#○-○ i like burkholderia

[wormgremlin]

Let's talk about scary diseases! Just some of my favorites. (I am not trying to fear monger or anything else; I just like 'em; there are lots of other diseases).

The black plague! Yersinia pestis!

Yes it still exists! There are intermittent outbreaks, especially in regions of the US including Tahoe and Colorado. It's a bacteria spread by fleas via rodents. I haven't heard of any AMR strains... yet. It is however still scary. There are occasional outbreaks, but at least within the US, they're fairly well contained. There are three types: bubonic (swelling of lymph nodes), pneumonic (respiratory), and septicemic.

Septicemic has no specific visible symptoms and is thought of as causing "sudden death." It can either be just septicemic or a result of untreated plague going septic. So regardless of susceptibility... can and will still kill you dead!

Meliodosis! Burkholderia mallei/pseudomallei!

A naturally multidrug resistant bacteria that is honestly under discussed. It's endemic in certain areas, makes its home in the soil and is sometimes aersolized during dry seasons. It causes severe granulomatous disease much like another famous antibiotic resistant bacterium. It was even known about in ancient Greece for causing disease in donkeys and horses... not surprising given the basket ball sized granulomas it can form.

It was using in the American Civil War as a bioweapon to infect horse water troughs. Horses and other equines can get it as well. It isn't antibiotic resistant because of humans, but because it encodes an eflux pump in its membranes to be able to deal with environmental toxins. We have no effective vaccine to date! It is treatable but requires extensive antibiotics.

The consumption! Mycobacterium! Tuberculosis!

It's called consumption for how it causes wasting. It's another granulomatous disease. It can also be a foodborne illness and is a large reason for the standardization of pasteurization of dairy. It's also that lovely respiratory illness that killed Satine in Moulin Rouge. It's incredibly tricky and actually infects and replicates inside the cells the body normally uses to kill bacteria! There are a lot of variants including multidrug resistant strains. It circulates in a lot of different countries, including the US despite their delusions. Multidrug resistant TB is a big issue in Russian prisons, with AIDS and other immunocompromised patients, with a lot of countries with lax antibiotic policies. The list goes on. But basically, yes it's scary.

The Green Brothers have recently taken massive offense about how TB is treated. Which good! TB treatment should be affordable and accessible... but sometimes, well the XDR strains are scary and hard to treat, man... There used to be a vax, of an attenuated version of bovine TB (M. bovis -- which they recently decided isn't actually it's own species), but well. It wasn't properly attenuated or mutated back, ND they basically injected a few kids eith TB... not good. Fun fact! The UK is having a really hard time getting TB out of their cow populations because badgers!

A pox upon your house! Pox viruses!

We eradicated smallpox... right? We did! Except here's the thing. Before small pox eradication, hobby scientists faced little regulation... people could have freezers full of small pox and experiment at home. And they did. The government tried to collect all the samples, but well... you never really know. Plus things like monkey pox roll around. Which yknow, not too bad all things considered. Easily vaccinated, small pox/monkey pox...

Unless someone happened to write a paper on how you can genetically modify mouse pox so no vaccine currently designed is effective at preventing disease and the same principles could be used with other pox virdae... that wouldn't happen right, who would do that *sweats* (it happened. They did it. And published it. Yay. Science.)

What would happen if the black plague had a resurgence?

It is still around and people contract the plague. We now have antibiotics to treat it. This is why antibiotic resistance is so scary.

[the-blue-phantom]

"write and submit an abstract for this paper" is my air of mystery not enough for you?

[jazzistolkienfanfics]

Breathing - Aragorn x reader (modern!AU)

hi! could you do prompt #53 with a female reader and aragorn? thank you!

@elvish-sky​ oh joy, another sad aragorn fic (jk jk). i wanted to write this one as a modern!AU because of some research i was doing before school ended for science and ... i just thought of the concept and liked it, okay hush

53. “You said you were okay!”

Type: Imagine Pairing: Aragorn x reader (modern!AU) Summary: Y/N hasn’t been entirely honest with her boyfriend, Aragorn. Warnings: angst, sadness, death, Word Count: 1,704 words

Y/N laughed loudly as the black Newfoundland puppy chased its fluffy tail, the dark fur sticking up as though it had been struck by lightning. 

Aragorn grinned at her, taking yet another long moment to watch her - to savour everything about his beautiful girlfriend. Just like every time she giggled, he wanted the seconds to last forever. He wanted every day he got to be with Y/N to last forever, because one day, they would be unable to make new memories. 

One day sooner than he would like. 

He tugged the sleeves of his RSPCA volunteer jacket down as he sat by her side, whistling for the dog to come and sit by his side. It obliged, just as all the animals in the shelter, or anywhere, always did.

Animal whisperer, Y/N would tease him. Like Doctor Dolittle!

Aragorn looked to her again, the smile still on Y/N’s face. Flushed s/c cheeks. Hooded e/c eyes with heavy bags under them, yet she still looked beauty. H/l messy h/c hair, kept out of her face by a f/c ribbon.

