text:
The Emergence of Vancomycin Resistance Staphylococci in Egypt: A Review
Azza Salah El-Demerdash*
Agriculture Research Center (ARC), Animal Health Research Institute (AHRI), Egypt
*Corresponding author: Azza Salah El-Demerdash, Agriculture Research Center (ARC), Animal Health Research Institute (AHRI), Egypt, Email: Dr.azzasalah@yahoo.com
Cite this article: Azza Salah El-Demerdash* . The Emergence of Vancomycin Resistance Staphylococci in Egypt: A Review. Op Acc J Bio Sci & Res 5(5)-2020
Staphylococcus aureus is a standout amongst the most pathogenic bacteria worldwide. The occurrence of methicillinresistant Staphylococcus aureus (MRSA) made vancomycin as the only therapeutic choice. Due to excessive use of vancomycin, diminished susceptibility and increased resistance against this antibiotic are reported worldwide. The current study aimed at investigating the emergence and development of vancomycin-resistant Staphylococcus aureus (VRSA) in Egypt. This paper highlighted the genetic basis and virulence determinants of vancomycin resistance in S. aureus. It also focused on important considerations in the detection of vancomycin resistance and the development of this resistance all over the years. Finally, the expanding reports on the emergence of VRSA in Egypt mentioned in this study, revealed the necessity for new and effective drugs against Staphylococcus infection and more attention should be paid to the proper prescription of this antibiotic as the only choice for S. aureus infections.
Keywords: Vancomycin; Resistance; Staphylococci; Egypt
Over the past few decades, there has been a disturbing increment in the prevalence of antibiotic-resistant pathogens and strains in serious infections [1, 2]. The occurrence of bacterial infection had diminished with the disclosure of penicillin in 1940 until Staphylococcus aureus began producing β-lactamase, which destroys the penicillin β-lactam core ring [3, 4]. This increase in resistance towards penicillin drove the development of methicillin drugs, which are virtually resistant against many genetic variants of the β-lactamase enzyme. Infection by S. aureus was well controlled using methicillin until the seclusion of the first strain of methicillin-resistantS. aureus (MRSA) in 1961 [4,5]. Since then, MRSA has become endemic in hospitals and nursing homes around the world [1,6, 7].
Vancomycin has served as the cornerstone of therapy for serious (MRSA) infections for 50 years. Despite the fact that microbiological resistance to vancomycin in S. aureus remains very rare, recent years have seen a shift upwards in vancomycin MICs [8, 9]. Vancomycin, a glycopeptide antibiotic, acts against Gram-positive bacteria only, by inhibiting the synthesis of the long polymers of (NAM-NAG) that form the backbone strands (polypeptide into the growing peptidoglycan (PG) chain) of the bacterial cell wall. It inhibits this process by the formation of a hydrogen bond with D.Ala.-D.Ala. Of the stem pentapeptide of bacterial cell wall which consequently blocks the release of terminal D.Ala [10] as shown in (Figure 1).
An elevated mutation rate of Enterococcus species led to the rapid development of vancomycin resistance, indicating that a high mutation frequency could be one of the factors that favor the emergence and transformation of vancomycin resistance to S. aureus [11]. The glycopeptide antibiotic vancomycin has long been reserved for treatment of infections with methicillin-resistant S. aureus (MRSA). But, over the past decade, vancomycin intermediately resistant S. aureus strains have emerged in many countries [12]. The first strain of S. aureus with reduced susceptibility to vancomycin was reported in Japan in 1997 and had a vancomycin MIC in the intermediate susceptibility range [13]. Presently, VRSA has been isolated in different countries; hence, the burden has become a global phenomenon. There have been no sufficient literature explaining the emergence of VRSA strains in Egypt as yet. Therefore, the current paper focuses on the problem of evolution vancomycin acquired resistance of gram-positive cocci in Egypt.
Figure 1: Mechanism of vancomycin action
Testing of Vancomycin Resistance in Vitro
MIC tests should be performed to determine the susceptibility of staphylococci isolates to vancomycin. The disc diffusion test doesn't differentiate vancomycinsusceptible isolates of S. aureus from vancomycinintermediate isolates, nor does the test differentiate among vancomycin-susceptible, intermediate and resistant isolates of coagulase-negative staphylococci, all of which will give similar size zones of inhibition [14]. S. aureus isolates with vancomycin MICs between 4 and 8 μg/ml are classified as vancomycin- intermediate and those with MIC ≥16 μg/ml as vancomycin resistant. These MIC cutoffs are different from those for coagulase-negative staphylococci and enterococci where isolates with vancomycin MIC ≥32 μg/ml are classified as vancomycin resistant.
Apart from vancomycin-intermediate S. aureus (VISA) and vancomycin-resistant S. aureus (VRSA), there is one more entity, heterogenous VISA (hVISA), which has a vancomycin MIC ≤2 μg/ml by routine testing methods, but has a great population of cells with reduced vancomycin susceptibility (in the disc diffusion method) [15].
