Antibiotic resistance is a serious global public health problem. ESBLs are enzymes that destroy expanded-spectrum beta-lactam antibiotics rendering these drugs ineffective. Infection with ESBL-producing K.pneumoniae are hard to treat and result in longer hospital stay and higher mortality rates. The Clinical Laboratory Standard Institute (CLSI) have standard methods for detection of ESBL producing strains of bacteria in infected patients to guide antibiotic therapy, reduce the risk of mortality and risk of transmission. The presence of K.pneumoniae and E.coli which produce ESBLs have been confirmed in natural environments such as soil and water but no standard methods exist to identify directly and quantify these bacteria to understand the risk of human exposure in these settings. The purpose of this research is to assess the ability of an agar dilution method, using a differential agar Bio-Rad Rapid E.coli 2 agar utilized in environmental water quality studies, to identify correctly ESBL-producing K.pneumoniae. The minimum inhibitory concentration (MIC) of ceftriaxone antibiotic for wild-type ESBL producing K.pneumoniae isolates were compared on Mueller-Hinton broth (MHB) and Bio-Rad Rapid E.coli 2 agar. Using the MIC values, the isolates were classified as susceptible, intermediate or resistant. The MIC of wild-type strains of K.pneumoniae were above 4μg/mL for both methods on all susceptibility tests performed. The results of this research suggest that Bio-Rad Agar dilution method performed well, correctly identifying these strains as resistant to ceftriaxone, an indication of ESBL production. The Bio-Rad agar dilution method can be considered as a viable standard method for direct identification of ESBL-producing K.pneumoniae in natural environments.

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Ceftriaxone is the most used third-generation cephalosporin anti-microbial agent in treating infections caused by gram-positive and gram-negative organisms. Chorea is a movement disorder characterized by involuntary and hyperkinetic movements of the affected body parts due to rapid and unpredictable contractions. We report an uncommon case of ceftriaxone-induced acute reversible chorea. 84-year-old male with a medical history of diabetes mellitus, hypertension, previous myocardial infarction, and gouty arthritis was admitted to the hospital with complaints of altered mental status (AMS) and right 1st metacarpal-phalangeal joint (MTP) swelling, erythema and ruptured wound draining pus-like fluid. The patient was febrile with a temperature of 101.3 F. The rest of the vitals were normal. The patient had an initial workup and was empirically started on ceftriaxone and vancomycin for skin and soft tissue infection. His wound cultures and blood cultures grew pan-sensitive streptococcus agalactiae. His antibiotics were de-escalated to ceftriaxone. X-ray showed severe soft tissue swelling and erosive changes at the base of the proximal phalanx of the first digit secondary to gout or osteomyelitis. MRI of the right foot was attempted, but the patient could not tolerate it. TTE was negative for Endocarditis. The patient had initial improvement in his AMS, but 72 hours later, he became increasingly confused with choreiform movements. Ceftriaxone was discontinued, and Ertapenem was started. Patient’s confusion and choreiform movements improved after the discontinuation of ceftriaxone. Patient was discharged to a rehabilitation facility with four weeks of IV Ertapenem. Ceftriaxone is a third-generation cephalosporin that inhibits mucopeptide synthesis in the bacterial cell wall. Ceftriaxone is a well-tolerated anti-microbial agent with a low toxicity profile. Common adverse effects include gastrointestinal disturbances, skin rashes, and hematological disorders. Neurological symptoms like encephalopathy is an uncommon adverse effect. Chorea is a movement disorder due to hereditary or acquired causes. Drug-induced chorea is one of the rare causes of acquired chorea. History and physical examination are essential in diagnosing acquired causes of chorea. Further workup with laboratory tests and neuroimaging are required to evaluate secondary causes. Chorea due to ceftriaxone is described in a patient with end-stage renal disease on hemodialysis in a case report previously, but our patient did not have any chronic kidney disease [1]. It is postulated that beta-lactam antibiotics increase neurological hyperexcitability by increased glutamate release in the striatum and cerebral cortex, causing movement disorders [2]. It is noted that pre-existing neurological conditions and excessive dosage are shown to be significant risk factors for cephalosporin neurotoxicity. Our patient, however, did not have any neurological condition but was treated with 2 grams of ceftriaxone daily before he had choreiform movements. Upon removal, the patient improved significantly within 36-48 hours. Ceftriaxone is a widely used anti-microbial with broad coverage. Although uncommon, recognizing that neurotoxicity due to third generation cephalosporins is essential. Prompt diagnosis and withdrawal of the offending agent is critical in improving the patient’s symptoms. Age, prior neurological conditions, kidney disease, and dosage must be carefully evaluated before administration.

