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Fight Broke Out In Brian Laundrie’s Family Home In Florida

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Again, the most typical case came into the headlines as a fight broke out near Brian Laundrie’s home between neighbor and protesters. The video of the fight between them went viral on social media and is available on several websites. Everyone knows that Brian Laundrie comes into the headlines when Gabby Petito missing after a road trip with him. The complete incident that happened with Gabby Petito is already widely famous among millions and everyone looking forward to knowing the truth. Gabby and Brian were on a road trip on 11th September but when Gabby’s parents trying to talk her through calls and messages, she can’t replying them.

Brian Laundrie who was a boyfriend of Gabby Petito

When two days pass out and Gabby has never come back home, her parents registered a missing case. After that, the police start their investigation and continuously tried a lot to talk with Brian Laundrie and his family. But, Brian and his family did not talk with the police except his sister. They all remain quiet in this matter and did not tell any information about what happened to Gabby. On 19th September 2021, the police found a dead body of Gabby in a remote area in northwestern Wyoming. After that, the missing case becomes a homicide and some situations take more typical turns.

Yes, Brian Laundrie who was a boyfriend of Gabby Petito has been absconding since the day when the police found her dead body. He is still absconding and the police search to catch him. In this case, he is the main suspect to kill Gabby but the reasons to do this will not come in front till Brian’s arrest. Currently, a minor incident takes place near Brian Laundry’s house, when a couple of protest outside Laundry’s family home and a neighbor in a red shirt starts yelling at them, accusing the couple of stepping out of their property.

Now, the incident that breaks out near the house of Brian Laundrie is covered by several reports as there are many reporters reporting the entire incident. The video of the complete moment has been also recorded by the reports who are available at the place. There is no update on Brian Laundrie’s whereabouts but we will update all the information when we get any report on this topic. This topic has become a very big incident as several people from every corner of the world are searching for the truth behind the murder of Gabby Petito. So, stay connected with us to get all the updates on time.



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Zuma speaks to grassroots supporters – The Maravi Post

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South Africa’s former president, Jacob Zuma, spoke Thursday to his supporters for the first time since being released on parole in early September.

The former ANC leader was released on medical grounds after serving two months of a 15-month prison sentence for contempt of court.

Jacob Zuma spoke via a video link as no one knows where the 79 year old is serving parole.

In his speech to supporters in Durban the former president lambasted the courts and criticised the graft investigations against him.

“Today we are a state governed by those who know what it is like to be oppressed and denied fundamental human rights. It is this state that has imprisoned me for contempt of court without trial. Something has gone terribly wrong in our country” lamented the former South African president.

South Africans head to the polls on November 1 to elect local councillors across the country.

Zuma’s arrest in July sparked a wave of violence and unrest that resulted in at least 350 deaths.

Source: Africanews

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Guillain-​Barré Syndrome Associated with COVID-19 Vaccination – The Maravi Post

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Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.

Author affiliations: Keelung Chang Gung Memorial Hospital, Keelung, Taiwan (S.-C. Shao, C.-H. Wang, M.-J. Hung, S.-C. Liao); National Cheng Kung University College of Medicine, Tainan, Taiwan (S.-C. Shao, K-C, Chang); Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan (K.-C. Chang, H.-Y. Chen); Chang Gung University College of Medicine, Taoyuan (M.-J. Hung, S.-C. Liao)

Guillain-Barré syndrome (GBS), an immune-mediated polyradiculoneuropathy with a ≈5% mortality rate, has an incidence worldwide of 0.81–1.91 cases/100,000 person-years (1). GBS has been reported to be associated with coronavirus disease (COVID-19) vaccination, but a comprehensive summary regarding this rare adverse event is still lacking. To determine clinical features of GBS associated with COVID-19 vaccination, we conducted hospital-based investigations in Taiwan along with a systematic review of published case reports.