Genomic Organization of Vancomycin Resistance
The first documented cause of vancomycin resistance in S. aureus due to the acquisition of the van genes occurred in Michigan in 2002 [16]. The second case of VRSA was isolated from a morbidly obese 70-year-old male in Pennsylvania [17]. The third case of VRSA was isolated from the urine of a long-term care facility patient [18]. The van genes were first found in1988 in an Enterococcus faecium isolated from France [19]. Transfer of vancomycin resistance from enterococci to staphylococci was detected and light- cycler PCR results illustrated that enterococci and staphylococci are known to exchange their genetic information (plasmid and related element) [20-22].
Six sorts of vancomycin resistance genes have been described on both a phenotypic and a genotypic premise in enterococci. Five of these sorts (van A, B, D, E, and G) correspond to acquired resistance and one sort (vanC) is an intrinsic property of Enterococcus gallinarum and Enterococcus flavescens. Classification of glycopeptide resistance is currently based on the primary sequence of the structural genes for the resistance ligases rather than on the levels of resistance to glycopeptides because the minimum inhibitory concentration (MIC) ranges of vancomycin and against the various types overlap. VanA-type strains display high levels of inducible resistance to both vancomycin and teicoplanin, whereas vanB-type strains have variable levels of inducible resistance to vancomycin only [23], [24]. VanDtype strains are characterized by constitutive resistance to moderate levels of the 2 glycopeptides [25] while vanC, vanE and vanG-type strains are resistant to low levels of vancomycin [26]. The vanA and vanB operons are situated on plasmids or in the chromosome [27], whereas the vanD [25], vanC [28], vanE [29] and vanG [30] operons have been discovered only in the chromosome. Along these lines, the incidence of van genes on Staphylococcus species responsible for the resistance to vancomycin was acquired by the action of vanA and vanB, where the enterococcus plasmid apparently behaved as a suicide conveyance vector to the plasmid in MRSA [31].
The vanA, vanR, vanS, vanH and vanX genes are basic for the articulation of the vanA phenotype (van A cluster) [32]. The transposon encodes a dehydrogenase (van H), which decreases pyruvate to d-Lac and the vanA ligase (van A), which catalyzes the formation of an ester bond between d-Ala and d-Lac. The resulting d-Ala-d-Lac depsipeptide replaces the d-Ala-d-Ala dipeptide in peptidoglycan synthesis, a substitution that decreases the affinity of the molecule for glycopeptides considerably. VanX, a D, D-dipeptidase that splits the d-Ala–d-Ala dipeptide synthesized by the host. Expression of the vanA gene cluster is regulated by the two-component regulatory system vanRvanS, which is responsible for recognition of the presence of glycopeptides in the culture medium and transcriptional activation of the resistance and regulatory genes [10]. As in vanA-type strains, acquired vanB-type resistance is due to synthesis of peptidoglycan precursors ending in the depsipeptide d-Ala-d-Lac instead of the dipeptide d-Alad-Ala [23, 33].
Virulence Determinants In VRSA
The alternative transcription factor sigma B (sB) is responsible for transcription of Staphylococcus aureus during the stress response. Many virulence-associated genes are directly or indirectly regulated by sB. Expression of sB-regulated virulence genes, including hla and fnbA, was related with the vancomycin-induced sB activity in VRSA strains and the raise in the cytotoxicity upon vancomycin treatment. The sub-minimum inhibitory concentration (sub-MIC) levels of vancomycin act as ecological stressors and activate the stress response sigma factor, sB [34].
The Consideration Of Genetic Basis And Regulation For Vancomycin Resistance In Egypt
Following a systematic literature search using the keywords vancomycin-resistant S. aureus, few reports were retrieved. A systematic review of all available resources suggested an increased rate of Vancomycin Intermediate S. aureus (VISA) and VRSA emergence in Egypt initiated since 2008. From the first report until 2010, 19 VISA and 2 VRSA from several intensive cares were detected [35, 36] at which Medhat et al. was the first one who identified two VRSA isolates from Mansoura University Hospital, children department and still susceptible to some antibiotics, which were not used widely such as, daptomycin, quinipristin\ dalfopristin and tigecycline, also detected hVISA and VISA had an antimicrobial susceptibility pattern similar to VRSA isolates.
Then, the highly resistant vancomycin- resistant S. aureus strains were obtained from clinical samples of patients at the critical care unit, Cairo Hospital, University. Furthermore, van A and van B resistant genes were detected for the first time by using real-time PCR with percentages of 27% and 36%, respectively [37]. Subsequently, 10 VRSA isolates were detected from outpatient clinics as well as inpatient departments mainly from the intensive care unit and orthopedic department at Zagazig University hospitals and five out of them harbored vanA gene [9]. Hassanein et al. [38] obtained three VISA and one VRSA. The vanA gene was detected in two isolates only (one VISA and one VRSA). Also, the tested VRSA strain was characterized by the production of virulence factors hemolysin, lecithinase, and protease.
