Miliary TB disease with TB meningitis

Context/background: Miliary tuberculosis is a condition that is fatal if not diagnosed and can present in the outpatient setting with vague symptoms that resemble a viral illness, therefore, can be easily missed. Recognition of this disease as a differential is important in the primary care setting, especially when caring for immigrant and International patient populations. Case Description: A previously healthy 35 yo female from Vietnam whom presented initially to the ER for headache and fever for the past 2 weeks. She was diagnosed with acute viral syndrome given her symptoms, normal labs, and head CT, and discharged home. A few days later, she presented to an urgent care because she began having blurry vision, nausea, vomiting, lethargy and had incoherent speech. She did not have any URI symptoms, cough or hemoptysis. At the urgent care, she was noted to have some neck stiffness, fatigue, unsteady gait, and fever to 103F. They had her return to the emergency room for further workup. In the ED, she had an LP that revealed lymphocytic-predominant pleiocytosis, elevated protein, and low glucose. ID was consulted, from LP alone, differential included early viral meningitis vs bacterial (pyogenic vs AFB vs other atypical pathogens such as Listeria, Brucella, Syphilis) vs Cryptococcus. She was started on CTX, vancomycin, and acyclovir while workup was pending. She had a CXR to look for evidence of prior TB, which resulted in ”diffuse pulmonary nodularity.” Differential included respiratory bronchiolitis, miliary tuberculosis and other fungal infections, hypersensitivity pneumonitis and viral infection. After CXR, she was placed on airborne precautions and in a reverse flow room given possibility of TB. Because she had neurological symptoms, she received a brain MRI, which showed ”small ring-enhancing lesions in the left frontal cortex and right frontal cortex.” The following day, CSF resulted was positive for TB by PCR, confirming the diagnosis. Treatment with rifampin, isoniazid, pyrazinamide, ethambutol (“RIPE”) was immediately started. Contacted by the county health department and they stated that even though there was a diagnosis, a sputum sample was needed to determine level of contagiousness. She was unable to produce sputum, even with induction (she had no cough), therefore she had bronchoalveolar lavage for sputum culture, resulted in 3+ (moderate) Mycobacterium tuberculosis. She continued the RIPE regimen and was discharged from the hospital the following day. Discussion: Although miliary TB is a rare form of TB (2% of TB cases), when missed it can be fatal, as mortality rate is between 15 to 30%. One of the main causes for high mortality includes late detection of disease caused by non-specific symptoms. Recognition of this disease as a differential is important in the primary care setting and when caring for international patient populations.https://digitalcommons.psjhealth.org/milwaukie_family/1000/thumbnail.jp

Increasing Vaccination Rates of Children up to 24 months old at PMG Milwaukie Family Medicine

Increasing Vaccination Rates of children up to 24 months old at PMG Milwaukie Family Medicine Authors: Justin Ferley DO; Rachel Jackson MD; Aubrey Miller MD; Sebastian Reeve MD; Christelle Serra Van-Brunt DO; Jamie Skreen DO; Jeffrey Sun DO; John Yates MD; Daniel Ruegg MD Introduction: Each year in the US, 42000 adults and 300 children die of vaccine preventable diseases. Yet across the country, clinics – including ours – fall short of the CDC Healthy People 2020 goals of pediatric vaccination rates. This resident-led quality improvement (QI) project aimed to improve our clinic vaccination rates in the under 24mo population. Methods: We identified 3 opportunities for vaccinating children under our clinic current processes: well child visits, medical assistants’ vaccinations visits, and acute care visits. Using a multidisciplinary approach comprising residents, MAs, clinical care coordinators and our nursing quality supervisor, we analyzed our current vaccinations processes and our iterative plan-do-study- cycles (PDSA) included: PDSA #1: standardize our work flow for vaccine reconciliation. PDSA #2: sending personal reminder lebers to patients and overall improving our vaccine recall/ reminder system. PDSA #3: Minimizing provider variation for vaccines given at the 12-18mo WCC. Results: We saw an improvement in our vaccinations rates after personalized reminder letters were sent out, outlining that we do not have a reliable vaccine schedule reminder system. We also noted that different providers created different vaccinations schedules in order to prevent giving 5 vaccines at the same $me – with no system in place to follow on missed vaccination, thus creating missed opportunities and suggesting that we need to implement a clinic-wide vaccine schedule. Conclusion: Our last PDSA cycle was interrupted by current CIVD-19 pandemic. We have however found valuable data to help improve our clinic’s vaccination rates, and plan to continue this project over the next 2 years.https://digitalcommons.psjhealth.org/milwaukie_family/1007/thumbnail.jp

Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure

Heart failure is a leading cause of mortality, yet our understanding of the genetic interactions underlying this disease remains incomplete. Here, we harvest 1352 healthy and failing human hearts directly from transplant center operating rooms, and obtain genome-wide genotyping and gene expression measurements for a subset of 313. We build failing and non-failing cardiac regulatory gene networks, revealing important regulators and cardiac expression quantitative trait loci (eQTLs). PPP1R3A emerges as a regulator whose network connectivity changes significantly between health and disease. RNA sequencing after PPP1R3A knockdown validates network-based predictions, and highlights metabolic pathway regulation associated with increased cardiomyocyte size and perturbed respiratory metabolism. Mice lacking PPP1R3A are protected against pressure-overload heart failure. We present a global gene interaction map of the human heart failure transition, identify previously unreported cardiac eQTLs, and demonstrate the discovery potential of disease-specific networks through the description of PPP1R3A as a central regulator in heart failure