We analyzed electronic medical records data from Taiwan’s largest multi-institutional healthcare system, including 9 branches of Chang Gung Memorial Hospital (2), where healthcare workers received first-priority COVID-19 ChAdOx1-S vaccine (Oxford/AstraZeneca, https://www.astrazeneca.com) starting March 22, 2021. We included healthcare workers vaccinated during March 22–May 31 and followed them for 30 days after vaccination. We identified GBS cases on the basis of code G610 from the International Classification of Disease, 10th Revision, Clinical Modification, or spontaneous adverse drug reaction reporting systems within the hospitals. Two authors (C.H.W. and S.C.L.) confirmed diagnosis and classification of GBS cases through chart reviews (3,4). This study was approved by the Institutional Review Board of Chang Gung Medical Foundation (approval no. 202101087B0).

To summarize clinical features of published cases from literature, we searched PubMed and Embase for reports posted through August 17, 2021, using relevant key terms such as “COVID-19,” “Guillain-​Barré syndrome,” and “vaccine” with suitable MeSH terms. Two independent reviewers (S.C.S., C.H.W.) performed the study selection and data extraction; a third-reviewer (S.C.L.) settled any differences between them. We excluded cases with coexisting COVID-19 or preexisting GBS. We included only publications with reports of clinical features related to GBS. We described basic characteristics, laboratory data, pathologic reports, treatment patterns, and prognosis of GBS cases associated with COVID-19 vaccination. The study protocol of this systematic review is published on PROSPERO (https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=265479).

We included 18,269 healthcare workers (mean age 40.6 years, range 18–87 years; 67.5% were women) who received ChAdOx1-S vaccine during the study period. After these 18,257 first-dose and 544 second-dose vaccinations, we identified 1 GBS case after a first dose of ChAdOx1-S vaccine in 1 of the hospitals participating in the study.

Figure

Systematic review of published literature in study of Guillain-​Barré syndrome associated with coronavirus vaccination, 2021. GBS, Guillain-​Barré syndrome.

Figure. Systematic review of published literature in study of Guillain-​Barré syndrome associated with coronavirus vaccination, 2021. GBS, Guillain-​Barré syndrome.

After a systematic review of published literature (Figure), we included 17 publications reporting an additional 38 cases of GBS related to COVID-19 vaccination (India, 10 cases; United Kingdom, 11 cases; Mexico, 7 cases; United States, 3 cases; France, 1 case; Italy, 3 cases; Malta, 1 case; Turkey, 1 case; and Qatar, 1 case) (Appendix Table). Including the case in Taiwan, these 39 cases occurred in persons with a mean age of 57.8 (range 20–86) years; 56.4% were male. Most of the reported case-patients received ChAdOx1-S (25/39), followed by BNT162b2 (12/39) (Pfizer-BioNTech, https://www.pfizer.com), Ad26.COV2.S (1/39) (Johnson & Johnson, https://www.jnj.com), and CoronaVac (1/39) (Sinovac Biotech, http://www.sinovac.com). The GBS rate after COVID-19 vaccination ranged from 1.8 to 53.2 cases/1 million doses. The initial symptoms of GBS included myalgia (12/39), paraparesis (5/39), quadriparesis (22/39), paresthesia (28/39), and facial palsy (23/39), and symptoms of dysautonomia also were observed during hospitalizations (3/39). The average time from vaccination to symptom onset was 11.3 days. A total of 34 case-patients received lumbar puncture; 30 had manifestations of albuminocytologic dissociation in the cerebrospinal fluid.

On the basis of the clinical diagnostic classification of GBS, we found that most case-patients had the classic form (22/39), followed by bilateral facial palsy with paresthesia (12/39), the paraparetic form (4/39), and GBS–Miller Fisher syndrome overlap variant (1/39). We defined all classic and paraparetic forms of GBS (26/26) as level 1 or 2 on the basis of the Brighton criteria (5). We identified the GBS subtype in 33/39 cases by electrophysiological examination; most reported case-patients had a diagnosis of acute inflammatory demyelinating polyneuropathy (23/33), followed by acute motor and sensory axonal neuropathy (4/33) and acute motor axonal neuropathy (3/33). For GBS management, 33 case-patients received intravenous immunoglobulin and 2 received plasmapheresis. One case-patient died; 9 case-patients required mechanical ventilation during hospitalization. The scores on the GBS disability scale (5) were only available for 30 cases; 12 scored >4 (i.e., indicating bedridden or chair-bound status) during follow-up or after discharge.