In 2014, profound cases of VRSA infection were detected in many intensive cares all over Egypt cities with little literature for the main source or origin of these isolates [1,39]. Also, all obtained VRSA isolates were harbored vanA gene. These raise the possibility of greatly increased mortality from simple infections and treatment-mediated failures Osman et al. [40], recorded intermediate resistant S. aureus in raw meat (51%) which might indicate the spread of vancomycin resistance in the community and imply food safety hazards.
The report of [41] was the first one of the comprehensive identification and confirmation of vancomycin- resistant S. aureus (VRSA) harboring van genes from meat samples in Egypt. The findings of VRSA in meats are a motive of concern, as they may suggest the spread of such microorganisms or their genetic material outside clinical boundaries. Eight VRSA isolates were obtained, vanA gene was detected in 3 isolates which were resistant to vancomycin with MIC≥128 μg/ml, whereas, four isolates carried vanB gene with MIC≥64 μg/ ml. These results confirmed the criteria, reporting that vanA-type strains display high levels of inducible resistance to vancomycin, whereas vanB-type strains have variable levels of resistance [23]. Moreover, the absence of van genes in one VRSA isolate by PCR even in the presence of phenotypic resistance to vancomycin. As proposed previously, cell wall thickening is the essential contributor for the development of vancomycin resistance. As a result, more vancomycin molecules are trapped in the peptidoglycan synthesis occurs [42].
The remarkable global concern of antibiotic-resistant pathogens (especially VRSA and MRSA) in the food chain and the potential for these resistant pathogens to spread through the food chain prompted the Codex Alimentarius Commission to establish an ad hoc Intergovernmental Task Force on antimicrobial resistance. The principle errand of this commission is to apply the a complete risk assessment methodology on utilization of antimicrobials belonging to both clinical and veterinary classes with special reference to beef meat that has been implicated to contribute to the emergence of multidrug resistance among humans through the scattering of resistance genes conveyed by resistant pathogens transmitted by contaminated meat [43-45]. However, until today all studies reinforce the development and increase the spread of these pathogens in Egypt resulting from misuse of antibiotics.
1. The occurrence of VRSA isolates demonstrates that resistance to vancomycin will appear because of overuse. We recommend that this drug should not be used (prescribed) except if it is highly indicated and only after susceptibility tests.
2. Most of the VRSA were profoundly resistant to most antibiotics. This may be because the control of antibiotic use isn't strictly followed by clinicians.
3. The infection-control practices, improved knowledge, and environmental hygiene may aid in controlling the propagation of vancomycin resistance
4. Alternative therapies should be considered to avoid treatment failure of staphylococcal infection.
1. Alam SMS, Kalam MA, Munna MS, Munshi SK, Noor R (2014) Isolation of pathogenic microorganisms from burn patients admitted in Dhaka Medical College and Hospital and demonstration of their drug-resistance traits. Asian Pacific J Trop Dis 4: 402-407.
2. Chessa D, Ganau G, Mazzarello V (2015) An overview of Staphylococcus epidermidis and Staphylococcus aureus with a focus on developing countries. J Infect Dev Ctries 9: 547- 550.
3. Khan SA, Feroz F, Noor R (2013) Study of extended-spectrum β-lactamase-producing bacteria from urinary tract infections in Bangladesh. Tzu Chi Med J 25: 39-42
4. Peacock S (2006) Staphylococcus aureus. Princ Pract Clin Bacteriol 2: 73-98.
5. Normark BH, Normark S (2002) Evolution and spread of antibiotic resistance. J Intern Med 252: 91-106.
6. Jones RN (2008) Key considerations in the treatment of complicated staphylococcal infections. Clin Microbiol Infect 14: 3-9.
7. Rahimipour F, Ghazvini K, Youssefi M (2018) Emergence of Vancomycin-Resistant Staphylococcus Aureus in Middle-East.
8. Rhee KY, Gardiner DF, Charles M (2005) Decreasing in vitro susceptibility of clinical Staphylococcus aureus isolates to vancomycin at the New York Hospital: quantitative testing redux. Clin Infect Dis 40: 1705-1706.
9. Shady AHM, El-Essawy AK, Salama MS, El-Ayesh AM (2012) Detection and molecular characterization of vancomycin resistant Staphylococcus aureus from clinical isolates. African J Biotechnol 11: 16494-16503.
10. Arthur M, Molinas C, Depardieu F, Courvalin P (1993) Characterization of Tn1546, a Tn3-related transposon conferring glycopeptide resistance by synthesis of depsipeptide peptidoglycan precursors in Enterococcus faecium BM4147. J Bacteriol 175: 117-127.
11. Schaaff F, Reipert A, Bierbaum G (2002) An elevated mutation frequency favors development of vancomycin resistance in Staphylococcus aureus. Antimicrob Agents Chemother 46: 3540-3548.
12. Ferreira-Carvalho BT, Figueiredo AM, others (2000) Spread of methicillin-resistant Staphylococcus aureus belonging to the Brazilian epidemic clone in a general hospital and emergence of heterogenous resistance to glycopeptide antibiotics among these isolates. J Hosp Infect 44: 301-308.
