and vomiting, restlessness and anxiety, periorbital edema, and skin rash [58,60,64]. Diagnostic Evaluation The history surrounding a widow spider bite is confusing if a spider was not seen. It is important to obtain a medical history, such as hypertension, pregnancy status, allergies, and tetanus immunization status.

Paul M discount tadalafil 2.5 mg overnight delivery, Grozinsky-Glasberg S buy tadalafil 20mg visa, Soares-Weiser K cheap 20 mg tadalafil otc, et al: Beta-lactam versus beta-lactam-aminoglycoside combination therapy in cancer patients with neutropenia discount tadalafil 5 mg online. Martino R, Viscoli C: Empirical antifungal therapy in patients with neutropenia and persistent or recurrent fever of unknown origin. Shaukat A, Bakri F, Young P, et al: Invasive filamentous fungal infections in allogeneic hematopoietic stem cell transplant recipients after recovery from neutropenia: clinical, radiologic, and pathologic characteristics. Singh N: Trends in the epidemiology of opportunistic fungal infections: predisposing factors and the impact of antimicrobial use practices. Weisser M, Rausch C, Droll A, et al: Galactomannan does not precede major signs on a pulmonary computerized tomographic scan suggestive of invasive aspergillosis in patients with hematological malignancies. Ellis M, Al-Ramadi B, Finkelman M, et al: Assessment of the clinical utility of serial beta-D-glucan concentrations in patients with persistent neutropenic fever. Cordonnier C, Ribaud P, Herbrecht R, et al: Prognostic factors for death due to invasive aspergillosis after hematopoietic stem cell transplantation: a 1-year retrospective study of consecutive patients at French transplantation centers. Wiesmayr S, Stelzmueller I, Tabarelli W, et al: Nocardiosis following solid organ transplantation: a single-centre experience. Bucaneve G, Micozzi A, Menichetti F, et al: Levofloxacin to prevent bacterial infection in patients with cancer and neutropenia. Paul M, Borok S, Fraser A, et al: Empirical antibiotics against Gram- positive infections for febrile neutropenia: systematic review and meta-analysis of randomized controlled trials. More recently, death rates have shown a more gradual decline, and were estimated at around 14,000 in 2012 [1]. The improved prognosis in the United States and the developed nations is hampered by limitations to diagnosis and care. Moreover, improvements of care and survival observed among developed nations still stand in sharp contrast to the global epidemic. Other radiographic findings include pneumatoceles, pneumothorax, nodules, lobar consolidation, and normal images [22]. The diagnosis can be confirmed only by identifying the organism in specimens obtained from the respiratory tract, either in sputum induced by inhalation of hypertonic saline or by bronchoscopy. A decision-analysis model and a retrospective study comparing these two strategies suggest that the outcomes are similar, but no clinical trial has ever evaluated whether initial empiric therapy or a more aggressive diagnostic strategy that includes bronchoscopy is preferable [23,24]. As the disease progresses and pulmonary compliance diminishes, pneumothorax is common and is associated with a particularly poor prognosis [28,29]. Corticosteroids may attenuate lung injury caused by the inflammatory response to killed organisms, allowing the patient to survive to receive more antimicrobial therapy. Corticosteroids offer no benefit for patients with less severe abnormalities in gas exchange at the start of therapy, or in whom they are administered more than 72 hours after anti-Pneumocystis treatment has begun. In patients with severe immune compromise, pulmonary infection or disseminated disease with Pseudomonas aeruginosa, Mycobacterium tuberculosis, cytomegalovirus, endemic fungi, and Aspergillus spp may also lead to respiratory failure [38]. Similarly, influenza-related morbidity and mortality are increased in severely immunocompromised patients. Treatment for severe disease is complicated by the tendency for elevated intracerebral pressure to develop. Treatment occurs in stages; the first stage is induction (duration ≥ 2 weeks), which involves infusion of an amphotericin B formulation together with oral flucytosine [44,45]. Focal encephalitis caused by Toxoplasma gondii most often presents with headache, altered mental