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An exception to the idea that “pathogenesis always starts with oropharyngeal colonization” is the case of infection by Pseudomonas spp buy 40 mg paxil with mastercard. Thus paxil 30mg sale, the findings of several studies have indicated that tracheal colonization by these pathogens may occur without previous oropharyngeal colonization (42–44). One prospective observational study evaluated 158,519 patients admitted to a single center over a four-year period (46). An existing high incidence of resistance to antibiotics in the hospital area or unit 4. Stay in a nursing home or an extended care facility Nosocomial Pneumonia in Critical Care 181 c. The detection of an increased load of oropharyngeal commensals (viridans group strepto- cocci, coagulase-negative staphylococci, and Corynebacterium spp. The authors of this study highlighted that the anaerobes recovered mirrored the bacteriology of the oropharynx and that only in four patients were they the only microorganisms isolated. No anaerobic bacterium was found in the blood or associated with necrotizing disease. Early-onset and late-onset disease can be distinguished using quantitative culture methods of diagnosis. When pneumonia develops within four or five days of admission (or intubation), microorganisms associated with community-acquired pneumonia are isolated with some frequency. In contrast, when disease develops after five days, few pathogens associated with community-acquired pneumonia are recovered, and gram-negative bacilli and S. Although indicators of late-onset disease, these bacteria can also cause early-onset pneumonia, especially in patients with severe comorbidities under recent antimicrobial treatment, making it more difficult to distinguish between early-onset and late-onset disease. Fungal or viral pathogens are rarely the causative agents in immunocompetent patients. Influenza, parainfluenza, adenovirus, and respiratory syncitial virus account for 70% of all nosocomial viral pneumonias. The diagnosis of these viral infections is often made by rapid antigen testing and viral cultures or serological assays. Within the categories described, the causes of nosocomial pneumonia also vary considerably according to geographic, temporal, and intra-hospital factors. In these subjects, respiratory tract function is impaired, lung volume is diminished, and airway clearance may be reduced. Trauma, surgery, medications, and respiratory therapy devices may additionally impair the capacity of the lungs to ward off infection. Notwithstanding, the most significant risk factor for nosocomial pneumonia is mechan- ical ventilation. In effect, the terms “nosocomial pneumonia” and “ventilator-associated pneumonia” are often used interchangeably. It has been described that when an endotracheal tube is introduced, many lines of host defense are bypassed, such that microorganisms gain direct access to the lower respiratory tract (26,83,87,89). Further, as the tube is inserted, possible damage to the tracheal mucosa will allow pathogens to achieve a foothold. Key components are (i) ensuring staff education and infection surveillance, (ii)preventing the transmission of microorganisms, and (iii) modifying host risk factors for infection. Effective infection-control measures, hand hygiene, and patient isolation to reduce cross- infections are routine mandatory practices (2,33,96,112,122). Senior management is accountable for ensuring that an adequate number of trained personnel are assigned to the infection prevention and control program 3. Senior management is accountable for ensuring that healthcare personnel, including licensed and nonlicensed personnel, are competent to perform their job responsibilities. Direct healthcare providers (physicians, nurses, aides and therapists) and ancillary personnel (house-keeping and equipment-processing personnel) are responsible for ensuring that appropriate infection prevention and control practices are used at all times 5. Hospital and unit leaders are responsible for holding their personnel accountable for their actions 6. Avoidance of H2 antagonist or proton pump inhibitors for patients without a high risk of gastrointestinal bleeding 2. Selective digestive tract decontamination for all patients undergoing ventilation 3. When the pH of the stomach contents is raised, its infective organism load may increase. Moreover, the preferential use of sucralfate or H2-blocking agents remains an unresolved issue (2). Accordingly, a semirecumbent position (95,98–101,144–146) and the use of an inflated esophageal balloon (in patients with a nasogastric tube and enteral feeding tube) during mechanical ventilation (147) can reduce gastroesophageal reflux and, thus, lower the risk of bronchial aspiration of gastric contents. The circuit should be replaced only when visibly soiled or not working properly (2). Endotracheal tube cuff pressure should be at least 20 cm H2O to prevent leakage of bacterial pathogens around the cuff into the lower respiratory tract (156,157). Contaminated condensates should be carefully emptied from ventilator circuits, and their entry into the endotracheal tube or in-line medication nebulizer should be avoided (157,161,162).