Similar to previous reviews on GBS associated with COVID-19, we found that both COVID-19 and COVID-19 vaccination mostly cause the classic form of GBS (under the clinical diagnosis classification) and the acute inflammatory demyelinating polyneuropathy subtype (based on electrodiagnostic features) within 2 weeks of infection or vaccination (68). However, the bilateral facial palsy with paresthesia variant and initial onset symptoms of facial diplegia were more frequently found in GBS case-patients after COVID-19 vaccination.

Case series and reports can indicate safety issues and outline clinical features of diseases, but they cannot establish robust causal relationships between COVID-19 vaccination and GBS. Despite the benefits (e.g., increase in the number of persons not susceptible to infection and decrease in severe outcomes after infection) of COVID-19 vaccination far outweighing the potentially severe adverse events after infection (9), our findings highlight the need for vigilance in patients with neurologic symptoms after COVID-19 vaccination and for postvaccination surveillance programs to assess causality of GBS.

Dr. Shao is a clinical pharmacist at Keelung Chang Gung Memorial Hospital. His research interests include the use of systematic review and meta-analysis to summarize current best evidence on clinical topics, specifically in regard to complications in COVID-19 patients.

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The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors’ affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.

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SARS-CoV-2 B.1.1.7 Variant Infection in Malayan Tigers, Virginia, USA – The Maravi Post

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Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.

Author affiliations: Cornell University, Ithaca, New York, USA (P.K. Mitchell, M. Martins, L.C. Caserta, R.R. Anderson, B.D. Cronk, E.L. Goodrich, D.G. Diel); Virginia Zoo, Norfolk, Virginia, USA (T. Reilly); Virginia Department of Health, Richmond, Virginia (J. Murphy)

On April 4, 2021, a 5-year-old male Malayan tiger (Panthera tigris jacksoni) at the Virginia Zoo (Norfolk, VA, USA) began exhibiting lethargy, labored breathing, coughing, intermittent upper respiratory sounds, hyporexia, and mucoid nasal discharge. On April 7, another 5-year-old male Malayan tiger began experiencing labored breathing, cough, clear nasal discharge, and hyporexia. On April 10, a third Malayan tiger, a 10-year-old male, had cough and later clear nasal discharge. The tigers’ clinical signs resolved by April 15, eleven days after the outbreak began.

Zoo staff collected nasal swab and fecal samples from the 5-year-old tigers on April 9 and the 10-year-old tiger on April 13 and submitted these to Cornell University’s Animal Health Diagnostic Center (AHDC; Ithaca, NY, USA). AHDC tested samples for Bordetella sp., Chlamydia felis, Mycoplasma cynos, M. felis, Streptococcus equi subspecies zooepidemicus, influenza virus, pneumovirus, feline calicivirus, and feline herpesvirus; all results were negative. All samples tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by EZ-SARS-CoV-2 Real-Time RT-PCR Test (Tetracore, Inc., https://tetracore.com). We isolated SARS-CoV-2 from respiratory and fecal specimens from the first tiger. Testing at the US Department of Agriculture National Veterinary Services Laboratories (Ames, IA, USA) confirmed SARS-CoV-2 infection. We screened the tiger samples using TaqPath COVID-19 RT-PCR Kit (Thermo Fisher Scientific, https://www.thermofisher.com), which revealed a spike gene dropout in samples from all 3 tigers; only the nucleoprotein and open reading frame 1ab gene targets were detected, suggesting B.1.1.7 variant infection.

Figure

Maximum-likelihood phylogenetic trees of severe acute respiratory syndrome coronavirus 2 from 3 Malayan tigers, Virginia, USA. Tiger samples are numbered in order of symptom onset. A) Subset of phylogenetic tree showing parent (G23236T) and grandparent (C4900T) nodes of the tiger sequences, with tips labeled as states of origin in the United States or Australia. B) Phylogenetic tree showing that other B.1.1.7 viruses detected in Virginia that contain the K558N mutation are not epidemiologically related to the sequences detected in tigers 1, 2, and 3. SNP, single-nucleotide polymorphism.

