Microbiology

Table 99.2 summarizes the common pathogens encountered during the preengraftment period. The most common portals of entry for bacterial infection during this period include central venous catheters and mucositis of the mouth and gut arising from the preparative regimen. Thus, not surprisingly, bacterial pathogens such as viridans streptococci and Gramnegative bacilli from the mouth and gastrointestinal tract, respectively, and skin organisms such as coagulase negative staphylococci are the most common bacterial pathogens encountered in the preengraftment period. Up to 12% of infections occur prior to transplant.4 Although Gram-negative infections were common during the 1980s, the use of prophylactic oral antibiotics such as fluoroquinolones and trimethoprim-sulfamethoxazole at the onset of neutropenia has led to a shift in the spectrum of bacterial pathogens seen in the preengraftment period. Gram-positive organisms now account for a majority of bacterial infections and for 50% of bacteremias.78 Coagulase negative staphylococci

Table 99.2 Common pathogens encountered during the preengraftment period

Pathogen Bacteria

Staphylococci Streptococci Gram-negative bacilli Clostridium difficile

Viruses

Herpes simplex 1 Herpes simplex 2 Community respiratory viruses

Fungi

Candida species

Aspergillus species

Site of origin/involvement

Skin, intravascular devices Mouth, GI tract GI tract Colon

Mouth, esophagus Genitals, anus, skin Upper respiratory tract, pneumonia

Originate from gut May involve bloodstream, mouth, esophagus, skin, intravascular devices; rarely viscera or bone marrow Pneumonia, sinusitis; rarely CNS and skin and viridans streptococci have emerged as dominant pathogens, and the latter have been associated with a shock syndrome.9 Penicillin resistance is an emerging problem in viridans streptococci.10 Gram-negative infections are the second most common cause of bacterial infections in the preengraftment period, and now include less common and more often multiresis-tant organisms such as Enterobacter, Acinetobacter, Klebsiella, Citrobacter and Stenotrophomonas species. Vancomycin-resistant enterococci and Clostridium difficile are important emerging pathogens, although diarrhea following HSCT is infectious in fewer than 15% of cases.11'12

HSV and community-acquired respiratory viruses (CRV) are the most common viral pathogens encountered in the preengraftment period. Autologous and allogeneic HSCT recipients appear to be at similar risk for these viral infections. HSV infections are almost always attributable to reactivation of latent asymptomatic infection in seropositive individuals. In the absence of prophylaxis, 70-80% of seropositive individuals will reactivate HSV in the preengraftment period, with a peak incidence at 2-3 weeks posttrans-plant. HSV type 1 (HSV 1) accounts for 85% of episodes and produces gingivostomatitis4; infection in the mouth may spread to the trachea, esophagus or lungs. In the initial posttransplant period, up to half of mouth lesions may be attributable to HSV 1.4 The remaining 15% of HSV reactivation episodes are due to HSV type 2 involving the genitals or other cutaneous sites.

Reactivation of other human herpes viruses (HHV) in the early posttransplant period, including HHV-6 and HHV-8, has been associated with the development of clinical symptoms. HHV-6 may reactivate in seropositive recipients of both autologous and allogeneic HSCTs, on average at 2-4 weeks posttransplant.1314 An anti-CD3 monoclonal antibody for prophylaxis against acute GVHD in allogeneic HSCT recipients appears to increase the risk of HHV-6 reactivation, which has been associated with the development of fever, rash, interstitial pneumonia, encephalitis, delayed white cell engraft-ment, and an increase in the severity of GVHD.1415 HHV-8 reactivation was recently reported to cause fever, rash, and hepatitis 2-3 weeks following autolo-gous HSCT.16 The pathogenetic significance of HHV-7 reactivation has been debated; HHV-7 may serve as a cofactor for the development of CMV disease following organ transplantation.17