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If cold alloantibody identified discount 40mg paxil with mastercard, alloantibody repeat reverse grouping with A1&B cells that lack corresponding ag 30 mg paxil overnight delivery. Control Same ingredients as reagent, except no Any neg typing rxn serves as control, e. Anti-C3d or anti-C3b-C3d Complement Helpful in investigation of immune hemolytic anemia. On row of ags at top of antigram, cross out those that are present on cells that didn’t react in any phase. An ab will react with all cells that possess the corresponding ag (except for abs that demonstrate dosage & only react with homozygous cells). Testing with selected cells If other abs can’t be ruled out, further testing with selected cells might be required. Cells selected for testing should be pos for only 1 ag corresponding to abs in question, e. Most often in multiply 2ºF during or shortly or cytokines transfused pts or women with multiple after tf, with no pregnancies. Transfusion-associated Rash, nausea, vomit- Viable T lymphs in None Irradiate components for pre- graft-vs. Transfusion Reaction Investigation Immunohematology Review 478 Signs & symptoms of possible Fever; chills; respiratory distress; hyper- or hypotension; back, flank, chest, or abdominal transfusion reaction pain; pain at site of infusion; hives (urticaria)*; jaundice; hemoglobinuria; nausea/vomiting; abnormal bleeding; oliguria/anuria. Signs of hemolytic reaction Hemolysis in post-tf sample, but not in pre-tf sample. Transfusion Reaction Investigation continued Immunohematology Review 479 Additional tests that may be Haptoglobin (↓with hemolysis). If baby is Rh pos, draw mother’s blood after delivery & perform rosette test to screen for large fetal bleed. If rosette test pos, quantitate fetal bleed by flow cytometry or Kleihauer-Betke acid-elution test. Examples of Equipment/Reagent Quality Immunohematology Review 484 Control Blood storage refrigerators & freezers, System for continuous temp monitoring & audible alarm. Centrifuges Determine optimum speed & time for different procedures upon receipt, after repairs, & periodically. Antihuman globulin Check anti-IgG activity each day of use by testing Rh-pos cells sensitized with anti-D. Clean catch Routine, culture Cleanse external genitalia & collect Less contamination. Suprapubic aspiration Culture Needle inserted through abdomen Avoids contamination. Protein Neg–trace Protein error of indicator Possible renal disease Buffered to pH 3. Orthostatic proteinuria— benign condition, protein is neg in 1st am specimen, pos after standing. Ketones Neg Sodium nitroprusside rxn ↑ fat metabolism Most sensitive to acetoacetic acid. Urobilinogen 1 Ehrlich unit or 1 Ehrlich’s aldehyde rxn or Liver disease, hemolytic Reagent strips don’t detect absence mg/dL diazo rxn disorders of urobilinogen, only↑. Failure to follow manufacturer’s Erroneous results instructions Failure to dip all test pads in urine False-neg rxns Prolonged dipping False-neg rxns Reagents may leach from pads. Expired strips Erroneous results Highly pigmented urine Atypical colors, false-pos rxns Pigment masks true rxns. Urobilinogen Highly pigmented urine Improperly preserved specimen (oxidation to urobilin), formalin. Sulfosalicylic All proteins, in- Acid precipitation False pos: radiographic dyes, Centrifuge & test supernatant. False neg: highly buffered alkaline urine Clinitest Reducing Copper reduction False pos:↑ascorbic acid Watch rxn to avoid missing pass substances False neg: “pass through” through. Lower urethra, Usually none ↑numbers usually seen in Prominent round vagina urine from females. Spherical, Renal pelvis, Seldom significant May form syncytia (clumps) pear-shaped, or ureters, bladder, polyhedral. Oval fat body Renal tubular epithe- Renal tubules Same as renal tubular Maltese crosses with lial cell containing fat epithelial cells polarized light droplets. Calcium oxalate Octahedral (8-sided) envelope form is most Occasionally found in slightly alk urine. Triple phosphate “Coffin-lid” crystal Ammonium biurate Yellow-brown “thorn apples” & spheres Seen in old specimens.