13. Hanaki H, Labischinski H, Inaba Y, Kondo N, Murakami H, Hiramatsu K (1998) Increase in glutamine-non-amidated muropeptides in the peptidoglycan of vancomycin-resistant Staphylococcus aureus strain Mu50. J Antimicrob Chemother 42: 315-320.
14. Cockerill FR (2011) Performance standards for antimicrobial susceptibility testing: twenty-first informational supplement. [place unknown]: Clinical and Laboratory Standards Institute (CLSI).
15. Howden BP, Davies JK, Johnson PDR, Stinear TP, Grayson ML (2010) Reduced vancomycin susceptibility in Staphylococcus aureus, including vancomycin-intermediate and heterogeneous vancomycin-intermediate strains: resistance mechanisms, laboratory detection, and clinical implications. Clin Microbiol Rev 23: 99-139.
16. Chang S, Sievert DM, Hageman JC, Boulton ML, Tenover FC, et al. (2003) Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene. N Engl J Med 348: 1342-1347.
17. Tenover FC, Weigel LM, Appelbaum PC, McDougal LK, Chaitram J, et al. (2004) Vancomycin-resistant Staphylococcus aureus isolate from a patient in Pennsylvania. Antimicrob Agents Chemother 48: 275-280.
18. Center for Disease Control (1997) Staphylococcus aureus with reduced susceptibility to vancomycin--United States, 1997. MMWR Morb Mortal Wkly Rep. 46: 765.
19. Leclercq R, Derlot E, Duval J, Courvalin P (1988) Plasmidmediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N Engl J Med 319: 157-161.
20. Lyon BR, Skurray RON (1987) Antimicrobial resistance of Staphylococcus aureus: genetic basis. Microbiol Rev 51 :88.
21. Nagarajan V, Secretion P (1993) In Bacillus subtilis and other Gram-Positive Bacteria (AL Sonenshein, JA Hoch, and R. Losick eds). Am Soc Microbiol Washington,DC 713-726.
22. Weaver KE, Rice LB, Churchward G (2002) Plasmids and transposons. In: The Enterococci. American Society of Microbiology 219-263.
23. Arthur M, Depardieu F, Reynolds P, Courvalin P (1996) Quantitative analysis of the metabolism of soluble cytoplasmic peptidoglycan precursors of glycopeptideresistant enterococci. Mol Microbiol 21: 33-44.
24. Lebreton F, Depardieu F, Bourdon N, Fines-Guyon M, Berger P, et al. (2011) D-Ala-D-Ser VanN-type transferable vancomycin resistance in Enterococcus faecium. Antimicrob Agents Chemother 55(10): 4606-4612.
25. Depardieu F, Kolbert M, Pruul H, Bell J, Courvalin P (2004) VanD-type vancomycin-resistant Enterococcus faecium and Enterococcus faecalis. Antimicrob Agents Chemother 48: 3892-3904.
26. Reynolds PE, Courvalin P (2005) Vancomycin resistance in enterococci due to synthesis of precursors terminating in D-alanyl-D-serine. Antimicrob Agents Chemother 49: 21-25.
27. Arthur M, Quintiliani R (2001) Regulation of VanA-and VanBtype glycopeptide resistance in enterococci. Antimicrob Agents Chemother 45: 375-381.
28. Arias CA, Courvalin P, Reynolds PE (2000) VanC Cluster of Vancomycin-ResistantEnterococcus gallinarum BM4174. Antimicrob Agents Chemother 44: 1660-1666.
29. Patiño LA, Courvalin P, Perichon B (2002) vanE gene cluster of vancomycin-resistant Enterococcus faecalis BM4405. J Bacteriol 184: 6457-6464.
30. Depardieu F, Bonora MG, Reynolds PE, Courvalin P (2003) The vanG glycopeptide resistance operon from Enterococcus faecalis revisited. Mol Microbiol 50: 931-948.
31. Weigel LM, Clewell DB, Gill SR, Clark NC, McDougal LK, (2003) Genetic Analysis of a High-Level Vancomycin-Resistant Isolate of Staphylococcus aureus. Science (80- ) 302: 1569-1571.
32. Woodford N, Adebiyi AMA, Palepou MFI, Cookson BD (1998) Diversity of VanA glycopeptide resistance elements in enterococci from humans and nonhuman sources. Antimicrob Agents Chemother 42: 502-508.
33. Coombs GW, Pearson JC, Daley DA, Le T, Robinson OJ, et al. (2014) Molecular epidemiology of enterococcal bacteremia in Australia. J Clin Microbiol 52: 897-905.
34. Chen H, Chen C, Fang C, Hsieh Y, Lin M (2011) Vancomycin Activates s B in Vancomycin-Resistant Staphylococcus aureus Resulting in the Enhancement of Cytotoxicity 6: 1-8.
35. Medhat A, Mesbah MR, El-Naggar MM, Khalil ESA, El-Kenawy MF (2008) The first two vancomycin resistant Staphylococcus aureus isolates in Mansoura University Hospital; epidemiology and antimicrobial study. Egypt J Med Microbiol 17: 31-43.