status, seizures, and focal neurologic signs [49], occasionally requiring intensive care management. Adjunctive corticosteroids and/or anticonvulsants (see Chapters 81 and 151) may be needed in individuals with significant mass effect and/or presentation with seizures. Close monitoring and administration of corticosteroids may be required if there is paradoxical worsening of neurologic function. Treatment with these agents may be associated with exacerbation of liver dysfunction and decompensation, particularly in individuals with advanced stages of cirrhosis (http://www. Alternatively, patients with an unrecognized infection, not yet manifested clinically, may develop an inflammatory reaction at the infected site (so-called unmasking). Corticosteroids may be used to suppress the aberrant inflammatory reaction, but there are no guidelines as to when to use them or the optimal dose and duration. Laboratory abnormalities, including pancytopenia, eosinophilia, and transaminase elevations, may either represent the patient’s baseline or indicate significant disease or drug toxicity. Among laboratory abnormalities that may safely be followed are macrocytosis as a normal accompaniment of zidovudine, stavudine, or tenofovir therapy (provided there are no hypersegmented polymorphonuclear leukocytes), mild indirect hyperbilirubinemia of patients on atazanavir or indinavir, and hyperuricemia of patients taking didanosine. Elevations of creatine phosphokinase in patients taking zidovudine or tenofovir may also be asymptomatic and benign, but some reflect clinical myositis caused by these drugs. Patients who received this drug even many years before may present with life-threatening hemorrhage from esophageal varices. Lactic acidosis is the consequence of increased anaerobic glycolysis by damaged mitochondria, coupled with decreased lactate clearance by the fatty liver. The appearance of nausea, vomiting, abdominal pain, dyspnea, or weakness in persons on long-term therapy with these agents may herald the onset of this life-threatening illness and should prompt measurement of serum lactate. Because patients may also develop severe lactic acidosis as a result of sepsis, empiric antibiotics should be administered, pending the results of microbiologic evaluations. In addition to standard care, case reports suggest that this disorder may improve with use of riboflavin, thiamine, L-carnitine, and coenzyme Q [73–75]. The same drugs and mechanism underlie a syndrome of severe neuromuscular weakness and respiratory failure that may mimic Guillain–Barré syndrome or botulism, and the same therapies have been proposed [76]. Abacavir hypersensitivity is a protean syndrome that may include fever, chills, nausea, diarrhea, rash, myalgia, aseptic meningitis, hepatitis, cough, or influenza-like illness within a few weeks of starting treatment. Discontinuation of the drug leads to resolution of symptoms, but rechallenge can produce an anaphylactic reaction with cardiovascular collapse and high fever [77,78]. Tenofovir nephrotoxicity rarely presents as Fanconi syndrome; with increases in serum creatinine, glycosuria, hypophosphatemia, and acute tubular necrosis. Electrolyte imbalance because of tubular dysfunction may be severe and require intensive repletion [81]. The critical care clinician is well-advised to manage these patients in close collaboration with an expert in antiretroviral treatment. When the gastrointestinal tract is significantly dysfunctional, all of the drugs in a patient’s regimen will inevitably be stopped at the same time, and no harm is likely if they can be resumed in a few days. For example, administration of proton-pump inhibitors causes significant reductions in the protease inhibitor atazanavir; an H2 blocker can be given safely 12 hours before or after atazanavir. The presence of acute kidney injury necessitates dose adjustments of all the nucleoside analogs except abacavir, and the components of fixed- dose combinations require individual adjustments. If renal function varies or is impaired for several days, the best way to assure consistently adequate and nontoxic levels of antiretrovirals is to change the regimen to drugs that do not require adjustment for renal insufficiency, when possible. First, is the enteral route expected to remain available to permit consistent and continuous drug administration?