Then, the things people tended to stare at. The bag by her side, much like the wheeled kind some people used to shop. The nose cannula hooked behind her ears, a long tube carrying oxygen from the bag. A surgery scar protruding from her f/c shirt’s neckline. 

Those things didn’t bother him. He loved her. 

“Are you okay?”

Aragorn blinked at Y/N’s question. Normally he was the one asking her that question, or supposed to be. “I-I’m perfect.”

She smiled again. “That’s good.”

He stood, pulling her to her feet as well. “Come on. My shift’s up.”

Y/N jokingly pouted. “But the puppies!”

This time, it was Aragorn who laughed. “We’ll come back next week, I promise.”

“Next week,” she echoed, a sadness in her voice that her boyfriend didn’t detect.

---

Y/N coughed, making a face as the last of her pills went down her throat. She took dozens every day - it was part of her necessary, pre-determined hospital routine. 

Her nurse, Legolas, (A/N - stan male nurses) passed her some water, which she gladly swallowed, hacking again. 

“Good job,” he grinned. “Everything’s doing okay. Lung function is at 54 percent, a little lower than last week, but it will get higher again.”

She’d definitely expected that, though her heart still sunk.

“I’ll let your boyfriend in now.” Legolas laughed at the annoyed look on his charge’s face. The sound faded as he took on a more serious tone. “But, you remember that it could get even worse anytime, especially-”

“I know,” Y/N interrupted, her voice scratched and broken. “I know.”

“Be careful,” the nurse reminded her again, as he left the room, Aragorn passing through the door before it could even swing shut. 

“Going alright?”

Y/N grimaced. “As well as can be expected. I hate my lungs.”

He took her hand, squeezing it tightly, like he would never, could never, let go. “I know you’re strong, Y/N/N. You can’t let CF beat you.”

Ah, yes. There it was - the casual reminder Y/N couldn’t go a day without hearing. Stressing how she was holding her life in an hourglass, which was rapidly running out of time.

Cystic Fibrosis. An often terminal lung condition, meaning Y/N’s lungs functioned at low percentages, causing difficulty in her breathing and weakened immune system. She was often lucky to spend more than a month out of the hospital, thought that hadn’t been the case recently.

She’d been continually relapsing, her lung function decreasing with every checkup. 

To put it simply, it sucked. Royally. 

“Here,” Aragorn offered her her nose cannula. “Hook up, and I’ll distract you.”

Y/N slipped it on, taking his hand and dragging her portable oxygen in The Granny Shopping Bag™️ with the other. smiling.

Well, at least, her mask was smiling. Inside, she didn’t know if she had the energy or will to anymore.

---

Y/N knew it was a risk, and she was exactly aware of the million and one ways this could go wrong. 

But she didn’t care. She was going to live whilst she still could. She was done with giving up her life, letting down her boyfriend, because of some stupid mucus. 

Besides, he didn’t know. He didn’t know it all, and she wasn’t going to stop them from being unable to make happy memories together by burdening him with more bad news. Being the protective guy he was, Aragorn probably wouldn’t even let her leave the hospital if her found out.

“Ready?” said-boyfriend-in-question asked.

“Hell yeah,” Y/N grinned, straightening the edges of her denim jacket. 

They stood at the archway entrance to the Rivendell National Park - a beautiful wonderland of pale trees and swirling leaves, in the deep of autumn.

Technically, Y/N wasn’t meant to engage in ‘prolonged physical activity’. But technically, she wasn’t even meant to be alive right now.

No one, least of all her, knew how much time she had left. Y/N wasn’t one to waste it. 

Together, she and Aragorn stepped through the archway, and explored the ‘whole new realm’.

---

After ten minutes, her lungs were burning, but she didn’t say anything.

Aragorn was looking so happy - a goofy smily affixed upon his face, his dark eyes lighting up as he swished his head from side to side to admire everything with childish wonder. 

The National Park was beautiful, but the air was thin, and Y/N was struggling not to audibly struggle. She hated being dependent on people, and she would. Not. Worry. Him.

Something felt different this time - her breathing was quickening even though she was walking extraordinarily slowly, and she was in more pain than she should’ve been

Y/N signalled for Aragorn to stop, doubling over and coughing until her throat was raw. She couldn’t breathe whilst the mucus was crawling up her airways, and she’d rather clear it than suffer.

“Get it out, Y/N,” Aragorn encouraged her as she straightened, worry sketched all over his face. 

Her coughing was done, and she went to take a nice big inhale, but ....

She.

Still.

Couldn’t.

Breathe.

Breathing should’ve been something natural, easy, if she had been just a normal young woman with her normal boyfriend. 

She wished that lying didn’t come to her easier than breathing.

Y/N collapsed, choking, almost about to pass out as Aragorn immediately fell to her side, pulling his phone from his pocket and dialling an emergency number.

“Oh my God,” he gasped, his breaths coming shortly as well as he scooped her up into his arms. “Oh, God. Y-You’re going to be okay, Y/N.”