36. Yaseen IH, Shareef AY, Daoud AS (2013) High prevalence of multidrugresistance MRSA and VRSA of different infections from Al-Jumhuory teaching hospital patients in Mosul. J Life Sci 7: 1255-1259.
37. Shindia, AA, Ragab FA, Nasrat H (2011) Emergence of High-Level Vancomycin-Resistant Staphylococcus aureus in the Critical care patients Cairo University Hospitals 5: 1281-1290.
38. Hassanein WA, EL- Zawahry YA, Reda FM, Abd E l- Rahman RA (2013) Molecular and microbiological studies on vancomycin. The Egyptian Society of Experimental Biology 9: 219-231.
39. Ghoniem EM, El Hendawy GR, Moteleb TMA, Hassan HA, Khalil HAER, et al. (2014) Characterization of vancomycin-resistant Staphylococcus aureus in the National Liver Institute. Menoufia Med J 27: 825.
40. Osman KM, Amer AM, Badr JM, Saad ASA (2015) Prevalence and Antimicrobial Resistance Profile of Staphylococcus Species in Chicken and Beef Raw Meat in Egypt. Foodborne Pathog Dis [Internet].
41. Ammar AM, Attia AM, Abd El-Aziz NK, Abd El Hamid MI, El-Demerdash AS (2016) Class 1 integron and associated gene cassettes mediating multiple-drug resistance in some food borne pathogens. Int Food Res J 23.
42. Cui L, Tominaga E, Neoh HM, Hiramatsu K (2006) Correlation between reduced daptomycin susceptibility and vancomycin resistance in vancomycin-intermediate Staphylococcus aureus. Antimicrob Agents Chemother 50: 1079-1082.
43. Doyle MP, Loneragan GH, Scott HM, Singer RS (2013) Antimicrobial resistance: Challenges and perspectives. Compr Rev Food Sci Food Saf 12: 234-248.
44. Card R, Vaughan K, Bagnall M, Spiropoulos J, Cooley W, et al. (2016) Virulence characterisation of Salmonella enterica isolates of differing antimicrobial resistance recovered from UK livestock and imported meat samples. Front Microbiol 7: 1-11.
45. Osman K, Alvarez-Ordóñez A, Ruiz L, Badr J, ElHofy F, et al. (2017) Antimicrobial resistance and virulence characterization of Staphylococcus aureus and coagulase-negative staphylococci from imported beef meat. Ann Clin Microbiol Antimicrob 16:1-10.


text:
Home > Faculty Scholarship > 267
Faculty Scholarship
Meek Mill's Trauma: Brutal Policing as an Adverse Childhood Experience
Todd J. Clark
Caleb Gregory Conrad
andré douglas pond cummings, University of Arkansas at Little Rock William H. Bowen School of LawFollow
Amy Dunn Johnson
Meek Mill's life and career have been punctuated by trauma, from his childhood lived on the streets of Philadelphia, through his rise to fame and eventual arrival as one of hip hop's household names. his 2018 track "Trauma," Meek Mill describes, in revealing prose, just how the traumatic experiences he endured personally impacted and harmed him. He also embodies a role as narrator in describing the same traumas and harms that impact the daily lives of countless similarly situated young Black people in the United States. As a child, Mill's lived experience was one of pervasive poverty and fear, as the world surrounding him consisted of large-scale poverty, addiction, crime, violence, and death. As a young man—at just 19 years of age—he was beaten by police, wrongfully arrested and incarcerated, and ultimately convicted of crimes that he did not commit, becoming another statistic as a young Black man swallowed by the American criminal justice system. Meek's story, lyrics and contributions to hip hop illuminate the Black experience with law enforcement. His personal involvements provide a powerful narrative for exactly how a racially biased criminal justice system perpetrates a trauma that extends far greater than the law has traditionally recognized. This article highlights this narrative through the lens that Meek Mill provides because of his current prominence in hip hop and the importance of his narrative claims. Despite his success in achieving the status of a true hip hop icon, Meek Mill suffered the kind of childhood adversity and trauma that emerging health care research indicates leads to debilitating health outcomes in adulthood.
Powerful health studies conducted over the past two decades have uncovered the startling impact of Adverse Childhood Experiences ("ACEs"). ACEs are traumatic events that occur in childhood, ranging from abuse and neglect to other traumatic experiences derived from household and community dysfunction. Today, ACEs are generally placed by health researchers into seven to ten categories of childhood adversities ranging from sexual, physical and emotional abuse to the incarceration of a family member, living with someone who abuses alcohol or drugs and poverty, community violence and homelessness. These identified categories of trauma, although not fully understood or grasped as late as the 1990s, were known to occur in the lives of children all over the United States; however, the overall impact of childhood trauma on an individual's long term health outcomes was only first measured in the now famous CDC-Kaiser Permanente ACE study. The findings of this study shook the health care world, forever altering the understanding of the link between childhood trauma and adult health outcomes. These links pushed researchers to look more deeply into the ultimate impact of traumatic childhood experiences on overall adult health. The groundbreaking study concluded that the more trauma a child experiences, the fewer years that child would live as an adult. In fact, in a 2009 study, CDC researchers determined that exposure to childhood trauma literally shortens an individual's lifespan. On average, a person with six or more ACEs died twenty years earlier than a person that had experienced no Adverse Childhood Experiences.