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Currently there are insufficient safety and tolerability data on Severe life-threatening malaria is nearly always due to mefloquine at its recommended dosage of 25 mg/kg body weight in P generic tadalafil 20mg online. Mefloquine shares cross resistance with quinine which is still an effective drug in our country discount tadalafil 5 mg with visa. Health planners of our country do to be treated in the same line of complicated malaria not advocate use of mefloquine generic 2.5mg tadalafil fast delivery. Advantage of artemether lumefantrine combination is that High degree of suspicion of severe malaria is of utmost lumefantrine is not available as monotherapy and has never been importance and any delay in initiation of treatment can used alone for the treatment of malaria order 20 mg tadalafil with visa. Lumefantrine absorption is enhanced by co-administration with fatty food like milk. Confirmation of the diagnosis is preferable but Drug sensitivity Recommended treatment one should not delay the treatment if it needs more than P. All these three interventions hours (total dose 25 mg base/kg) are equally important and to be taken care of simultaneously. In case of vivax malaria to prevent relapse primaquine should be given in a dose of 0. Chloroquine should not be given in empty stomach and in high the patient antimalarials should be given according to the fever. A single dose of deficiency, they should preferably be screened for the same prior primaquine (0. Clindamycin 20 mg/kg/day in 2 divided doses Then 12 hours after the start of loading dose give a for 7 days maintenance dose of 10 mg salt/kg over 2 hours. Doxycycline is preferred to tetracycline as it can be given once daily clindamycin is added to quinine as soon as the patient is and does not accumulate in renal failure. The dose of quinine should be divided between two sites, half the dose in each anterior thigh. Tetracycline or doxycycline pump over 30 minutes, followed immediately by 10 mg or clindamycin should be added as above. Artemisinin are the most rapidly acting of all known • If there is no clinical improvement after 48 hours of antimalarial drugs, they often produce a 10,000 fold parenteral therapy the maintenance dose of quinine reduction of parasites per asexual cycle. Thus they can stop parasite • Quinine should not be given subcutaneously as this maturation, particularly from the less pathogenic may cause skin necrosis. Convulsions may be supportive management very subtle with nystagmus, salivation or twitching of an isolated part of the body. Effort should be given to exclude • Rapid clinical assessment with respect to level of other treatable causes of coma (e. Patients should be given good nursing care, pressure, rate and depth of respiration, anemia, state of convulsions should be treated with diazepam/midazolam hydration and temperature. Children with hyperparasitemia due to acute destruction • Oxygen therapy and respiratory support should be of red cells may develop severe anemia. Also maintain intake output chart and watch for Deep breathing with indrawing of lower chest wall without hemoglobinuria. Correct Blood smear examination every 6–12 hours for hypovolemia, treat anemia and prevent seizures. Asexual parasitemia generally disappears after 72 hours It is common in children below 3 years especially with of therapy. It also occurs in • In case of quinine parasite count may remain patients treated with quinine. Manifestations are similar unchanged or even rise in first 18–24 hours which to those of cerebral malaria so it can be easily overlooked. However, parasite count should fall after blood glucose are not available assume hypoglycemia 24 hours of quinine therapy and should disappear in symptomatic patient and treat accordingly. Of the various complications of falciparum malaria the bibliography common and important ones in children are as follows: 1. Guidelines for Diagnosis and Treatment of Malaria in India • Respiratory distress (acidosis) 2009. This may affect viscera, skin or mucous membranes caused organism is capable of producing rapid tissue destruction by infection due to parasites of genus Leishmania. In India, etiological agent is a protozoal parasite, Leishmania The diagnosis of kala-azar is usually clear from clinical donovani, a hemoflagellate. Parasitization of reticuloendothelial differentiated from tropical splenomegaly, malaria, system, such as spleen, liver, lymph node and bone marrow, Hodgkin disease, leukemia, tuberculosis and hemolytic accounts for the salient features of the disease. When the onset is typhoid-like, kala-azar should be differentiated from enteric fever, septicemia, miliary epidemiology tuberculosis, brucellosis and hepatic amebiasis. Kala-azar Kala-azar is distributed worldwide with about 12 million with malaria-like onset needs differentiation from malaria, people infected and about 1. In India, it is endemic in Bihar, West Bengal, Orissa, Assam, Sikkim Laboratory diagnosis and eastern Uttar Pradesh but sporadic cases have been reported from different parts of the country. Human beings are bone marrow, spleen, liver and lymph node aspirates or the only reservoir of infection in India. The splenic aspiration or less confined to rural areas, especially those along rivers and smear examination is the most sensitive (95–98%) (Ganga-Brahmaputra) and lakes. Bone marrow aspiration is usually without any risk and positive in 75–85% clinical features of cases. Lymph node aspiration and liver biopsy are positive The incubation period is 2–6 months but there may be wide in 60% and 50% of cases, respectively. A large majority in kala-azar usually shows anemia, thrombocytopenia, of the cases have insidious onset though acute onset may leukopenia with neutropenia, marked eosinopenia and rarely be seen with high fever and rapidly enlarging spleen. Fever, serological Tests hepatosplenomegaly and pallor are seen in more than 95% • aldehyde test (Napier test):It is simple and non-specific of cases. The increase in immunoglobulin skin, polymorphic waxy non-ulcerating nodules and sparse, is the basis of this test. The sensitivity of this test is falling and brittle hairs are the additional manifestations. Rarely it may present as bleeding; may occur in children with cirrhosis, malaria and multiple epistaxis, hematemesis, melena and retinal hemorrhage. In this test, 1 or 2 drops of formalin (40%) are The serious complications may occur in kala-azar added to 1–2 mL of patient’s serum in a test tube. The and include pneumonia, dysentery, severe hemorrhage, egg white jellification of serum with opacification within agranulocytosis, acute glomerulonephritis, amyloidosis, 2–20 minutes indicates strongly positive reaction, and 226 papilledema, jaundice and cancrum oris. Some authors recommend this drug as first line anti- the disease during and after therapy. It a phosphocholine analog which was developed as anti- is simple, cheap and effective. A titer of 1:1600 or above malignant drug has shown to be highly active against is taken as positive.

