Oral antibiotic therapy for acute pyelonephritis

Pinson, Andy G.; Philbrick, John T.; Lindbeck, George; Schorling, John B.

doi:10.1007/bf02599462

Cited by 23 publications

(3 citation statements)

References 29 publications

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“…Regarding the treatment of cystitis, the literature has demonstrated that β‐lactam antibiotics are not as effective, that they require a longer duration of therapy and are associated with more recurrences than non‐β‐lactam agents [36–39]. Despite recommendations against the use of β‐lactam agents in urinary tract infections [40–42], these agents continue to be used widely. Until such time as clinical data confirm that E. coli isolates with elevated MICs for cephalothin can be reliably treated with oral ampicillin–amoxicillin, DKML favors a more cautious approach.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of VITEK 2 for analysis of Enterobacteriaceae using the Advanced Expert System (AES) versus interpretive susceptibility guidelines used at Dynacare Kasper Medical Laboratories, Edmonton, Alberta

Blondel-Hill

Hetchler²,

Andrews³

et al. 2003

Clinical Microbiology and Infection

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Section: Discussionmentioning

confidence: 99%

Evaluation of VITEK 2 for analysis of Enterobacteriaceae using the Advanced Expert System (AES) versus interpretive susceptibility guidelines used at Dynacare Kasper Medical Laboratories, Edmonton, Alberta

Blondel-Hill

Hetchler²,

Andrews³

et al. 2003

Clinical Microbiology and Infection

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“…Equally as important is the need for an initial period of observation for hydration and subsequent triage. [79] A meta-analysis of the existing literature on oral therapy for pyelonephritis [84] indicates that patients who do not have diabetes or sepsis and who are not immunocompromised, can tolerate oral intake, and do not have chronic illness can be treated for upper UTI with oral agents. From these data, a regimen for the outpatient treatment of pregnant women with acute pyelonephritis may be extrapolated; however, the application of ambulatory therapy for upper UTI in pregnancy appears to be quite limited.…”

Section: Nonpregnant Patientsmentioning

confidence: 99%

Pyelonephritis in Pregnancy

Jolley

Wing

2010

Drugs

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Acute pyelonephritis is one of the most common indications for antepartum hospitalization. When acute pyelonephritis is diagnosed, conventional treatment includes intravenous fluid and parenteral antibacterial administration. There are limited data by which to assess the superiority of one antibacterial regimen over the other in terms of efficacy, patient acceptance and safety for the developing fetus; however, it is important to consider antimicrobial resistance patterns in the local community when choosing an agent. Moreover, there are growing public health concerns regarding antimicrobial resistance to commonly prescribed medications for urinary tract infections in pregnancy. There is a small body of evidence to support the ambulatory treatment of pregnant women with pyelonephritis in the first and early second trimesters, but the majority of women will be managed as inpatients. This article provides a suggested algorithm for the treatment of pyelonephritis during pregnancy. Acute Pyelonephritis in PregnancyAcute pyelonephritis is one of the most common indications for antepartum hospitalization, complicating 1-2% of all pregnancies. Women with asymptomatic bacteriuria (ASB), traditionally defined as a urine culture from mid-stream collection with a single isolate of more than 100 000 THERAPY IN PRACTICE

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“…Pyelonephritis, one of the most serious forms of urinary tract infection (UTI), is an infection of the upper urinary tract involving bacterial invasion of the renal parenchyma, and is usually caused by the ascent of bacteria from the bladder to the renal medulla via the ureters (1,2). Up to a quarter of the hospitalizations for UTI involve infection of the kidney or pyelonephritis, causing serious conditions including sepsis and septic shock (3).…”

Section: Introductionmentioning

confidence: 99%

TcpC secreting uropathogenic E. coli promoted kidney cells to secrete MIP-2 via p38 MAPK pathway

Fang

Zhang

et al. 2017

Molecular Medicine Reports

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Pyelonephritis is an infection of the upper urinary tract with characteristic histological change to neutrophil infiltration in the kidney. The majority of pyelonephritis is caused by uropathogenic Escherichia (E.) coli (UPEC) bearing distinct virulence factors. Toll/interleukin‑1 receptor domain‑containing protein C (TcpC) encoded by E. coli is an important virulence factor in the majority of strains of UPEC and inhibits macrophage‑mediated innate immunity, which serves an essential role in the pathogenesis of pyelonephritis. In the present study, it was demonstrated that TcpC induced kidney cells to produce macrophage inflammatory protein‑2 (MIP‑2; also known as C‑X‑C motif chemokine 2). MIP‑2 concentration in kidney homogenates from TcpC‑secreting UPEC CFT073 (TcpCwt) murine pyelonephritis models was significantly higher compared with that in kidney homogenates from tcpC knockout CFT073 (TcpC‑/‑) models. In vitro, TcpCwt dose‑dependently promoted MIP‑2 secretion in HEK‑293 cells. The concentration of MIP‑2 in culture supernatants of HEK‑293 co‑cultured with TcpCwt was profoundly higher compared with that of HEK‑293 co‑cultured with TcpC‑/‑. In the presence of anti‑TcpC antibody, the enhancement effect of TcpCwt on MIP‑2 production was completely abrogated, suggesting that the enhanced production of MIP‑2 was mediated by secreted TcpC. Furthermore, it was demonstrated that TcpC‑/‑ treatment had no effect on the p38 mitogen activated protein kinase (MAPK) signaling pathway, while TcpCwt treatment resulted in the activation of p38 MAPK in HEK‑293 cells, as indicated by a simultaneous increase in p38 and phosphorylated‑p38. In addition, inhibition of p38 MAPK with SB203580 significantly decreased MIP‑2 concentration and neutrophil recruitment activity in the supernatants of HEK‑293 cells co‑cultured with TcpCwt. This indicates that TcpC may promote MIP‑2 production in kidney cells through the p38 MAPK signaling pathway. Taken together, the data of the present study demonstrated that TcpC can induce MIP‑2 production, which may contribute to the characteristic histological change associated with pyelonephritis. This data has provided novel evidence to further clarify the pathogenesis of pyelonephritis and novel directions on the pathogenicity of TcpC‑secreting UPEC.

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Oral antibiotic therapy for acute pyelonephritis

Cited by 23 publications

References 29 publications

Evaluation of VITEK 2 for analysis of Enterobacteriaceae using the Advanced Expert System (AES) versus interpretive susceptibility guidelines used at Dynacare Kasper Medical Laboratories, Edmonton, Alberta

Evaluation of VITEK 2 for analysis of Enterobacteriaceae using the Advanced Expert System (AES) versus interpretive susceptibility guidelines used at Dynacare Kasper Medical Laboratories, Edmonton, Alberta

Pyelonephritis in Pregnancy

TcpC secreting uropathogenic E. coli promoted kidney cells to secrete MIP-2 via p38 MAPK pathway

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