This reality, that traumatic childhood experiences are directly and inextricably linked to negative health outcomes, is now widely recognized in the public health and clinical literature. Dr. Robert Block, former President of the American Academy of Pediatrics, has warned that "[a]dverse childhood experiences are the single greatest unaddressed public health threat facing our nation today." More recently, this literature has begun to explore the connection between trauma and race, outlining how structural violence and historical trauma—particularly violence and discrimination experienced by Black, indigenous, and persons of color—is often experienced both at the individual and community levels. Such work has focused on improving economic opportunities for trauma- stricken communities, improving the physical/built environment, and supporting the development of healthy social-cultural environments. The prevailing framework for addressing the ACEs crisis has been a medical model focused on interventions for individual survivors and communities rather than addressing the glaring systemic issues that directly contribute to the vast majority of the trauma suffered by those communities and the individuals and families that inhabit them. Largely and undeniably absent from the body of work on childhood trauma, and the proposed solutions to confronting and rectifying its deadly impact, is the exploration of how the American legal and justice systems, from municipal law enforcement to the appellate courts, stands at the epicenter of the current crisis.
Each of the recognized categories of ACEs listed in medical screening instruments used by physicians to identity trauma have a direct nexus to the justice system. If we as a society are committed to treating ACEs as the public health crisis that they are, it is incumbent upon us to examine where and how our legal system is complicit in perpetuating trauma upon minority children. In addition, we need to consider how it can intervene—both at the individual and structural levels—to eliminate practices that contribute to multi-generational cycles of trauma and work to equip those with justice-system involvement to succeed and build the resilience necessary to heal minority individuals and communities who have been stricken by trauma and its life-long negative consequences. Indeed it is the responsibility of our justice system, as a major contributor to so-called "social determinants of health."
Meek Mill, in his intimate autobiographical tracks of "Trauma," "Oodles O'Noodles Babies," and "Otherside of America," describes experiencing not just several instances of childhood trauma as identified by the CDC-Kaiser Permanente study, but as a teenager, he suffered additional cruel trauma at the hands of U.S. police and a criminal justice system that wrongly imprisoned and unfairly positioned him in a revolving door between probation and prison. The data tells us that the trauma Meek experienced as a child and teenager statistically predicts a poorer life expectancy for him than those individuals that experienced no trauma or little trauma as a child and youth. Because of the anti-Black culture of policing in America, and because of the deep systemic racism that permeates the criminal justice system, simple exposure to U.S. policing and its courts should qualify as an Adverse Childhood Experience for Black and minority children—one that contributes to harmful adult outcomes, including a shortened life expectancy. Mill's personal childhood trauma as described in his music carefully extrapolates the ways that American policing and the criminal justice system literally traumatized and endangered his young Black life, as it does so many Black children.
This article begins in Section I by providing an in-depth examination of ACEs research, including how the groundbreaking original ACE study discovered the direct link between high ACE scores and poor health outcomes and the prevalence of ACEs in the Black community. It then turns, in Section II, to a brief discussion of the broad ACE category of social disadvantage, and how a child growing up in an environment built on a foundation of poverty and violence will inevitably have more trauma, more ACEs, and be harmed through his or her experience of toxic stress. Section III will provide an overview of anti-Black policing and how law enforcement, as currently constituted, traumatizes minority communities and youth. Section IV explains how criminal charging, jailing, and sentencing traditions have disproportionately targeted Black men, contributing to the trauma that their children and families experience with the loss of a loved one to death or incarceration. The article next argues that minority youth exposure to U.S. law enforcement agents and the justice system at large functions as an ACE for youth of color in a way that is simply not present for non-minority youth and, as such, should be added to the list of ACEs that are formally recognized by public health officials. Finally, the article concludes with how Meek Mill himself is seeking to reform a system rife with debilitating trauma. Throughout each section, Meek Mill, and the raw lyrics from some of his most personal tracks, will serve as an illustration, and example, of how social disadvantage, police misconduct and brutality, and the American criminal justice system at large, cause harmful and lifelong trauma for Black Americans.
Todd J. Clark et. al., Meek Mill's Trauma: Brutal Policing As an Adverse Childhood Experience, 33 St. Thomas L. Rev. 158 (2021).
Law and Race Commons, Law and Society Commons, Law Enforcement and Corrections Commons
Available at: https://lawrepository.ualr.edu/faculty_scholarship/267
Bowen Law Links

redpajama_set_name: RedPajamaCommonCrawl


Rabia got married when she was only 12 years old. She and her husband, and—years later—their two children, lived relatively happy lives, following their traditional Asian religion.
But when Rabia turned 30, she developed the symptoms of leprosy. Her husband kicked her out of the house because of it. In one fell swoop, the divorcee lost her husband of 18 years, her two young children and a life of normalcy. She moved to another village where there were some other people suffering from leprosy, too.