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These methods usually provide retrospective confirmation of the diagnosis tadalafil 2.5mg lowest price, and although this is important for accurate epidemiologic surveillance buy tadalafil 5mg lowest price, these tests do not help in clinical decision-making at the point of care cheap tadalafil 20mg without a prescription. A single elevated immunoglobin M (IgM) antibody titer is likely not helpful discount 10mg tadalafil with amex, either, because false positives can occur [113]. Most broad-spectrum antibacterial agents such as cephalosporins, penicillins, and sulfa drugs are inactive against R. The treatment of choice for nonpregnant adults and children weighing more than 45 kg is doxycycline [116], 100 mg twice daily for 7 to 10 days. The risk of dental staining by tetracyclines in children is small for short courses of therapy; this consideration should not delay treatment [118]. Therapy of pregnant women is problematic because tetracyclines are associated with maternal hepatotoxicity and fluorescent yellow discoloration of fetal deciduous teeth. Calcification of permanent teeth does not begin until after birth; discoloration of permanent teeth would not be expected. Although teratogenicity has not been proven with chloramphenicol, maternal aplastic anemia or reversible bone marrow suppression may occur. Gray baby syndrome has occurred in neonates treated with chloramphenicol, and may occur in infants born to women treated with chloramphenicol near term. Most authorities recommend therapy of pregnant women in the first or second trimester with chloramphenicol, 50 to 75 mg/kg/d in divided doses. Corticosteroid therapy has not been studied in a controlled manner, although older literature has recommended it for patients with widespread vasculitis and encephalitis [122]. Risk factors for mortality include central nervous system involvement, renal dysfunction at presentation, a delay in the institution of therapy, therapy with an agent other than a tetracycline [116], and increased age. Several of these diseases are discussed briefly below and others are discussed in other chapters, such as serious epidemic viral pneumonias (Chapter 83) and biologic agents of mass destruction (Chapter 130). Ehrlichiosis and anaplasmosis are tick-borne Rickettsial diseases that present as a fever with few localizing symptoms or signs. Headache, myalgias, malaise, and rigors are seen in nearly all cases; gastrointestinal or respiratory symptoms may occur in a minority of cases [125]. It is found in the same geographic areas as babesiosis and Lyme disease and transmitted by Ixodes scapularis and by Ixodes pacificus, the same ticks that transmit Borrelia burgdorferi and Babesia species. Ehrlichia ewingii infection has been reported to cause a granulocytic ehrlichiosis in the Southeastern United States, primarily in immunocompromised hosts [115]. In contrast to most tick-borne illnesses, ehrlichiosis and anaplasmosis are more frequently seen in middle-aged and older individuals [126,127]. Cases most often present in spring and summer, but have been reported in every month of the year [126]. Leukocyte counts are generally low or normal with a shift to immature forms; elevated transaminases and thrombocytopenia are typically found if patients are followed carefully [125,127]. The diagnosis may be confirmed by the observation of clumps of organisms within leukocytes, termed morulae, but the sensitivity of microscopy in the first week of illness is only 60%, even in very experienced hands [127]. Cases have been reported in association with cat bites and with nontraumatic exposure to the oral secretions of dogs. Several other species of the Capnocytophaga genus are normal oral flora of humans, and may cause bacteremia in the setting of cancer chemotherapy [132,133]. Ampicillin-sulbactam is a good empiric choice for serious soft tissue infection when there is a history of a dog bite. Clindamycin can be used for culture-proven cases of monomicrobial infection with Capnocytophaga in the case of penicillin allergy [132], but it is not active against Pasteurella multocida, which is a common pathogen in cases of dog or cat bites. Hashikawa S, Iinuma Y, Furushita M, et al: Characterization of group C and G streptococcal strains that cause streptococcal toxic shock syndrome. Jamart S, Denis O, Deplano A, et al: Methicillin-resistant Staphylococcus aureus toxic shock syndrome. Takahashi N, Imanishi