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Parkinsons sjukdom (PD) är ett tillstånd som ger en försvårad och försämrad livskvalité. I dagsläget finns det endast symtomatiska läkemedel men ingen bot med vilken sjukdomen upphör eller som bromsar förloppet. Pågående forskningsarbete utgår bland annat från att ta fram nya läkemedel men även också undersöka om redan befintliga läkemedel går att använda som behandling av PD. Många av de redan befintliga läkemedlen som testas är de som har förmågan att påverka proteinet α-synuklein (α-syn) och dess aggregering, som visats vara en central orsak till uppkomsten av PD. I föreliggande litteraturstudie undersöktes på vilket sätt en del läkemedel vars indikation är PD och även andra sjukdomstillstånd såsom astma, påverkar (ex. påskyndar eller inhiberar) in-vitro aggregering av α-syn. Därutöver genomfördes en detaljerad analys av de utvalda läkemedlen och deras effekt på α-syn aggregering utifrån deras kemiska egenskaper med avseende på löslighet (hydrofila, lipofila, amfifila) och inbindning till α-syn. Här kunde det visas att aggregering av α-syn inhiberades av alla utvalda läkemedel förutom dexametason, som istället påskyndade aggregeringskinetiken för proteinet. Dessutom uppvisade fasudil, ceftriaxon, dopamin, entakapon och tolkapon inbindning till delar av (hydrofila, hydrofoba eller amfifila) vilka delade samma fysikalkemiska egenskaper som α-syn. Därtill uppvisade utvalda läkemedel med till viss del plana strukturer (ex. aromatiska ringar) direkt inbindning till α-syn, vilka också rapporterats ha en något högre grad av transport över blod-hjärnbarriären, dock måste dessa fynd mer noggrant undersökas. Sammanfattningsvis visade alla utvalda läkemedel förutom dexametason anti-aggregeringsegenskaper (hämmande) mot α-syn genom att antingen indirekt eller direkt binda till proteinet och därmed hindra proteinet från att börja binda till sig själv. Mer studier måste genomföras för att studera effekten av läkemedelsexponering på α-syn för att identifiera viktiga segment av proteinet som kan utgöra läkemedelsmål för inhibering av α-syn aggregering. / Parkinson's disease (PD) is a condition that leads to an aggravated and worsened quality of life. At present, there are only symptomatic drugs for PD but no cure that eradicate the disease nor halter the disease progression have been found. Current research is being carried out to develop new drugs, but efforts also investigate whether existing drugs can be used as treatment for PD. Many of the already existing drugs being tested are those that have the ability to interact with a protein called α-synuclein (α-syn), that has been implicated to be a major player for onset of PD. In the present literature study, it was investigated in what way some drugs, whose indication is PD but also other diseases such as asthma, affect (i.e. propagate or inhibit) the in-vitro aggregation kinetics of αsyn. Additionally, a detailed analysis of the investigated drugs and their effect on the aggregation pathway was made to characterize common chemical features of the selected drugs based upon choice of solvents and binding to α-syn. Here, it could be shown that aggregation of α-syn is inhibited upon exposure to all selected drugs except dexametason which instead propagated aggregation of α-syn. In addition, fasudil, ceftriaxone, dopamine, entacapone and tolcapone was found to bind to parts (hydrophilic, hydrophobic or amphiphilic) of α-syn similar to their solubility features. Moreover, the selected drugs that were found to bind to α-syn seemed to exhibit planar in structure (i.e. aromatic rings) and also be associated to pass the blood-brain barrier to a greater extent, however these findings need to be more thoroughly investigated. In summary, all drugs but dexametason were shown to inhibit aggregation of α-syn invitro by either indirectly or directly affecting the aggregation of the protein. Further investigations need to be carried out to study the effect of drug exposure on α-syn aggregation in order to propose key segments of α-syn that can act as drug targets for inhibition of protein aggregation.