The distribution of the drug throughout the various compartments and tissues that are accessed result in an equilibrium concentration discount 30mg paxil free shipping, and from that point effective paxil 30mg, the elimination of the drug proceeds in a consistent fashion. A semilogarithm plot is used for the concentration at each time point and this yields a linear configuration to the elimination plot. Extrapolation of the semilogarithm elimination plot to time-zero permits calculation of the volume of distribution (Vd) of the drug in this specific set of clinical circumstances. The volume of distribution equals the total dose of drug given (D) divided by 6 the time-zero theoretical concentration (T0), or D/(T0) ¼ Vd. Thus, 1 g of an antibiotic (1 Â 10 mg) with an extrapolated (T0) ¼ 50 m/mL results in a Vd ¼ 20,000 m, or 20 L. The linear configuration of drug elimination over time permits calculation of the biological elimination half-life (T1/2). The T1/2 is the period of time required for the equilibrated plasma concentration of the drug to decline by 50%. The expectation is that the plasma concentration reflects the dynamic processes of equilibration of the central pool (i. Antibiotics are generally considered to have a single T1/2 that describes elimination of the drug, but some may have a second T1/2 that describes clearance at low concentrations. Antibiotic Kinetics in the Multiple-System Trauma Patient 523 Figure 1 Illustrates the clearance curve of a theoretical antibiotic. Vd is a theoretical calculation that can be influenced by factors other than the actual body water of drug distribution. Knowledge of the Vd and T1/2 allows the design of dose and dosage intervals for the antibiotic. If our theoretical drug in Figure 1 was deemed to have toxicity at concentrations above 80 m/mL then it would be desirable to have the concentration below that threshold for the treatment interval. Thus, a rational configuration of the use of this drug would be a 1 g dose that was re- dosed every eight hours. Antibiotics with a significant post-antibiotic effect can have treatment intervals that are greater than would be predicted by the above model. Nevertheless, the above strategy is generally used for the design of the therapeutic application of drugs in clinical trials. The design is derived from studies in healthy volunteers and clinical trials are generally performed in patients without critical illness. Biotransformation is the process by which the parent drug molecule is metabolized following infusion. Biotransformation may occur via a number of pathways, although hepatic metabolism is most common. It may occur within the gastrointestinal tract, the kidney epithelium, the lungs, and even within the plasma itself. Hepatic biotransformation may result in the metabolite being released within the blood, resulting commonly in attenuation of action and facilitation of 524 Fry elimination via the kidney. Hepatic metabolism may result in the inactivated metabolite being eliminated within the bile. Clearly, abnormalities within the organ responsible for biotransformation will affect the process. The cytochrome P-450 system requires molecular oxygen, so poor perfusion or oxygenation of the liver from any cause will impact hepatic metabolism of specific drugs. Some drugs are eliminated unchanged by the kidney into the urine, or excreted by the liver into the bile. Excretion of unchanged drug via the biliary tract, which in turn can be reabsorbed, may create an enterohepatic circulation that results in prolonged drug presence in the patient. When either the intact drug or metabolic product is dependent on a specific organ system for elimination, intrinsic disease becomes an important variable in the overall pharmacokinetic profile. Extensive torso and extremity injuries result in soft tissue injuries that activate the human systemic inflammatory response. This systemic inflammatory response requires extensive volume resuscitation for maintenance of intravascular volume and tissue perfusion. Blunt chest trauma requires intubation and prolonged ventilator support, and exposure of the lung to environmental contamination. The patients are immunosuppressed from the extensive injuries, transfusions, and protein-calorie malnutrition. Following the injury itself, infection becomes the second wave of activation of systemic inflammation. Infection becomes a complication at the sites of injury, at the surgical sites of therapeutic interventions, and as nosocomial complications at sites remote from the injuries. Fever and hypermetabolism are common and add an additional compounding variable at a time when antimicrobial treatment is most important in the patient’s outcome. Antibiotics are invariably used in the febrile, multiple-injury patient, but they are dosed and re-dosed using the model of the healthy volunteer initially employed in the development of the drug.