K, Uchiyama T: Overall picture of an emerging neonatal infectious disease induced by a superantigenic exotoxin mainly produced by methicillin-resistant Staphylococcus aureus. Durand G, Bes M, Meugnier H, et al: Detection of new methicillin- resistant Staphylococcus aureus clones containing the toxic shock syndrome toxin 1 gene responsible for hospital- and community- acquired infections in France. Zimbelman J, Palmer A, Todd J: Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection. Kaul R, McGeer A, Norrby-Teglund A, et al: Intravenous immunoglobulin therapy for streptococcal toxic shock syndrome—a comparative observational study. Linner A, Darenberg J, Sjolin J, et al: Clinical efficacy of polyspecific intravenous immunoglobulin therapy in patients with streptococcal toxic shock syndrome: a comparative observational study. Darenberg J, Ihendyane N, Sjolin J, et al: Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial. Prevention of Invasive Group A Streptococcal Infections Workshop Participants: Prevention of invasive group A streptococcal disease among household contacts of case patients and among postpartum and postsurgical patients: recommendations from the Centers for Disease Control and Prevention. Sinave C, Le Templier G, Blouin D, et al: Toxic shock syndrome due to Clostridium sordellii: a dramatic postpartum and postabortion disease. Fischer M, Bhatnagar J, Guarner J, et al: Fatal toxic shock syndrome associated with Clostridium sordellii after medical abortion. Booy R, Habibi P, Nadel S, et al: Reduction in case fatality rate from meningococcal disease associated with improved healthcare delivery. Sakran W, Raz R, Levi Y, et al: Campylobacter bacteremia and pneumonia in two splenectomized patients. Working Party of the British Committee for Standards in Haematology Clinical Haematology Task Force: Guidelines for the prevention and treatment of infection in patients with an absent or dysfunctional spleen. Bruneel F, Hocqueloux L, Alberti C, et al: The clinical spectrum of severe imported falciparum malaria in the intensive care unit: report of 188 cases in adults. Dondorp A, Nosten F, Stepniewska K, et al; South East Asian Quinine Artesunate Malaria Trial group: Artesunate versus quinine for treatment of severe falciparum malaria: a randomised trial. Butler T: Capnocytophaga canimorsus: an emerging cause of sepsis, meningitis, and post-splenectomy infection after dog bites. However, patients with autoimmune diseases, neoplasia, or transplantation become highly susceptible to infection by virtue of their associated therapies or by the nature of their underlying illness. Infection has been and remains a leading cause of death among patients with leukemia and lymphoma and a major cause of morbidity and mortality in patients with solid tumors or transplants [1–4]. Rapid progression of fungal, bacterial, and mycobacterial infections occurs in patients given monoclonal antibodies to treat Crohn’s disease and autoimmune diseases such as rheumatoid arthritis [5–7]. Traditionally, infection has accounted for up to 75% of deaths in patients with acute leukemia or Hodgkin’s disease [1,8] or in transplant recipients [3,9], but with advances in prophylaxis and management, deaths because of infections have decreased to about 50%, whereas death owing to graft versus host disease, relapse of malignancy, and multiorgan failure have increased [10–13]. Although a great variety of microorganisms have been noted to cause severe, life-threatening infections in immunocompromised hosts, the clinician can formulate a diagnostic plan and decide on empiric therapy by giving careful consideration to the nature, duration, and severity of the immunosuppression that is causing the patient’s predisposition to infection. Infection can arise as a consequence of derangements in host defenses that result from the primary disease, the medical and surgical treatment of the condition, or a combination of these factors. Additionally, immunocompromised patients are likely to manifest their infections in ways that are characteristically different from those of patients with intact immune responses. A level of suspicion of infection with certain organisms depends on the specific immune defect, the duration of immunosuppression, surgical and medical interventions, colonization with nosocomial pathogens, and previous latent or asymptomatic infections that may reactivate after immunosuppression.

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