Funny how good they’d both become at lying.

With that thought, Y/N’s eyes fluttered shut, without the energy to keep themselves open.

“Y/N!”

---

Aragorn sat in the waiting room with a feeling like acid being poured down his throat and then regurgitated. 

She shouldn’t have collapsed like that - it was highly medically improbable given what he knew about Y/N and her Cystic Fibrosis. Unless ... there was something he didn’t know.

He shook his head as soon as that thought came to him. He trusted Y/N. She trusted him. He had to have faith in her.

The sound of footsteps encouraged him to look sideways, where he saw Y/N’s nurse, Legolas, with four cups of coffee in his arms.

“Expecting someone else?” Aragorn laughed as he was handed one of the cups.

“Oh, no,” Legolas replied, with an unbelievably straight face. “I intend to drink all the coffee.”

“How is Y/N?” 

The nurse winced. “I will be honest with you - she isn’t going so well right now. The fact that she was still walking with you ... that’s pretty amazing given her lung function and diagnosis.”

“What do you mean?” Aragorn furrowed his eyebrows. “She-she’s fine, isn’t she?”

Legolas stared. “Y/N didn’t tell you, did she? Oh, that stubborn little-”

“Tell me what?”

He averted Aragorn’s eyes. “Tell you that she was diagnosed with Burkholderia Cepacia and she was given another six months to live with her current lung function.”

“What?” All the air rushed out of his lungs, and suddenly, he knew how Y/N felt when it was hard for her to breathe. “H-How long has it been?”

Again, the blond looked awkwardly to the floor.

“How long?!” It was a shout this time, and Aragorn could feel himself on the brink of tears. His beautiful girlfriend, lost to the void ... he could not cope with it.

“Seven months.”

He fell back in his chair, coffee discarded, his shaking hands covering his face as his cheeks dripped with tears. This couldn’t be happening. This could not be happening.

A doctor rushed out from the ER, making a beeline for Legolas. Her nametag read ‘Tauriel’, her long red hair flying behind her as she ran towards them.

Her face was sober.

“He-he should come. Now.” She motioned towards Aragorn who stood immediately.

“Is Y/N alright?”

Dr. Tauriel did not answer his question, just motioning for him to follow her. 

---

Y/N wasn’t moving. For such a joyful young woman, she was lying unbelievably still. 

There was a crowd of doctors around her, but they all moved back at the sight of Aragorn.

“I’m sorry.” 

He didn’t know who said it ... all he could think about was how much paler Y/N looked than her normal s/c. 

“She-she’s just a-asleep, r-right?” Aragorn stuttered on the words as more tears fell down his face. “Y/N’s o-okay?”

Dr. Tauriel shook her head. “I’m so sorry. We-we couldn’t do anything.”

“You said you were okay!” Aragorn cried, talking to Y/N even though she couldn’t hear him - would never hear him again. Jut like he would never hear her. “You told me you were okay ...”

“Get him out of here,” someone said quietly, and Aragorn was pulled to the door.

He threw one final look over his shoulder. 

Y/N’s hair was spread out over the pillow. Her hands had been folded over her chest. She still had her nose cannula in, but that had never made her less beautiful.

Even in death, she still looked like an angel.

She was still the most beautiful person Aragorn had ever known.

A/N - guys this is my new favourite fic so please spread it! @elvish-sky​ thank you so much for this request, and everyone, thank you for reading!

[bpod-bpod]

Fuse and Conquer

Hijacking the host cytoskeleton is a popular pathogen trick, but the bacterium Burkholderia thailandensis takes this strategy even further. Once inside a host cell, B. thailandensis (in green) uses the host’s actin fibres (in red) to promote fusion with other cells, forming giant cells in which it rapidly replicates. Studying this behaviour in mouse macrophages, researchers uncovered how the immune system fights back: activated by type I interferon, molecules known as guanylate-binding proteins (GBPs) prevent the bacteria from manipulating actin, ultimately hindering cell fusion. Without GBPs, the macrophages are more likely to fuse when infected by B. thailandensis, and mice lacking GBPs are more susceptible to infection. Closely-related pathogens B. mallei and B. pseudomallei, which cause serious diseases in humans, also rely on cell fusion to spread, so unpicking this process in B. thailandensis is a useful step towards understanding their strategies.

Written by Emmanuelle Briolat

Image from work by David E. Place and colleagues, published on the cover of PLOS Pathogens

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN, USA

Published in PLOS Pathogens, April 2020

You can also follow BPoD on Instagram, Twitter and Facebook

[mcatmemoranda]

Going through questions:

Nitroblue tetrazolium testing is used for diagnosis of Chronic Granulomatous Disease (CGD). Normally, neutrophils will turn blue on nitroblue tetrazolium testing because of the respiratory burst in phagolysosomes, but there is no blue color change in CGD because there is no production of oxidative species. CGD is due to an X-linked Recessive NADPH oxidase mutation. NADPH oxidase catalyzes production of reactive oxygen species, which kill bacteria. NADPH also catalyzes activation of granule proteases, like elastase, in phagosomes. Mutation of NADPH oxidase gene-> deficient NADPH oxidase-> neutrophils and macrophages can't kill bacteria that they phagocytose. This leaves pts susceptible to recurrent fungal and bacterial infections, especially catalase + bugs (staph aureus, serratia marcenscens, aspergillus, burkholderia cepacia, and nocardia). The skin, lungs, liver, and lymph nodes are often infected in these pts. For diagnosis of CGD, you want to measure neutrophil superoxide production with either the Nitroblue Tetrazolium (NBT) test or with flow cytometry using dihydrorhodamine (DHR). The DHR test is better.