Figure. Maximum-likelihood phylogenetic trees of severe acute respiratory syndrome coronavirus 2 from 3 Malayan tigers, Virginia, USA. Tiger samples are numbered in order of symptom onset. A) Subset of phylogenetic tree…

We performed whole-genome sequencing on all samples by using MinION (Oxford Nanopore Technologies, https://nanoporetech.com), as previously described (1). We assembled reads using the ARTIC ncov-2019 protocol (ARTIC Network, https://artic.network) and Medaka (Oxford Nanopore Technologies) for variant calling. We obtained near-complete (29,702–29,710-bp) assemblies from all nasal swab specimens (GenBank accession nos. MZ305031–3) but no assemblies from fecal samples. We identified respiratory specimen genomes as lineage B.1.1.7 (Alpha variant) by using Pangolin version 2.4.2 (https://github.com/cov-lineages/pangolin). We used Nextstrain (https://nextstrain.org) for phylogenetic analysis of tiger-derived sequences and other B.1.1.7 sequences downloaded from GISAID (https://www.gisaid.org) on April 15, 2021 (2,3). Tiger-derived sequences all were identical, except 1 manually corrected homopolymer repeat error, and fell into a clade defined by a C4900T mutation containing other samples collected primarily in the United States. Tiger-derived sequences differed from others in the clade by 1 single-nucleotide polymorphism in the spike gene (K558N) (Figure, panel A). Using the vdb tool (4), we found 46 additional B.1.1.7 sequences that had the K558N mutation in GISAID on July 22, 2021; all were collected from Virginia during March 27–July 7, 2021. However, phylogenetic analysis of these sequences and the tiger-derived sequences showed divergence of 11 single-nucleotide polymorphism, minus the divergence producing the K558N mutation (Figure, panel B), indicating the sequences are not related epidemiologically.

The source of the tigers’ infection is unknown. The zoo has been open to the public, but transmission from a visitor is unlikely because tiger exhibit areas are separated from visitors by either a glass enclosure or >9 m distance. The most plausible explanation is that >1 tiger acquired the virus from a keeper because they had close contact. However, no employees tested positive for SARS-CoV-2 nor had symptoms during the 4 weeks before the tigers’ symptom onset. Nine keepers were responsible for the animals’ daily care; 2 other persons prepared animal diets daily. Employees were required to wear facemasks always, indoors and outdoors; everyone wore standard 2-ply surgical masks or homemade cloth facemasks. Staff also were required to wear gloves when handling and preparing food and when servicing animal areas. Furthermore, staff were required to step into an accelerated hydrogen peroxide disinfectant footbath when entering the tiger building and diet kitchen. The 3 tigers might have been infected by an employee, or 1 tiger was infected, then transmission occurred to the others. Two tigers lived in the same enclosure and had no direct contact with the third, but all 3 rotated through common enclosure spaces.

After identification of the tiger infections, 4 additional zoo animals were tested: 1 lion (Panthera leo) with lethargy and hyporexia ≈1 week after SARS-CoV-2 diagnosis in the tigers; another asymptomatic lion because of age and proximity to the first lion; and 2 degus (Octodon degus) that died in late March and had interstitial pneumonia on necropsy. AHDC tested nasal swab samples from the lions and frozen spleen and cecum samples from the degus by reverse transcription PCR; all results were negative for SARS-CoV-2.

Our findings underscore felid susceptibility to SARS-CoV-2, which also has been detected in captive snow leopards (Panthera uncia) and pumas (Puma concolor) (5). Other nonhuman species, including gorillas (Gorilla gorilla), minks (Neovison vison), and ferrets (Mustela putorius furo), have acquired SARS-CoV-2; additional species have been shown to be susceptible experimentally (57). Domestic cats and dogs in the United Kingdom and United States reportedly had B.1.1.7 infections, suggesting that mutations characterizing this lineage are not constrained to a host range (8; L. Ferasin et al., unpub. data, https://doi.org/10.1101/2021.03.18.435945). Monitoring animals for SARS-CoV-2 infection is critical to determining potential host range, particularly as new virus variants emerge and spread.

Dr. Mitchell is a research associate in the Department of Population Medicine and Diagnostic Sciences at Cornell University. His primary research interest is molecular epidemiology of infectious diseases.

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The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors’ affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.

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