Moraxella nonliquefaciens superinfecting herpes simplex keratitis

2021 ◽  
pp. 112067212110195
Author(s):  
Carmen Alejandra Porcar Plana ◽  
Jaime Matarredona Muñoz ◽  
Jaime Moya Roca ◽  
Ezequiel Campos Mollo
Keyword(s):  
Herpes Simplex ◽  
Antibiotic Therapy ◽  
Combined Treatment ◽  
Visual Outcome ◽  
Empiric Antibiotic Therapy ◽  
Predisposing Factor ◽  
Aggressive Approach ◽  
Corneal Infection ◽  
Ocular Infections ◽  
Herpes Simplex Keratitis

Introduction: Moraxella nonliquefaciens ( M. nonliquefaciens) is a low pathogenicity microorganism, which rarely causes ocular infections, unless there is a predisposing factor. The main clinical manifestation of M. nonliquefaciens ocular infections is endophthalmitis and only five cases of corneal infection have been reported. This work shows an update in M. nonliquefaciens corneal infections, and the first reported case of keratitis due to M. nonliquefaciens superinfecting herpes simplex infection. Case report: A 84-year old woman with worsening of her herpes simplex keratitis, diagnosed, and treated 2 days before. The slit lamp showed deep paracentral infiltrate and hypopyon. A corneal sample was collected for culture prior to initiation of empiric antibiotic therapy with vancomycin and ceftazidime fortified, oral acyclovir, and cyclopentolate. The strain was identified as M. nonliquefaciens and topical antibiotic therapy was adjusted to ciprofloxacin and ceftazidime. After 2 weeks, the epithelial defect and the infiltrate were resolved and prednisolone was added to the regimen. As the corneal oedema and neovascularization decreased, acyclovir, and prednisolone were slowly tapered. About 4 months later, the visual outcome was 20/50 and the ophthalmic examination showed a clear cornea with a paracentral leucoma. Conclusion: Keratitis due to M. nonliquefaciens is rare and should be suspected in patients with local predisposing factors such as corneal damage or previous corneal infection. Prompt and appropriate combined treatment for the predisposing lesions and the keratitis may improve the prognosis and avoid a more aggressive approach.

scholarly journals Herpes Simplex Keratitis in Patients with SARS-CoV-2 Infection: A Series of Five Cases

Medicina ◽  
2021 ◽  
Vol 57 (5) ◽  
pp. 412
Author(s):  
Nora Majtanova ◽  
Petra Kriskova ◽  
Petra Keri ◽  
Zlatica Fellner ◽  
Juraj Majtan ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Initial Assessment ◽  
Assessment Tests ◽  
Ocular Manifestations ◽  
Ocular Infections ◽  
Herpes Simplex Keratitis ◽  
Simplex Virus ◽  
Local Antibiotic ◽  
Hsv 1

Herpes simplex virus type 1 (HSV-1) is a leading cause of infectious blindness worldwide. Most of the initial infection cases manifest as acute epithelial keratitis. Reactivation of herpesviruses is common in critically ill patients, including patients with severe Coronavirus disease (COVID-19). However, the data on COVID-19-related ocular infections is sparse, despite recent observations that more than 30% of COVID-19-infected patients had ocular manifestations. We report five cases of HSV-1 keratitis in COVID-19 patients. In total, five COVID-19 patients underwent ophthalmic examination, showing similar symptoms, including photophobia, tearing, decreased vision, eye redness, and pain. After initial assessment, tests of visual acuity and corneal sensitivity, a fluorescein staining test, and complete anterior and posterior segment examinations were performed. A diagnosis of HSV-1 keratitis was confirmed in all cases. Therapy was initiated using a local and systemic antiviral approach together with local antibiotic and mydriatic therapy. The complete reduction of keratitis symptoms and a clear cornea was achieved in all patients within 2 weeks. SARS-CoV-2 infection may be a risk factor for developing HSV-1 keratitis, or it may act as a potential activator of this ocular disease.

scholarly journals Successful de-escalation antibiotic therapy using cephamycins for sepsis caused by extended-spectrum beta-lactamase-producing Enterobacteriaceae bacteremia: A sequential 25-case series

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 782-786
Author(s):  
Tsukasa Kuwana ◽  
Junko Yamaguchi ◽  
Kosaku Kinoshita ◽  
Satoshi Hori ◽  
Shingo Ihara ◽  
...  
Keyword(s):  
Septic Shock ◽  
Antibiotic Therapy ◽  
Vital Signs ◽  
Apache Ii ◽  
Empiric Antibiotic Therapy ◽  
Apache Ii Score ◽  
Beta Lactamase ◽  
Extended Spectrum Beta Lactamase ◽  
Escalation Therapy ◽  
Extended Spectrum

AbstractCarbapenems are frequently used to treat infections caused by extended-spectrum beta-lactamase-producing Enterobacteriaceae (ESBL-E), but carbapenem-resistant Enterobacteriaceae bacteria are a clinical concern. Although cephamycins (cefmetazole; CMZ) have been shown to be effective against mild cases of ESBL-E infection, data on their use for severe ESBL-E infections with sepsis or septic shock remain scarce. Herein, we discuss a de-escalation therapy to CMZ that could be used after empiric antibiotic therapy in ICU patients with sepsis or septic shock caused by ESBL-E bacteremia. A sequence of 25 cases diagnosed with sepsis or septic shock caused by ESBL-E bacteria was evaluated. The attending infectious disease specialist physicians selected the antibiotics and decided the de-escalation timing. The median SOFA (Sequential Organ Failure Assessment) and APACHE II (Acute Physiology and Chronic Health Evaluation II) severity scores were 8 and 30; the rate of septic shock was 60%. Infections originated most frequently with urinary tract infection (UTI) (56%) and Escherichia coli (85%). Eleven patients were de-escalated to CMZ after vital signs were stable, and all survived. No patients died of UTI regardless of with or without de-escalation. The median timing of de-escalation antibiotic therapy after admission was 4 days (range, 3–6 days). At the time of de-escalation, the median SOFA score fell from 8 to 5, the median APACHE II score from 28 to 22, and the rate of septic shock from 55% to 0%. We conclude that for sepsis in UTI caused by ESBL-E bacteremia, de-escalation therapy from broad-spectrum antibiotics to CMZ is a potential treatment option when vital signs are stable.