IL-12 presented to naive helper T cells by macrophages causes naive helper T cells to differentiate into Th1 cells, which release IFN-gamma; IFN-gamma activates cytotoxic CD8+ T cells and macrophages to kill intracellular pathogens. Mycobacterium is an intracellular pathogen that is killed this way. People with IL-12 deficiency can't mount a cell-mediated immune response and are susceptible to mycobacterium infection. Interferon gamma is given to treat these pts.

In OnlineMedEd, Dustyn said that in graft vs host disease, the lymphocytes in the donor tissue trigger the recipient to make antibodies against the recipient. In this question I just answered, it says that T lymphs in the donated organ are sensitized to the recipient's MHC Ag and then they attack the host's tissues. Donor T cells from the donated organ go into the host's tissues, become sensitized to the host's MHC antigens, and then the donor CD4+ and CD8+ T cells destroy host cells. The GI tract, the skin, and the liver are usually affected. The pt can get a rash that includes the palms and soles.

IL-2 is made by CD4+ helper T cells and activates more CD4+ helper T cells, cytotoxic CD8+ T cells, Natural Killer cells, monocytes, and B cells. T cells and natural killer cells activated by IL-2 kill renal cancer and metastatic melanoma. I posted a picture showing how immumosuppressants work. So IL-2 causes activation of macrophages and NK cells, proliferation and differentiation of helper T cells, growth and secretion of IFN-gamma from T cells, and proliferation of B cells.

Macrophages, B cells, dentritic cells = Antigen-Presenting Cells (APCs); they have MHC Class II, which they use to present angtigens to CD4+ helper T cells.

Type IV (T cell-mediated/delayed type) HSR = T lymphs release cytokines that cause induration 24-48 hours after exposure to the Ag. So cytokines, CD8+ T cells, and macrophages cause the type IV HSR. Poison ivy is a type IV HSR.

Poison ivy, poison oak, and poison sumac make urushiol, which attaches to proteins (haptenization)-> T-cell mediated immune response. CD8+ T cells destroy keratinocytes with the haptenated proteins.

Accumulation of ADA-> destruction of lymphocytes. Adenosine is converted to inosine by adenosine deaminase (ADA). ADA also catalyzes the conversion of deoxyadenosine to deoxyinosine. If ADA is absent, then deoxyadenosine is converted to dATP and that causes lymphocyte apoptosis. Hairy cell leukemia is a lymphocyte cancer, which can be treated with ADA inhibitor (cladribine). ADA deficiency also causes SCID, which is lack of B and T cells.

Hib vaccine is made with the polysaccharide capsule of Hib conjugated to tetanus toxoid carrier protein (or N. meningitidis outer membrane protein). The protein conjugation elicits T cell mediated immune response-> B cell activation-> memory B cells, which causes long term immunity. The capsule isn't effective at eliciting the T cell response in pts younger than 2 years old because their humoral immunity is underdeveloped. So conjugating the capsule polysaccharide to a protein increases the humoral response against the capsule via T cell activation. T cells-> B cell stimulation-> memory B cells.

Steroids cause neutrophil count to increase because it prevents them from marginating (lining up against the walls of blood vessels). Steroids can cause hypomania and psychosis. Steroids decrease basophils, eosinophils, lymphs, and monocytes.

Mycophenolate inhibits IMPDH, which prevents conversion of inosine monophosphate to guanosine monophosphate. This prevents DNA and RNA synthesis in lymphs. Mycophenolate is used to prevent transplant rejection.

Eosinophils release major basic protein, which causes the induration that occurs 2 to 10 hours after exposure to an allergen. It's responsible for the late phase of a dermatologic type I HSR and is IgE-mediated. Major basic protein damages tissue. Wheal and flare is the early phase of a type I HSR in the skin. The late phase induration of the skin is due to release of major basic protein from eosinophils. Contrast this with type IV HSR, which is T cell-mediated and takes days, rather than hours, to develop.

Classical complement pathway starts with C1 binding to 2 IgGs or 2 IgMs. C1 binds Fc region of heavy chain near the hinge point. After IgM binds to an antigen, the C1 binding site is revealed and C1 can bind to it, activating complement.