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The statistical term for communicating that chance produced an unrepresentative sample is to say that the sample reflects sampling error generic paxil 30mg with mastercard. Sampling error occurs when random chance produces a sample statistic (such as X) that is not equal to the popula- tion parameter it represents (such as ) purchase 10mg paxil mastercard. Sampling error conveys that the reason a sam- ple mean is different from is because, by chance, the sample is unrepresentative of the population. That is, because of the luck of the draw, the sample contains too many high scores or too many low scores relative to the population, so the sample is in error in representing the population. The problem is that then the sample appears to come from and represent that other population. Thus, although a sample always represents some population, we are never sure which population it represents: Through sampling error the sample may poorly represent one population although it doesn’t look like it represents that one, or the sample may accurately represent some other popula- tion altogether. Therefore, we should have obtained a sample mean of 500 if our sample was perfectly representative of this population. Maybe because of the luck of the draw, we selected too many students with high scores and not enough with low scores so that the sam- ple mean came out to be 550 instead of 500. Thus, it’s possible that chance produced a less than perfectly representative sample, but the population being represented is still that ordinary population where is 500. After all, these are Prunepit students, so they may belong to a very different population of students, having some other. For example, maybe Prunepit students belong to the population where is 550, and their sample is perfectly representing this population. The solution to this dilemma is to use inferential statistics to make a decision about the population being represented by our sample. The next chapter puts all of this into a research context, but in the following sections we’ll examine the basics of deciding whether a sample represents a particular population. Therefore, we can determine whether our sample is likely to come from and thus represent a particular population. If chance is likely to produce our sample from the population, then we decide that our sample does come from and represent that population, although maybe with a little sampling error. However, if chance is unlikely to produce our sample from the population, then we decide that the sample does not represent that population, and instead represents some other population. It’s possible that some quirk of chance produced such an unrepresentative sample, but it’s not likely: I type errorless words only 20% of the time, so the probability of an errorless paragraph is extremely small. Thus, because chance is unlikely to produce such a sample from the population of my typing, you should conclude that the sample represents the population of a competent typist where such a sample is more likely. Deciding Whether a Sample Represents a Population 195 On the other hand, say that there are typos in 75% of the words in the paragraph. This is consistent with what you would expect if the sample represents my typing, but we have a little sampling error. Although you expect 80% typos from me over the long run, you would not expect precisely 80% typos in every sample. Rather, a sample with 75% errors seems likely to occur simply by chance when the population of my typing is sampled. Therefore, you can accept that this paragraph represents my typing, albeit somewhat poorly. As you’ve seen, we determine the probability of a sample mean by computing its z-score on the sampling distribu- tion of means. Therefore, think of a sampling distribution as a “picture of chance,” showing how often chance produces different sample means when we sample a particular raw score population. The next step is to calculate the z-score for our sample mean of 550 so that we can determine its likelihood. In reality we would not always expect a perfectly represen- tative sample, so we would not expect a sample mean of precisely 500 every time. Instead, if our sample is representing this population, then the sample mean should be close to 500. Thus, this is a mean that we’d expect to see if we are representing this population. In fact, to put it simply, we obtained an expected mean that happens often with this pop- ulation. We assume the discrepancy is due to sampling error where, by chance, we obtained a few too many high scores so our X turned out to equal 550 instead of 500. However, say that, instead, our sample has a z-score at location B back in Figure 9. Thus, this is a mean we would not expect to see if we are representing this population. To put it simply, we obtained an unexpected mean that almost never happens with this population! Instead, it makes more sense to conclude that the sample represents and comes from some other raw score population (having some other ), where this sample is more likely. Be sure you understand the above logic before proceeding, because it is used in all inferential procedures.

