Transplant infections

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  • (BQ) Part 1 of the document Transplant infections presents the following contents: Introduction to transplant infections, risks and epidemiology of infections after transplantation, specific sites of infection, bacterial infections.

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  • (BQ) Continued part 1, part 2 of the document Transplant infections presents the following contents: Viral infections, fungal infections, infection control, immune reconstitution strategies for prevention and treatment of infections, hot topics.

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  • Kidney Transplantation (See Table 126-4) Table 126-4 Common Infections after Kidney Transplantation Period after Transplantation Infection Site Early Month) (6 Urinary tract Bacteria (Escherichia Klebsiella, Enterobacteriaceae, Pseudomonas, Enterococcus) associated bacteremia pyelonephritis; Candida coli, (fever, CMV Bacteria (late bone urinary tract marrow suppression, hepatitis); virus with (nephropathy, and graft infections usually not associated BK bacteremia); virus graft with BK (nephropathy, failure, failure, generalized vasculopathy) vasculopathy) Lungs Bacteria ...

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  • Adenovirus can be isolated from HSCT recipients at rates varying from 5 to 18%. Although hemorrhagic cystitis, pneumonia, gastroenteritis, and fatal disseminated infection have been reported, adenovirus infection, which (like CMV infection) usually occurs in the first or second month after transplantation, is often asymptomatic. A role for cidofovir therapy has been suggested, but the efficacy of this agent is unproven. Infections with parvovirus B19 (presenting as anemia or occasionally as pancytopenia) and enteroviruses (sometimes fatal) can occur.

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  • Graft Failure While complete and sustained engraftment is usually seen posttransplant, occasionally marrow function either does not return or, after a brief period of engraftment, is lost. Graft failure after autologous transplantation can be the result of inadequate numbers of stem cells being transplanted, damage during ex vivo treatment or storage, or exposure of the patient to myelotoxic agents posttransplant. Infections with cytomegalovirus (CMV) or human herpes virus type 6 have also been associated with loss of marrow function.

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  • Diffuse interstitial infiltrates suggest viral, parasitic, or Pneumocystis pneumonia. If the patient has a diffuse interstitial pattern on chest x-ray, it may be reasonable to institute empirical treatment with TMP-SMX (for Pneumocystis) and a quinolone (for Chlamydophila, Mycoplasma, and Legionella) or an erythromycin derivative (e.g., azithromycin) while considering invasive diagnostic procedures. Noninvasive procedures, such as staining of sputum smears for Pneumocystis, serum cryptococcal antigen tests, and urine testing for Legionella antigen, may be helpful.

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  • Pneumocystis jiroveci pneumonia, once seen in 5–10% of patients, can be prevented by treating patients with oral trimethoprim-sulfamethoxazole for 1 week pretransplant and resuming the treatment once patients have engrafted. The risk of infection diminishes considerably beyond 3 months after transplant unless chronic Most GVHD transplant develops, centers requiring recommend continuous continuing immunosuppression. trimethoprim-sulfamethoxazole prophylaxis while patients are receiving any immunosuppressive drugs and also recommend careful monitoring for late CMV reactivation.

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  • Bacterial Infections In the first month after hematopoietic stem cell transplantation, infectious complications are similar to those in granulocytopenic patients receiving chemotherapy for acute leukemia (Chap. 82). Because of the anticipated 1- to 3week duration of neutropenia and the high rate of bacterial infection in this population, many centers give prophylactic antibiotics to patients upon initiation of myeloablative therapy. Quinolones decrease the incidence of gram-negative bacteremia among these patients.

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  • Middle-Period Infections Because of continuing immunosuppression, kidney transplant recipients are predisposed to lung infections characteristic of those in patients with T cell deficiency (i.e., infections with intracellular bacteria, mycobacteria, nocardiae, fungi, viruses, and parasites). The high mortality rates associated with Legionella pneumophila infection (Chap. 141) led to the closing of renal transplant units in hospitals with endemic legionellosis.

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  • Kidney transplant recipients are also subject to infections with other intracellular organisms. These patients may develop pulmonary infections with Nocardia, Aspergillus, and Mucor as well as infections with other pathogens in which the T cell/macrophage axis plays an important role. In patients without IV catheters, L. monocytogenes is a common cause of bacteremia ≥1 month after renal transplantation and should be seriously considered in renal transplant recipients presenting with fever and headache.