There are more steps in WBCs leaving the vessels to get to the cytokines than what he mentioned in OnlineMedEd. The steps of inflammation are: margination, rolling, activation, tight adhesion and crawling, and transmigration. He grouped it differently in the video. Rolling is when the neutrophil slows down via interaction of its sialylated carbohydrate groups with selectins on endothelial cells. For example, sialyl Lewis X or PSGL-1 on neutrophils with selectins on endothelial cells. Then integrins on the endothelial surface (ICAM-1) stop the WBCs. In the tight adhesion and crawling phase of inflammation, CD18 beta 3 integrins on neutrophils bind to ICAM on endothelial cells. Then PECAM lets neutrophils slide through the spaces between the blood vessel wall cells during transmigration. Leukocyte adhesion deficiencies (LADs) prevent leukocytes from migrating from the blood to the site of cytokine release. LAD type 1 = no CD18-> no beta 2 intergins-> skin infections with no pus and delayed separation of umbilical cord.

C1 inhibitor deficiency leads to cleavage of C2 and C4-> excessive activation of complement system; also causes angioedema and GI symptoms.

Hemolytic Disease of the Fetus and Newborn (HDFN) occurs when the mom has type O blood and thus makes IgG against type A and B blood. If this mom's baby has type A, B, or AB blood, her IgG can diffuse across the placenta and cause hemolysis in the baby. But moms with type A or B blood make IgM antibodies (anti-B if the mom has type A blood; anti-A if the mom has type B blood), which can't cross the placenta, and thus don't cause hemolysis in the newborn. In contrast to Rh disease, HDFN can occur during the first pregnancy because the mom makes anti-B and anti-A IgGs in response to similar antigens that are encountered early in life.

Leukotriene B4 causes neutrophil chemotaxis.

[read-sky-at-night]

It All Happened so Fast

Alright, so right after I finished The Paper Wasp, I was all set to take a couple days off from reading and start the next book on my Net Galley checklist. But then I saw a trailer for Five Feet Apart. I had seen the trailer and the movie poster before, the book was even on my To Read List, and was curious so I checked to see if it was available at my local library (where I normally get my books.) It wasn’t. But suddenly I got this urge that felt like I have to read this now, like I don’t want to wait for it to come in if I place a hold for it. I got a good deal through Kindle, downloaded it and oh lord you guys I felt so many things.

So just in case anyone doesn’t know, the book is about two teens with Cystic Fibrosis (CF,) Stella and Will. The general rule for those with CF to stay six feet apart to lower the risk of spreading bacteria, but Will also has Burkholderia cepacia, which makes him more susceptible to infections. The two’s friendship slowly blossoms and because of love and junk and fuck the system, Stella and Will settle on five feet of space between them and discover that love is worth the risk. 

I enjoyed this book a lot. I felt myself get invested with the characters and their journey. Some parts were predictable and others I did not see coming. For me, it wasn’t a drag to get through. I enjoyed the nurses and Poe, Stella’s friend who also has CF. The dialogue was charming and witty and the emotional stuff really gets ya. It’s one I’ll be keeping in my collection. 

[garbage-empress]

When I saw the headline I thought it would be something like Staph, not fucking Burkholderia pseudomallei. B. pseudomallei is put on the "tier 1 select agent" list because it has strong potential as a bioterror weapon. Also on that list are Bacillus anthracis (anthrax) and Yersinia pestis (black plague).

Walmart is recalling nearly 4,000 bottles from a line of aromatherapy spray products linked with a bacterial disease outbreak. A bottle of “Better Homes & Gardens Lavender & Chamomile Essential Oil Infused Aromatherapy Room Spray with Gemstones” tested positive for B. pseudomallei, a rare and sometimes deadly bacteria that causes melioidosis.

[askedfortoo-much]

The Mystery of Burkholderia Cepacia That Nobody Is Discussing

Burkholderia Cepacia - a Quick Outline

Pay a visit to our site to discover the QC microorganisms your lab needs in quite a few easy-to-use formats. The instructions for use for virtually any ultrasound equipment has to be consulted to guarantee compatibility before using any kind of disinfectant on their transducers. Thus it could be beneficial to use advanced technologies and methods to detect its presence in the medicinal item. Detection techniques of B. cepaciain pharmaceutical superior control have been quite slow using traditional media and at times traditional methods don't detect this bacterium. It's possible to come across such products on the internet or at sporting goods stores. www.sdrugs.com/?c=drug&s=toxinil

Together with their antinematodal and antifungal properties, they are also able to degrade a wide assortment of toxic compounds. Phages are the absolute most ubiquitous bacteria fighters on Earth. The colonies were created up of gram-negative rods. Burkholderiain pharmaceuticals Microbial contamination is a significant reason behind product recall in the USA. There is a huge difference between helpful and harmful kinds of bacteria. You'll locate those in the next various sorts of bacteria list.

Who Else Wants to Learn About Burkholderia Cepacia?

You are able to view it like a PDF. Because there are currently no compendial procedures for detection of BCC, we've provided suggestions for a prospective validation approach and a number of points to think about when designing your validation studies. Up to now, there aren't any studies evaluating the efficacy of a range of transducer covers used during an ultrasound guided procedure. The outcomes are exciting. If negative data aren't fully reported, we'll speak to the principal investigators for these data.