Many years passed, and Rabia remarried and had another child, but she never consulted any doctors about the disease. By the time she was 56 years old, the leprosy had spread over her entire body. She had lost the ends of her fingers and toes, and sores covered her.
Some Sisters of Compassion, Gospel for Asia-supported women missionaries specially trained to care for leprosy patients and others in desperate need, began serving in Rabia's village. When they visited Rabia's house, she told them wounds covered one of her legs and asked if they could cure her.
The women missionaries comforted the downtrodden woman and assured her the Lord Jesus could heal her sores through their simple, practical dressing of the wounds.
As they dressed Rabia's wounds, the Sisters of Compassion sang songs of praise to God and prayed for her. They shared the Word of God with Rabia, and as she heard the Word, she slowly started to trust in this God they told her about. He was healing her, just as the missionaries had said He would.
Rabia decided to visit the Sunday worship service the missionaries had told her about, and in the weeks afterward, she kept going back. Eventually, she came to a point where she decided she wanted to know Christ herself, so she invited Him into her heart.
Rabia kept believing the Lord would heal her of leprosy—and He did!
Seeing this, many in her village have begun to recognize Christ's power to heal and redeem lives. In addition, Rabia is coming to a deeper understanding that Christ accepts her, loves her and honors her, and He will never cast her out.
Praise God for His love for this once-outcast woman.
You can join Him in His work by praying for others like Rabia who are suffering from leprosy.
Praise God for healing this wonderful woman. He still heals today as He did when He walked this Earth. I am so grateful for the testimony this woman has to reach others for Christ. I will be praying for her and the others in her village . God bless her and the women who helped lead her to Christ.
Praise the Lord. Nothing is too hard for our Lord.
All the glory be to Our Marvellous and Still Healing God who is the same, yesterday, today and forever, Praise God, Amen.
Jesus is the great healer.glory to god halleluia!
Let the glory of God be revealed to many in Asia as the missioneries work tirelessly to fulfill the Lord's great commission. May the almighty God make your sandles survive or unworn so that you can go greater distances for those that have not yet heard the gospel also have the chance to hear it.
Praise Him for He is worthy.. He 4gave my sins making me whole, the same God that healed our sister Rabia. jim in Las Vegas…………please pray for peace in Jerusalem………………..
May God bless all supporters,volunteer workers, prayer partners and friends of Gospel For Asia.
Praise the Lord for GFA. To God be the glory.


text:
No. 15 KU tops No. 16 K-State 64-49 to maintain Big 12 hopes
Win keeps Jayhawks in hunt for 15th straight conference championship
Updated: 10:46 PM CST Feb 25, 2019
WEBVTT BY YOUR KANSAS CITY HONDA DEALERS. LEN: KANSAS CITY EYES ITS FIRST BIG 12 CHAMPIONSHIP SINCE 2013. SUNFLOWER SHOWDOWN TIPS OFF TONIGHT. THE JAYHAWKS MISSED THE FIRST SEVEN SHOTS. K STATE TAKES ADVANTAGE. NAILS THE THREE-POINTER. SNEE SCORES 80 THE FIRST HALF. KANSAS COMES BACK. COMING OFF T BENH. STATE. KEEPS THIS ONE CLOSE. NICE FEED FOR THE SLAM. CATS PULL WITHIN TWO. THAT SPARKS A BIG RUN FOR THE JAYHAWKS. ON A 10-3 RUN. DOTSON TRIES FOR THE HOOP AND THE FOUL. JAYHAWKS LED BY SEVEN AT THE HALF. SECOND HAL LIGHTFOOT GETS THE BLOCK ENFORCES THE TURNOVER. THE JAYHAWKS START TO TAKE OVER. UNDERNEATH LAWSON ANOTHER BIG NIGHT. HOOPING FOUL. A 13 POINT LEAD. ANOTHER DOUBLE DOUBLE F LAWSON. CHARLIE MOORE SINKS A THREE-POINTER. A 16 POINT LEAD. THE JAYHAWKS WIN BY 15, 64-49. LAWSON SCORED 18 AND PULLED DOWN 14 REBOUNDS. LIFE WOULD HAD THREE BLOCKS. WE GO LIVE TO PRESS CONFERENCE RIGHT NOW. A LETTER PEOPLE HAVE INJURIES NOW, SICKNESS, YO JUST GOT A DEAL WITH IT. >> I KNOW THE GAME JUST ENDED BUT WHAT WAS THE MESSAGE TO THE TEAM? >> ONE, IT IS DONE AND OVER WITH. WE NEED TO WORRY ABOUT BAYLOR. ON SATURDAY, THE TOUGHEST GAME OF THE SCRATCH -- THE STRETCH. IT DIDN'T MATTER IF WE WON OR LOST TONIGHT. THEY ARE VERY PHYSICAL AND VERY HUNGRY. WE GOT T COME READY TO PLAY AND HANG TOGETHER AND BE COACHABLE. THAT'S THE BIGGEST THING. WE'RE IN FIRST PLACE. THAT IS BRUCE WEBER TALKING AFTER LOSING TO THE JAYHAWKS. THE WILDCATS REMAIN IN THE LEAD WITH THREE GEAMES TO GO. TH HOST OKLAHOMA STATE ON WEDNESDAY WITH FOUR GAMES TO GO. THE JAYHAWKS ARE A GAME BACK. KANSAS AT OKLAHO