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  • Virus-Associated Malignancies In addition to malignancy associated with gammaherpesvirus infection (EBV, KSHV) and simple warts (HPV), other tumors that are virus-associated or suspected of being virus-associated are more likely to develop in transplant recipients, particularly those who require long-term immunosuppression, than in the general population. The interval to tumor development is usually 1 year. Transplant recipients develop nonmelanoma skin or lip cancers that, in contrast to de novo skin cancers, have a high ratio of squamous cells to basal cells.

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  • part 2 book "antibiotic and chemotherapy expert consult" presentation of content: anthelmintics, antiprotozoal agents, antiretroviral agents, other antiviral agents, treatment, abdominal and other surgical infections, infections associated with neutropenia and transplantation, infections associated with implanted medical devices,... and other content.

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  • Harrison's Internal Medicine Chapter 126. Infections in Transplant Recipients Infections in Transplant Recipients: Introduction The evaluation of infections in transplant recipients involves consideration of both the donor and the recipient of the transplanted organ. Infections following transplantation are complicated by the use of drugs that are necessary to enhance the likelihood of survival of the transplanted organ but that also cause the host to be immunocompromised.

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  • In many transplantation centers, transmission of infections that may be latent or clinically inapparent in the donor organ has resulted in the development of specific donor-screening protocols.

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  • Herpes Simplex Virus Within the first 2 weeks after transplantation, most patients who are seropositive for HSV-1 excrete the virus from the oropharynx. The ability to isolate HSV declines with time. Administration of prophylactic acyclovir (or valacyclovir) to seropositive HSCT recipients has been shown to reduce mucositis and prevent HSV pneumonia (a rare condition reported almost exclusively in allogeneic HSCT recipients). Both esophagitis (usually due to HSV-1) and anogenital disease (commonly induced by HSV-2) may be prevented with acyclovir prophylaxis.

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  • PCR can be used to monitor EBV production after hematopoietic stem cell transplantation. High or increasing viral loads predict an enhanced likelihood of developing EBV-LPD and should prompt rapid reduction of immunosuppression and search for a focus of disease. If reduction of immunosuppression does not have the desired effect, administration of a monoclonal antibody to CD20 (rituximab or others) for the treatment of B cell lymphomas that express this surface protein has elicited dramatic responses and currently constitutes first-line therapy for CD20-positive EBV-LPD.

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  • Middle-Period Infections T. gondii (Chap. 207) residing in the heart of a seropositive donor may be transmitted to a seronegative recipient. Thus serologic screening for T. gondii infection is important before and in the months after cardiac transplantation. Rarely, active disease can be introduced at the time of transplantation. The overall incidence of toxoplasmosis is so high in the setting of heart transplantation that some prophylaxis is always warranted.

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  • Late Infections The incidence of Pneumocystis infection (which may present with a paucity of findings) is high among lung and heart-lung transplant recipients. Some form of prophylaxis for Pneumocystis pneumonia is indicated in all organ transplant situations (Table 126-5). Prophylaxis with TMP-SMX for 12 months after transplantation may be sufficient to prevent Pneumocystis disease in patients whose degree of immunosuppression is not increased. As in other transplant recipients, infection with EBV may cause either a mononucleosis-like syndrome or EBV-LPD.

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  • As in other transplantation settings, reactivation disease with herpes-group viruses is common (Table 126-3). Herpesviruses can be transmitted in donor organs. Although CMV hepatitis occurs in ~4% of liver transplant recipients, it is usually not so severe as to require retransplantation. Without prophylaxis, CMV disease develops in the majority of seronegative recipients of organs from CMVpositive donors, but fatality rates are lower among liver transplant recipients than among lung or heart-lung transplant recipients.

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  • In the absence of compelling data as to optimal timing, it is reasonable to administer the pneumococcal and H. influenzae type b conjugate vaccines to both autologous and allogeneic HSCT recipients beginning 12 months after transplantation. A series that includes both the 7-valent pneumococcal conjugate vaccine and the 23-valent Pneumovax is now recommended (following CDC guidelines). The pneumococcal and H. influenzae type b vaccines are particularly important for patients who have undergone splenectomy.

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