We will be able to help you make a decision as to what information your school needs to understand about your kid's care. The outcomes of this theoretical and technical research is going to be detailed within this study. You may even combine terms from various languages. PrecautionsQuanti-CultPLUS comprises live micro-organisms and ought to be used solely by individuals with microbiological training. This is a product which is sold to consumers for direct use and to hospitals and healthcare facilities for administration to patients. Consumers, pharmacies, and healthcare facilities which have a liquid product which is being recalled should quit using the item immediately.

Care has to be taken because Burkholderia cepacia is also quite a serious human pathogen. Burkholderia cepacia is characterized by means of a resistance to several antibiotics. Laboratory specialists first test samples to see whether the bacterium is present, and then try to eradicate the pathogen from cultures with distinct forms of antibiotics. This bacterium is very dangerous however because it may take many different routes once it infects and present itself in many distinct manners. https://www.nrcs.usda.gov/wps/portal/nrcs/detailfull/soils/health/biology/?cid=nrcs142p2_053862

In addition, CDC states the bacteria is known to be resistant to a lot of common antibiotics, making infection harder to deal with. Additional testing is underway to ascertain whether bacteria from such samples match the outbreak strains. Surgical debridement might be helpful. They can be beneficial for instance, gut bacteria help us to digest food but some are responsible for a range of infections. BCC bacteria exist throughout the surroundings. It's utilized by several bacteria and archaea.

What You Must Know About Burkholderia Cepacia

The clinical significance and pathogenic potential of these various genomovars aren't yet known. The PCR-RFLP procedure was shown to be in excellent agreement with strain identification offered by the various study participants. Study findings imply that biofield treatment has a notable effect on the phenotypic character and biotype quantity of multidrug resistant strain of B. cepacia. When multiple interventions were introduced in various moments the authors analysed the single intervention based on the related size of the result.

It's your duty to do your part. We should maintain the momentum. Although it's important to practice approaches to avoid catching germs, it's not possible to have total control over your surroundings. You might have a right to compensation. His major interests in the use of technology to enhance the human condition.

The New Fuss About Burkholderia Cepacia

Nevertheless, strict infection control guidelines to stop the spread of this organism within this vulnerable patient population ought to be enforced. Individuals should realize that an old therapy is back, he states. That which we do know is that it may become very resistant to antibiotics and it can make a lot of lung damage. To the latter, the right mix of drugs that will influence a durable cure has to be chosen.

As it is resistant to numerous antibiotics, effective therapies and treatments aren't straightforward. Background Cystic fibrosis is an inherited disease and individuals who have this disease produce large quantities thick mucus that's tricky to clear. Symptoms are like an array of diseases and are frequently misdiagnosed, which can cause fatality.

Replacement of genomovar III-A infection by strains of different genomovars wasn't observed during the analysis period. Symptoms connected with infections caused by B. cepacia are extremely much like the signs of different diseases of the lungs like pneumonia and cystic fibrosis. Cases of MDR infection was increased suddenly, which contributes to ineffective therapy and risk of spreading infections. These infections could be associated with a fulminant necrotising pneumonia.

Most Noticeable Burkholderia Cepacia

Even back then, but the treatment was divisive in the health care world. There were not any further instances. When employing a mask, it's important to wash the youngster's face after use.

Moreover, the treatment process used to keep the caliber of water on spacecraft has to be robust and operate for extended periods with minimal crew intervention. Although this strategy is often successful, the maximal effects might not be clinically apparent for many months. In the past ten years considerable progress was made in understanding the pure biology and clinical infections brought on by this fascinating group of bacteria. Following that, others started to seek Strathdee's help in receiving viruses to treat their superbugs. It can put lives in danger.

New Step by Step Roadmap for Burkholderia Cepacia

The beginning phases of infection also have been related to the scavenging of iron. The goal of this is to lessen exposure to bacteria that may stay airborne for as much as 30 minutes after testing. Inside this case we present acute suppurative thyroiditis brought on by Burkholdeira cepacia, that is an uncommon infectious agent in adults. Its capacity to survive such conditions is as a result of its ability to create a biofilm. The second portion of the study involved a decremental PEEP titration to locate the important closing pressure. The upcoming key step within this experiment was to have the ability to isolate and immobilize the lipase to be able to be capable of using it as needed for the transesterification procedure.

In case you have phages which are already characterized in a phage bank, they are sometimes tested against a new bacterial threat, rather than having to return to something like sewage every moment. Moreover, there is ordinarily a resistance to a lot of beta-lactam agents which is based on the creation of chromosomally-encoded beta-lactamases or altered penicillin binding proteins. However, there's no consensus on which method might be superior. That's the reason why we're attempting to find different laboratories involved, since they might have the phage I don't have. B. cepacia complex was demonstrated to be invasive in tissue culture cell lines (32) and invasiveness could possibly be a significant factor in the growth of bacteremia within this immunocompromised patient population.