CRV infections may develop in both autologous and allogeneic HSCT recipients and tend to mirror the seasonal occurrence of influenza, parainfluenza, respiratory syncytial virus (RSV), and rhinovirus infections in the community. Outbreaks of RSV and influenza have been described on stem cell transplant units.1819 Prevention of infection and containment of outbreaks require meticulous attention to infection control practices, cohorting of infected individuals, immunization against influenza of health care workers and at-risk HSCT candidates pretransplant, and influenza prophylaxis on HSCT units during outbreaks.219 Influenza, parainfluenza, and RSV may produce lower respiratory tract infection in the early posttransplant period with significant morbidity and mortality2021; tracheobron-chitis and pneumonia are usually heralded by the onset of upper respiratory tract symptoms, such as rhinor-rhea, sinus congestion, and sore throat. Lymphopenia appears to be a risk factor for progression to lower respiratory tract infection in HSCT recipients with influenza.21 Other pathogens, such as Aspergillus species, are frequently isolated in patients with influenza involving the lower respiratory tract. Antiviral therapy in HSCT recipients with influenza with a neuraminidase inhibitor is preferred to amanti-dine or rimantidine, as neuraminidase inhibitors appear to shorten the duration of viral shedding.21 Inhaled ribavirin and intravenous immunoglobulin have been advocated for those with RSV. The optimal therapy for a parainfluenza lower respiratory tract infection has not been defined; in a recent study involving allogeneic and autologous HSCT recipients with parainfluenza pneumonia, inhaled ribavirin with or without immunoglobulin did not improve sur-vival.22 Adenovirus infections occur in up to 6% of pediatric HSCT recipients, often following engraft-ment, but occasionally in the preengraftment period.23 Hemorrhagic cystitis, hemorrhagic colitis, pneumonia, nephritis, and hepatic failure are the most common presentations; disseminated disease has been reported.

Invasive fungal infections due to molds and Candida species are important clinical problems in the preengraftment period. Autologous HSCT recipients have a lower incidence of these infections compared with those receiving allogeneic transplants. Prior to 1990, Candida albicans, C. tropicalis, and C. parapsilosis were the most common causes of invasive fungal infections in this setting. However, the demonstration in the early 1990s of the utility of fluconazole prophylaxis in reducing the incidence of superficial and invasive fungal infections in HSCT recipients and its subsequent widespread use24 25 has led to a decline in the incidence of infections from these organisms. Fluconazole prophylaxis in HSCT recipients has also led to the emergence of the fluconazole-resistant yeasts C. krusei and C. glabrata as important pathogens in the preengraftment period, and to the emergence of aspergillosis as the most common invasive fungal infection following HSCT.

Candidal infections can present in the preengraft-ment period as superficial cutaneous infection, thrush, esophagitis, urinary tract infections, fungemia, or as disseminated infection involving the skin, viscera, and bone marrow. Although infection most often arises from organisms that colonize mucosal surfaces, infection of intravascular devices or contamination of infusates such as total parenteral nutrition (TPN) fluid are occasional causes of candidal bloodstream infections. Risk factors for invasive candidal infections include prolonged and severe neutropenia, breakdown of mucosal barriers, and the use of broad spectrum antibiotics, corticosteroids, and TPN.26

Invasive molds are a growing cause of morbidity and mortality in the preengraftment period, especially in allogeneic HSCT recipients.27 Invasive aspergillosis following HSCT occurs in a bimodal distribution, with peak onsets at 16 days and 96 days following HSCT.27 While the overall incidence of invasive aspergillosis is higher in allogeneic HSCT recipients, early onset disease is more common in autologous HSCT recipients.27 Risk factors for early onset disease occurring within 40 days of HSCT include transplantation for hematologic malignancy without first remission, HLA-mismatched related donor, HSCT outside a laminar airflow room, and HSCT during summer months.27 Pneumonia, often with cavitation, is the most common clinical syndrome; invasive aspergillosis can also involve the sinuses, brain, and skin. Other emerging fungal pathogens include Fusarium species and the Zygomycetes. Fusariosis typically presents as fungemia with hematogenous spread to the skin, and occurs in a trimodal distribution following allogeneic HSCT, with peak incidences prior to engraft-ment, at 62 days, and beyond 1 year following HSCT.28 Survival is poor, especially in those with neutropenia. Zygomycetes, which present with sinopulmonary disease and for which iron overload and decompensated diabetes mellitus represent risk factors, have been increasingly seen in HSCT recipients receiving antifungal prophylaxis with voriconazole.26'29'30

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