Klebsiella pneumoniae infections after liver transplantation:Drug resistance and distribution of pathogens,risk factors,and influence on outcomes

BACKGROUND Liver transplantation(LT)is the only curative treatment for end-stage liver disease.However,LT recipients are susceptible to infection,which is the leading cause of early mortality after LT.Klebsiella pneumoniae infections(KPIs)in the bloodstream are common in LT recipients.We hypothesized that KPIs and carbapenemresistant Klebsiella pneumoniae(CRKP)infections may affect the outcomes of LT recipients.AIM To assess KPI incidence,timing,distribution,drug resistance,and risk factors following LT and its association with outcomes.METHODS This retrospective study included 406 patients undergoing LT at The Third Xiangya Hospital of Central South University,a tertiary hospital,from January 2015 to January 2023.We investigated the risk factors for KPIs and assessed the impact of KPIs and CRKP infections on the prognosis of LT recipients using logistic regression analysis.RESULTS KPI incidence was 7.9%(n=32),with lung/thoracic cavity the most frequent site of infection;the median time from LT to KPI onset was 7.5 d.Of 44 Klebsiella pneumoniae isolates,43(97.7%)and 34(77.3%)were susceptible to polymyxin B or ceftazidime/avibactam and tigecycline,respectively;>70%were resistant to piperacillin/tazobactam,ceftazidime,cefepime,aztreonam,meropenem,and levofloxacin.Female sex[odds ratio(OR)=2.827,95%confidence interval(CI):1.256-6.364;P=0.012],pre-LT diabetes(OR=2.794,95%CI:1.070-7.294;P=0.036),day 1 post-LT alanine aminotransferase(ALT)levels≥1500 U/L(OR=3.645,95%CI:1.671-7.950;P=0.001),and post-LT urethral catheter duration over 4 d(OR=2.266,95%CI:1.016-5.054;P=0.046)were risk factors for KPI.CRKP infections,but not KPIs,were risk factors for 6-month all-cause mortality post-LT.CONCLUSION KPIs occur frequently and rapidly after LT.Risk factors include female sex,pre-LT diabetes,increased post-LT ALT levels,and urethral catheter duration.CRKP infections,and not KPIs,affect mortality.

Establishment of a Predictive Diagnostic Model for Acute Mycoplasma Pneumoniae Infection in Elderly Patients with Community-acquired Pneumonia

We established a diagnostic model to predict acute Mycoplasma pneumoniae （M. pneumonia） infection in elderly Community-acquired pneumonia （CAP） patients. We divided 456 patients into acute and non-acute M. pneumoniae infection groups. Binary logistic regression and receiver operating characteristic （ROC） curves were used to establish a predictive model. The following independent factors were identified： age 〉 70 years; serum cTNT level 〉 0.0S ng/mL; lobar consolidation; mediastinal lymphadenopathy; and antibody titer in the acute phase 〉 1：40. The area under the ROC curve of the model was 0.923 and a score of 2 7 score predicted acute M. pneumoniae infection in elderly patients with CAP. The predictive model developed in this study has high diagnostic accuracy for the identification of elderly acute M. pneumoniae infection.

Incidence of Extended-Spectrum Be-ta-Lactamase-Producing Klebsiella pneumoniae among Patients and in the Environment of Hassan II Hospital, Settat, Morocco

Aim: The aim of the current study is to determine: (1) the prevalence of extended-spectrum β-lactamase-producing K. pneumoniae (ESBL-Kp) isolated from clinical samples and a hospital environment in Hassan II Hospital (Settat, Morocco);(2) the associated risk factors of ESBL-Kp infections;(3) the link between clinical and environmental isolates. Methods: During the study period (April 2010 to March 2011), all patients infected and hospital environment sites contaminated by K. pneumoniae were considered as the potential study population and environmental site. The clinical data were collected to identify risk factors for ESBL carriage of K. pneumoniae infection. Screening of ESBL-and carbapenemase-producing isolates was performed by using a double-disk synergy test and the modified Hodge test, respectively. ESBL-Kp isolates were tested for the presence of genes encoding β-lactamases and were investigated by PCR. The clonal relationship between ESBL-producing isolates was analysed by ERIC- and REP-PCR method. Results: The overall prevalence of ESBL-Kp among clinical and environmental K. pneumoniae isolates was 35.13% (13/37) and 4.04% (4/99), respectively. The main risk factors for carrying ESBL-Kp were renal disease (46.15%), recent surgery (53.84%), previous hospitalisation (76.92%), and the presence of many invasive devices (53.84%). All ESBL isolates were multidrug resistant. The blaCTX-M group1and blaSHV (70.58% for each) were the most prevalent followed by blaTEM (52.94%). Thirteen strains expressed at least two bla genes. One isolate was positive in the modified Hodge test and was a blaOXA-48 producer. ERIC and Rep-PCR methods revealed an epidemic clonal dissemination of these isolates. Conclusion: The emergence of OXA-48 carbapenemase, endemic clonal dissemination and multi-drug resistance of ESBL-Kp isolates in our institution is highly alarming.

PENTOXIFYLLINE AMELIORATES PULMONARY DAMAGE CAUSED BY STREPTOCOCCUS PNEUMONIAE INFECTION IN MOUSE

Streptococcus pneumoniae stimulated mouse peritoneal macrophagc to release tumor necrosis factor-α (TNFα) in vitro. When penicillin was added into the medium with bacteria, TNFα release was accelerated. Pentoxifylline (PTX), a phosphodiesterase inhibitor, significantly attenuated TNFα release caused either by Streptococcus pneumoniae or by its lysates. In this experiment, 150 Kunming mice were infected with Streptococcus peumoniae through inspiration. Dynamic changes of TNFα concentration in serum and bronchoalveolar lavage fluid were determined, and pulmonary pathological changes were also observed. It was found that PTX significantly attenuated TNFα activity in serum and bronchoalveolar lavage fluid, and inhibited white blood cell chemotaxis, emigration and infiltration. In conclusion, Streptococcus pneumoniae infection stimulates the release of TNFα which is probably the major mediater that causes tissue damage during Streptococcus pneumoniae infection. The mechanism is probably that Steptococcus pneumoniae and its lysates activate TNFα gene transcription. As penicillin accelerates TNFα release, treatment with penicillin alone may aggravate the tissue damage. Combined treatment with PTX may be more reasonable.