[wumblr]

"if you're asking permission, that's uh... that's really not my department... but if you're asking if it's physically possible, i mean... neither of the two guys who separately edited their own genomes on youtube specifically used mitochondrial ddda editing, newly announced this week based on a secretion of burkholderia cenocepacia -- but like, otherwise, yea -- oh shit, they're teaming the fortress 2 or whatever idk i've never played it" --scout from tf2

me, using a ddr gamepad to edit my own genome via mitochondrial ddda, eventually resulting in the epigenetic termination of my whole clone line in 200 years' time:

[medicowesome]

Medicowesome secret project Click to know more about what is the secret project and how you can contribute!

Life of a blind man Photography and writing by Jaskunwar Singh A beautiful writing on struggles and compassion. An Alcoholics Tale A poem on Alcoholism written by A.P. Burkholderia This dark poem paints an imagery on the signs of alcoholic liver disease. Embryo - Male or female? Afees Ahmad links a religious script written hundreds of years ago with what medical genetics knows today A nice read for people who like to strengthen their faith through science. Bio-statistics A poem on Biostatistics by Parbinva It's by the last verse that you realize the poet isn't talking about stats... Ghrelin Ivan Chong's calligraphy It's a mystery why 'Ghrelin' is his favorite word... Who am I? A riddle on a medical condition written by whoopingcough Can you figure out which condition the poet is talking about? Exam time Jaskunwar Singh writes on what he goes through during his exam time Somehow relatable to all of us, isn't it?

[mcatmemoranda]

ED pts I saw today:

Woman with otitis externa (perichondritis - infection of the cartilage in the ear) treated by urgent care with cephalexin came in with persistent ear pain and new R sided facial numbness. It appears to be Bell’s palsy. Bell’s palsy is usually caused by viral infections, but this pt has no recent URI. She could potentially have malignant otitis externa, which can cause Bell’s palsy. So we got blood cultures, ESR, CRP, CT temporal bone with IV contrast. Gave her IV ciprofloxacin 400 mg and Zosyn 3.375 grams.

Otitis externa affects the pinna and canal, but not the eardrum

Otitis media involves the part medial to the eardrum and distal to the oval window of the cochlea

From UpToDate:

●Definition − Malignant (necrotizing) external otitis (also termed malignant otitis externa) is an invasive infection of the external auditory canal and skull base, which typically occurs in older adult patients with diabetes mellitus.

●Microbiology − Malignant external otitis is caused by Pseudomonas aeruginosa in more than 95 percent of cases. Since P. aeruginosa is not a normal component of ear canal flora even in diabetic patients, its recovery indicates the presence of a pathogen. Occasional reports of cases caused by other organisms have included Aspergillus species, Staphylococcus aureus, Proteus mirabilis, Klebsiella oxytoca, Burkholderia cepacia, and Candida parapsilosis. Infection with these other organisms characteristically occurs in immunocompromised hosts, such as those with AIDS or cancer.

●Clinical presentation − Patients with malignant external otitis classically present with exquisite otalgia and otorrhea, which are not responsive to topical measures used to treat simple external otitis. The pain is generally more severe than that found in simple external otitis, although the two may be difficult to distinguish in their early stages.

●Complications − As the infection advances, osteomyelitis of the base of the skull and temporomandibular joint osteomyelitis can develop. Progression of the osteomyelitis can be associated with cranial nerve palsies. Other central nervous system complications are rare but can be fatal when they occur. These include meningitis, brain abscess, and dural sinus thrombophlebitis.

●Diagnosis − The diagnosis of malignant external otitis is based upon a constellation of clinical, laboratory, and radiographic findings. ESR, CRP, culture of ear drainage, blood cultures, CT temporal bone with contrast.

●Imaging − Anatomic localizing procedures, such as computed tomography (CT) and magnetic resonance imaging (MRI) scans, can be useful for both diagnosis and follow-up. CT is the better test for identifying bony erosion, while MRI is better for establishing extent of disease and monitoring response to therapy. MRI may also identify very early cases prior to appearance of bony erosion on CT.

●Antibiotic selection − For empiric therapy of immunocompetent patients with uncomplicated malignant external otitis, we suggest ciprofloxacin (Grade 2C). Initial combination therapy with ciprofloxacin plus an antipseudomonal beta-lactam is appropriate for patients with advanced infection or severe immunocompromising conditions (like my pt who is on methotrexate for RA); they can be transitioned to ciprofloxacin following clinical improvement. (See 'Systemic antimicrobial therapy' above.)

●Duration of therapy − The duration of antibiotic treatment is generally six to eight weeks, as indicated for osteomyelitis. Patients with treatment failure should undergo biopsy for culture and susceptibility testing.

