The rapidly changing epidemiology of Staphylococcus aureus and evolution of strains with enhanced virulence is a significant issue in global healthcare. Hospital-associated methicillin-resistant S. aureus (HA-MRSA) lineages are being completely replaced by community-associated S. aureus (CA-MRSA) in many regions. Surveillance programs tracing the reservoirs and sources of infections are needed. Using molecular diagnostics, antibiograms, and patient demographics, we have examined the distributions of S. aureus in Ha’il hospitals. Out of 274 S. aureus isolates recovered from clinical specimens, 181 (66%, n = 181) were MRSA, some with HA-MRSA patterns across 26 antimicrobials with almost full resistances to all beta-lactams, while the majority were highly susceptible to all non-beta-lactams, indicating the CA-MRSA type. The rest of isolates (34%, n = 93) were methicillin-susceptible, penicillin-resistant MSSA lineages (90%). The MRSA in men was over 56% among total MRSA (n = 181) isolates and 37% of overall isolates (n = 102 of 274) compared to MSSA in total isolates (17.5%, n = 48), respectively. However, these were 28.4% (n = 78) and 12.4% (n = 34) for MRSA and MSSA infections in women, respectively. MRSA rates per age groups of 0–20, 21–50, and >50 years of age were 15% (n = 42), 17% (n = 48), and 32% (n = 89), respectively. However, MSSA in the same age groups were 13% (n = 35), 9% (n = 25), and 8% (n = 22). Interestingly, MRSA increased proportional to age, while MSSA concomitantly decreased, implying dominance of the latter ancestors early in life and then gradual replacement by MRSA. The dominance and seriousness of MRSA despite enormous efforts in place is potentially for the increased use of beta-lactams known to enhance virulence. The Intriguing prevalence of the CA-MRSA patterns in young otherwise healthy individuals replaced by MRSA later in seniors and the dominance of penicillin-resistant MSSA phenotypes imply three types of host- and age-specific evolutionary lineages. Thus, the decreasing MSSA trend by age with concomitant increase and sub-clonal differentiation into HA-MRSA in seniors and CA-MRSA in young and otherwise healthy patients strongly support the notion of subclinal emergences from a resident penicillin-resistant MSSA ancestor. Future vertical studies should focus on the surveillance of invasive CA-MRSA rates and phenotypes.
A 32-year-old female, with a history of secondarily-generalized convulsive epilepsy, mental retardation, and a psychiatric illness, developed neuroleptic malignant syndrome while receiving carbamazepine and amitriptyline concurrently. We hypothesize that the addition of amitriptyline to carbamazepine caused a decrease in the serum level of carbamazepine, resulting in NMS. We conclude that combination therapy with carbamazepine and amitriptyline should be avoided in patients who are predisposed to NMS. The purpose of this paper is to warn physicians against combination therapy with carbamazepine and tricyclic antidepressants which may be conducive to neuroleptic malignant syndrome in susceptible patients.
There is a plethora of data in the EEG literature on the characteristics of the most prominent component of interictal epileptiform discharges (IED), namely the negative (fast) phase. Surprisingly, however, little attention has been drawn to the after-coming slow wave (ASW), and its pathological as well as clinical significance. In this paper, we will address the significance of prominent (high amplitude) ASW, giving rise to a triphasic morphology of the IED (focal triphasic sharp waves and spikes—FTSW). We will discuss this EEG pattern with respect to its clinical, neurophysiological, and neuropathological significance. This investigation was conducted on a heterogeneous group of patients at KKH, Ha'il, KSA. Our data revealed that FTSW were rare EEG events occurring primarily in the first two decades of life. Ninety percent of the patients with FTSW had epilepsy, presenting clinically with generalized convulsive seizures, often without partial onset. The majority of these patients responded favorably to anticonvulsant monotherapy. We were surprised to find that half of the patients with FTSW had chronic and/or static CNS pathology, particularly congenital CNS anomalies. Even though more than one mechanism may be involved in the pathogenesis of FTSW, we believe a deeply seated pacemaker as the source of this EEG pattern is the most compelling theory. The presence of FTSW should alert clinicians to the possibility of an underlying chronic and/or static CNS pathology, in particular congenital CNS anomalies, underscoring the significance of neuroimaging in the work-up of this population. Moreover, it is conceivable that the prominent ASW may contribute to the interictal intellectual dysfunction of these patients, justifying aggressive anticonvulsant therapy.
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