Histoplasma l Oral lichen planus Distinguished by culture purchase paxil 20mg without prescription, capsulatum l Behcet’s disease serology and/or biopsy paxil 10 mg with mastercard. Acute necrotizing l Leukemic gingivitis Leukopenia suggests inflammation, ulcerative gingivitis l Scurvy agranulocytosis or cyclic ulceration (Vincent’s angina) l Agranulocytosis neutropenia. Herpangina l Cyclic neutropenia hyperkeratosis, purpura, and l Acatalasia corkscrew hairs are seen in scurvy. Acute infectious Ecballium elaterium) uvulitis may be associated l Trauma with epiglottitis. Infectious glossitis l Vitamin B complex deficiency Culture will be positive in erythematous due to type b l Nontropical sprue bacterial/fungal glossitis. Atrophic thrush l Iron deficiency l Alcoholism l Amyloidosis l Regional enteritis Blanching of half of 1. Bacterial l Giant cell arteritis Fever >1028F favors the tongue endocarditis l Air embolism (Liebermeister endocarditis. Kaposi sarcoma l Venous lake or varicosity Biopsy will distinguish the violaceous 2. Acute suppurative l Subacute (de Quervain) Fever >1028F suggests thyroiditis thyroiditis infection. Scanning/ l Thyroid amyloidosis biopsy for others l Infarction of a thyroid nodule Hemoptysis 1. Bronchiectasis l Lupus pneumonitis l Long trauma/contusion l Foreign body l Arteriovenous malformation l Mitral stenosis l Pseudohemoptysis Inspiratory stridor 1. Lobar pneumonia l Pleural effusion Fever, egophony, increased loss of l Tension pneumothorax fremitus in pneumonia. Tropical pulmonary l Bronchiolitis obliterans eosinophilia l Hypersensitivity pneumonitis 5. Septic thrombophle- l Trousseau syndrome Fever >1028F and positive superficial vein bitis l Thromboangiitis obliterans blood cultures in septic l Chemical phlebitis thrombophlebitis Palpable arterial 1. Mycotic aneurysm l Polyarteritis nodosa Fever, positive blood cultures in aneurysm l Traumatic aneurysm mycotic aneurysm. Mycotic or luetic l Noninfectious ascending Fever, positive blood cultures or suprasternal ascending aortic aortic aneurysm in mycotic aneurysm. Acute viral or l Collagen vascular diseases Clinical context for post- rub bacterial (esp. Peritoneal/ peritonitis l Recent significant weight loss ascites culture or biopsy. Acute salpingitis l Acute appendicitis Stool culture, specific serology quadrant with a tuboovarian l Cecitis/typhlitis in enteric infections. There may be hepatomegaly hepatitis l Drug-induced hepatitis a friction rub over a hepatic 2. Serology, (pyogenic, amebic, constrictive pericarditis ultrasonography, culture to Toxoplasma) l Hepatic sickle cell crisis distinguish the various 3. Bacterial septic l Gout Arthrocentesis with microscopy articular arthritis arthritis l Pseudogout (including polarized lens) 2. Septic arthritis/ l Reactive arthritis Blood and joint fluid culture/ tenderness osteomyelitis l Trauma/fracture microscopy. Pyocele l Testicular torsion impaired blood flow in l Polyarteritis nodosa torsion and an inhomogeneous collection in a pyocele. Creutzfeldt–Jakob l Drugs (l-dopa, lithium, imaging for other disease methadone, lamotrigine) possibilities. Herpes zoster l Retroperitoneal hemorrhage serology, and imaging to (a) T12 to L4— 3. Absent patellar reflex (b) L5 to S3—hip extension, abduction, and internal rotation of thigh, flexion of leg, and all movements of foot. Absent Achilles reflex (c) Entire plexus—variable weakness of hip girdle, thigh and foot muscles Paraplegia/paresis 1. Spinal epidural l Arachnoiditis due to epidural Significant spinal pain suggests with a sensory abscess drug injection, hemorrhage epidural abscess. Listeria l Ataxia-telengiectasia syndrome serology, imaging to monocytogenes l Friedrich’s ataxia distinguish among the other meningitis l Spinocerebellar ataxia etiologies. Rickettsia l Paraneoplastic disorder (Rickettsia rickettsii, l Vitamin E deficiency Coxiella burnetti) l Exposure to toxins (lead, 9. Francisella Tularensis Descending Botulism l Miller–Fisher syndrome Fever and asymmetry suggest paralysis with Bulbar poliomyelitis polio. Hematology: Basic Principles and Practice (Hematology: Basic Principles & Practice). Murray and Nadel’s Textbook of Respiratory Medicine edition: Text with Continually Updated Online Reference (Textbook of Respiratory Medicine. Ophthalmologic Clues to Infectious Diseases 4 and Their Mimics in Critical Care Cheston B. Cunha Department of Medicine, Brown University, Alpert School of Medicine, Providence, Rhode Island, U.