scholarly journals Purple urine bag syndrome is a rare manifestation of bacteriuria on bladder catheter: case report

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Othmane Mohib ◽  
Thomas Roland ◽  
Margot Fontaine ◽  
France Laurent ◽  
Camelia Rossi
Keyword(s):  
Antibiotic Therapy ◽  
Rare Complication ◽  
Total Duration ◽  
Empiric Antibiotic Therapy ◽  
Healthcare Team ◽  
Urine Ph ◽  
Urine Retention ◽  
Bladder Catheter ◽  
Purple Urine Bag Syndrome ◽  
Purple Urine

Abstract Background Purple urine bag syndrome (PUBS) is a complication of bacterial colonisation of bladder catheters in which urine turns purple in the tubing, as well as in the catheter bag. This rare phenomenon can be very worrisome and stressful for the patients and their families, as well as for the healthcare team taking care of them. Recognising this complication is essential in order to avoid misdiagnosis and erroneous treatment. We report a case of PUBS in a 71-year-old female patient. Case presentation A 71-year-old woman with previous medical history of schizophrenia was admitted to the emergency department for anorexia and suspicion of psychotic decompensation. Acute urine retention and rectal faecal impaction were clinically suspected and confirmed by bladder ultrasound and rectal examination, respectively. The patient underwent bladder catheterisation as well as a rectal enema. The day after her admission, our medical team was approached by the nurse in charge of the patient because of purple urine in her catheter bag and tubing. The diagnosis of PUBS was made with the help of the Oxford urine chart. A dipstick urinalysis revealed alkaline urine (pH = 8), and the urine culture was subsequently positive for Proteus mirabilis, which is sensitive to quinolones, beta-lactams and nitrofurantoin. The bladder catheter was changed. The patient received empiric antibiotic therapy with Levofloxacin 500 mg once daily. After obtaining the antibiogram, the targeted antibiotic therapy was adapted with oral Cefuroxime 500 mg three times a day for a total duration of seven days of antibiotic therapy. There was no recurrence of purple urine. Conclusion PUBS is a rare complication of bacteriuria, which induces a purple colouration of the tubing as well as the catheter bag. It is a simple spot diagnosis, as there is no other known cause of purple urine. This is why we believe that the Oxford urine chart represents a very interesting and easily accessible tool to help clinicians to investigate any abnormal urine colour.

Compliance With ATS-IDSA Guideline Recommendations for Empiric Antibiotic Therapy in Pneumonia

CHEST Journal ◽  
2010 ◽  
Vol 138 (4) ◽  
pp. 856A
Author(s):  
Kyle W. Bierman ◽  
Lee E. Morrow ◽  
Joshua D. Holweger ◽  
John T. Ratelle ◽  
Mark A. Malesker
Keyword(s):  
Antibiotic Therapy ◽  
Empiric Antibiotic Therapy ◽  
Empiric Antibiotic

scholarly journals Herpes Simplex Virus Type 1 Corneal Infection Results in Periocular Disease by Zosteriform Spread

2001 ◽  
Vol 75 (11) ◽  
pp. 5069-5075 ◽  
Author(s):  
Bretton C. Summers ◽  
Todd P. Margolis ◽  
David A. Leib
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Skin Lesions ◽  
Ocular Infection ◽  
Trigeminal Ganglia ◽  
Corneal Infection ◽  
Recombinant Viruses ◽  
Viral Spread ◽  
Reporter Activity ◽  
Simplex Virus

ABSTRACT In humans and animal models of herpes simplex virus infection, zosteriform skin lesions have been described which result from anterograde spread of the virus following invasion of the nervous system. Such routes of viral spread have not been fully examined following corneal infection, and the possible pathologic consequences of such spread are unknown. To investigate this, recombinant viruses expressing reporter genes were generated to quantify and correlate gene expression with replication in eyes, trigeminal ganglia, and periocular tissue. Reporter activity peaked in eyes 24 h postinfection and rapidly fell to background levels by 48 h despite the continued presence of viral titers. Reporter activity rose in the trigeminal ganglia at 60 h and peaked at 72 h, concomitant with the appearance and persistence of infectious virus. Virus was present in the periocular skin from 24 h despite the lack of significant reporter activity until 84 h postinfection. This detection of reporter activity was followed by the onset of periocular disease on day 4. Corneal infection with a thymidine kinase-deleted reporter virus displayed a similar profile of reporter activity and viral titer in the eyes, but little or no detectable activity was observed in trigeminal ganglia or periocular tissue. In addition, no periocular disease symptoms were observed. These findings demonstrate that viral infection of periocular tissue and subsequent disease development occurs by zosteriform spread from the cornea to the periocular tissue via the trigeminal ganglion rather than by direct spread from cornea to the periocular skin. Furthermore, clinical evidence is discussed suggesting that a similar mode of spreading and disease occurs in humans following primary ocular infection.

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