Dedric Lawson had 18 points and 14 rebounds to cement his front-runner status for Big 12 player of the year, and No. 15 Kansas pounded No. 16 Kansas State 64-49 on Monday night to keep alive its hopes of a 15th consecutive conference championship.Devon Dotson added 16 points and fellow freshman Quentin Grimes had 12 for the Jayhawks (21-7, 10-5), who moved within a game of the league-leading Wildcats (21-7, 11-4) with three to play.Texas Tech, which roughed up the Jayhawks on Saturday, is a half-game back in second place.There was a sense of desperation in the air inside Allen Fieldhouse, where Kansas — despite all the injuries and unrest this season — had not lost in 19 games. And it manifested itself in the kind of cutthroat defense that coach Bill Self's teams have become accustomed to playing over the years.The Wildcats shot just 32 percent from the field, struggled with turnovers at key junctures and never seemed as comfortable as they were at Bramlage Coliseum, where they roared past the Jayhawks nearly three weeks ago to seize control of the conference race.Kamau Stokes led the Wildcats with 12 points, but nobody on coach Bruce Weber's team got into much of a rhythm. Floor leader Dean Wade was held to eight points and five boards before fouling out with 3:35 to go, and leading scorer Barry Brown Jr. finished with four points on 1-of-8 shooting.It was a masterful defensive effort by a Kansas team that had been searching for an identity.The Jayhawks doubled Wade in the post. They got big man Makol Mawien into early foul trouble. And they ultimately forced off-balance jumpers and deep 3s as the shot clock was winding down.Meanwhile, Kansas turned its defense into just enough offense to rip off a 12-2 run midway through the half, and that was responsible for the 34-27 lead the Jayhawks took to the locker room.The in-your-shorts defense was just as responsible for extending the lead in the second half.Kansas State missed three shots on its first trip down the floor, three more on its next, and its first 10 out of the break. The Jayhawks took advantage by converting a couple easy layups, and Grimes shrugged off a season-long slump to hit an open 3-pointer and push the lead to 41-27 with 16 minutes to go.Suddenly, a field house stirring with anticipation and jammed to the rafters was roaring.Wildcats guard Xavier Sneed went to the bench midway through the second half with cramps, and that seemed to spoil a brief surge. The Jayhawks' defense took care of every other Kansas State run, closing the door not only on a comeback but any hopes of delivering a knockout blow in the Big 12 title chase.
Dedric Lawson had 18 points and 14 rebounds to cement his front-runner status for Big 12 player of the year, and No. 15 Kansas pounded No. 16 Kansas State 64-49 on Monday night to keep alive its hopes of a 15th consecutive conference championship.
Devon Dotson added 16 points and fellow freshman Quentin Grimes had 12 for the Jayhawks (21-7, 10-5), who moved within a game of the league-leading Wildcats (21-7, 11-4) with three to play.
Texas Tech, which roughed up the Jayhawks on Saturday, is a half-game back in second place.
There was a sense of desperation in the air inside Allen Fieldhouse, where Kansas — despite all the injuries and unrest this season — had not lost in 19 games. And it manifested itself in the kind of cutthroat defense that coach Bill Self's teams have become accustomed to playing over the years.
The Wildcats shot just 32 percent from the field, struggled with turnovers at key junctures and never seemed as comfortable as they were at Bramlage Coliseum, where they roared past the Jayhawks nearly three weeks ago to seize control of the conference race.
Kamau Stokes led the Wildcats with 12 points, but nobody on coach Bruce Weber's team got into much of a rhythm. Floor leader Dean Wade was held to eight points and five boards before fouling out with 3:35 to go, and leading scorer Barry Brown Jr. finished with four points on 1-of-8 shooting.
It was a masterful defensive effort by a Kansas team that had been searching for an identity.
The Jayhawks doubled Wade in the post. They got big man Makol Mawien into early foul trouble. And they ultimately forced off-balance jumpers and deep 3s as the shot clock was winding down.
Meanwhile, Kansas turned its defense into just enough offense to rip off a 12-2 run midway through the half, and that was responsible for the 34-27 lead the Jayhawks took to the locker room.
The in-your-shorts defense was just as responsible for extending the lead in the second half.
Kansas State missed three shots on its first trip down the floor, three more on its next, and its first 10 out of the break. The Jayhawks took advantage by converting a couple easy layups, and Grimes shrugged off a season-long slump to hit an open 3-pointer and push the lead to 41-27 with 16 minutes to go.
Suddenly, a field house stirring with anticipation and jammed to the rafters was roaring.
Wildcats guard Xavier Sneed went to the bench midway through the second half with cramps, and that seemed to spoil a brief surge. The Jayhawks' defense took care of every other Kansas State run, closing the door not only on a comeback but any hopes of delivering a knockout blow in the Big 12 title chase.