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In addition purchase paxil 40mg without prescription, patient clustering purchase paxil 20mg line, a greater likelihood of antibiotic use, and a larger proportion of elderly patients may facilitate transfer of the organism (1). The rates of colonization in the feces among hospitalized patients are 10% to 25% and 4% to 20% among residents of long-term facilities as opposed to 2% to 3% among healthy adults in the general population. Other factors that increase the vulnerability of the elderly are underlying severe disease, nonsurgical gastrointestinal procedures, and poor immune response to C. In addition, there is a higher likelihood of comorbidities in older patients that may lead to more frequent hospitalizations and exposure to antibiotics compared with the younger population. Immunity Host immune response plays an essential role in determining whether patients become colonized with C. As mentioned previously, most patients remain asymptomatic following acquisition of C. Patients with a normal immune system who are exposed to toxin A, mount serum IgG antitoxin A antibody in response to C. In elderly patients and patients with severe underlying illnesses, the immunologic response may be blunted leading to lower serum antibody response to toxin A. In the colon, the spores convert to their vegetative, toxin-producing form and become susceptible to killing by antimicrobial agents. Toxin A is a 308-kDa enterotoxin that produces acute inflammation, leading to intestinal fluid secretion and mucosal injury (33). Toxin B is a 270-kDa cytotoxin that is 10 times more potent than toxin A in mediating mucosal damage in vitro. Both toxins act intracellularly by inactivating proteins in the Rho subfamily, which regulate the F-actin cytoskeleton. This results in disaggregation of actin, opening the tight junctions between cells, and resulting in cell retraction and apoptosis manifested as characteristic cell rounding in tissue culture assays and shallow ulceration on the intestine mucosal surface (17,34). Both toxins are also proinflammatory, inducing release of cytokines, phospholipase A2, platelet-activating factor (33), tumor necrosis factor-a, and substance P. This results in the activation of the enteric nervous system, leading to neutrophil chemotaxis and fluid secretion. While most strains produce both toxins, some produce toxin B only but can be equally virulent as strains with both toxins. Colonization rates of 25% to 80% are seen in healthy infants and neonates but clinical illness is rare (3). For unclear reasons, colonization appears to wane with advancing age, and 276 Hjalmarson and Gorbach Table 2 Definition of Clostridium difficile infection 1. Presence of symptoms >3 unformed stools over 24 hours for at least 2 days in the absence of ileus and 2. Positive stool test for the presence of toxigenic Clostridium difficile or its toxins or 3. Colonization increases to 20% to 30% of hospitalized adults (26), but clinical symptoms develop in only one-third of those who become colonized (34). However, colonized individuals shed pathogenic organisms and serve as a reservoir for environmental contamination. Symptoms can begin as early as the first day of antibiotic use or as late as eight weeks after completion of the precipitating antibiotic course (25). For mild disease, the diarrhea is usually the only symptom, involving <10 episodes a day without systemic symptoms. The diarrhea is frequently watery with a characteristic foul odor, but it can also be mucoid or mushy. Moderate disease, defined as <10 bowel movements per day, leukocytosis <15,000 cells/mL, and creatinine <1. Severe disease defined as >10 bowel movements per day, leukocytosis >15,000 cells/mL, elevated creatinine (>1. The first warning sign of fulminant colitis may be diminishing diarrhea, due to decreased colonic muscle tone. A study of 44 patients undergoing colectomy for fulminant colitis reported that 5 (11%) presented with frank peritonitis, hypotension, or both (40). Characteristic laboratory findings include leukocytosis that may be severe and hypoalbuminemia. Hypoalbuminemia is the result of large protein losses attributable to leakage of albumin and may occur early in the course of the disease (25). Evidence of colitis includes fever, abdominal cramps, leukocytosis, and presence of leukocytes in the feces. Endoscopic Clostridium difficile Infection in Critical Care 277 examination reveals pseudomembranes in the colonic mucosa (see “Diagnosis”). Prominent complications include toxic megacolon requiring colectomy, leukemoid reactions, septic shock, and death (10,11,37). The most commonly reported is polyarthritis involving large joints occurring one to four weeks after infection (34). Generally, these infections are polymicrobial, making it difficult to ascertain the pathogenic role of C. The clinical presentation is usually very similar to the original presentation (42) and generally occurs one to eight weeks, but usually within two weeks, after completion of anticlostridial therapy.