[troisenator]

Rules: Reblog with your answers (and the rules, please) and tag 10 other blogs (or however many you’d like) whose answers you want to hear. That’s it! Was tagged by: NO ONE  Time Where You Are Now: 10:00 PM Pacific Last Thing You Watched On TV: Parks & Rec Favorite Color: Blue Favorite Ice Cream Flavor: Cookies & Cream What You Ate For Dinner Tonight: Chicken, Egg, Broccoli  Currently Wearing: Gym Clothes Favorite Movie Character: Winter Soldier Top Places To Visit On Your Bucket List: Machu Picchu, Tokyo, Italy, London, Edinburgh Harry Potter House: Hufflepuff  If You Read FanFic, Last One You Read: NO. Favorite Sleeping Position: On my stomach, half curled to the right If You Could Instantly Teleport Yourself Anywhere Right Now: Next to my dog.  I tag: @killingchivalry @revflooper @that-drew-bot @burkholderia @crazycade @juniorskeptictumblorg @kupokuupo @queenofqeeks @littlekingfox @damianism

[frankkjonestx]

A bacterial toxin enables the first mitochondrial gene editor

Bacterial weaponry has an unexpected use in human cells.

A protein secreted by bacteria to kill other microbes has been re-engineered to tweak DNA inaccessible to other gene editors, scientists report online July 8 in Nature. The advance paves the way for one day fixing mutations in mitochondria. Those energy-producing organelles are inherited from a mother and have their own DNA, distinct from the genetic information — from both parents — that’s stored in a cell’s nucleus.

“I’ve been a mitochondrial biologist for 25 years, and I view this as an extremely important advance for the field,” says Vamsi Mootha, a Howard Hughes Medical Institute investigator at Massachusetts General Hospital in Boston and the Broad Institute of MIT and Harvard.

Mutations in mitochondrial DNA cause over 150 distinct syndromes and affect 1,000 to 4,000 children born in the United States each year. There are no cures for these diseases and currently, the only way to prevent a child from inheriting dysfunctional mitochondria is a controversial “three-parent baby” method (SN: 12/14/16). This in vitro fertilization technique requires mitochondria from a donor egg, in addition to genetic information from a mother and father.

An approach for developing cures for genetic diseases is gene editing, a technique that makes changes directly to DNA. Perhaps the most famous gene editor, CRISPR/Cas9 is a molecular scissors that cuts DNA. Researchers have also previously used molecules called TALENs to cut up mitochondrial DNA in mice and eliminate defective organelles (SN: 4/23/15). A newer technology, called base editors, bolts proteins that can change DNA bases — represented by the letters A, C, G and T —  to a modified version of the CRISPR-associated protein Cas9 (SN: 10/25/17). These editors chemically transform one DNA base into another, essentially fixing typos that can lead to disease. This technology, however, works only on DNA in nuclei, not mitochondria.

The toxin secreted by the bacteria Burkholderia cenocepacia unexpectedly proved to be the solution needed to create a mitochondria-friendly base editor. Marcos de Moraes, a microbiologist at the University of Washington in Seattle, deduced that the toxin killed bacteria by causing disruptive DNA mutations. But for months, he couldn’t untangle how the process worked at a molecular level. He was on the verge of moving on from the project when a single late-night experiment made everything fall into place.

It was like a soap opera, de Moraes says. He’d suspected early on that the toxin protein attached to DNA and modified one DNA letter, cytosine (C), so it resembled a different one, thymine (T). These intentional DNA typos were what brought down the toxin’s victims. But what de Moraes learned from that fateful late-night experiment was that, unlike all other cytosine-converting proteins, the toxin made changes to double-stranded DNA rather than single-stranded DNA.

This seems like a minor difference, but it has major implications. Thus far, base editors have used proteins like Cas9 to pry apart target DNA into single strands before making a change. But pieces of RNA required for the function of these proteins can’t get into mitochondria. A base editor based on the B. cenocepacia toxin, which works on double-stranded DNA, would no longer need to depend on Cas9.

The prospect of developing a mitochondria-friendly tool spurred conversations with David Liu, a chemical biologist and HHMI investigator at Harvard University and the Broad Institute of MIT and Harvard.

The new cytosine-converting enzyme, however, was as lethal to mammalian cells as it was to bacterial prey. The first step in “taming the beast” was modifying the toxin so it didn’t just indiscriminately mess up double-stranded DNA, Liu says. The researchers split the protein into nontoxic halves; the two pieces changed cytosine to thymine only when they were brought together to the same spot of DNA.

“It’s quite brilliant,” says Carlos Moraes, a mitochondrial biologist at the University of Miami in Florida who was not involved in the work.

To direct the enzyme halves’ activity, the researchers attached TALE proteins, short pieces of protein that could be chosen to target specific stretches of DNA. In cell culture experiments, the mitochondrial editor successfully converted cytosine to thymine at intended mitochondrial DNA locations, with efficiencies ranging from 5 to 49 percent.

Future work will aim to improve efficiency, develop new types of mitochondrial editors that can produce other DNA base changes, and see if mitochondrial gene editing works in animals.

“This is just the first step,” says Shoukhrat Mitalipov, a mitochondrial biologist at the Oregon Health & Science University in Portland who was not involved in the work. “But in the right direction.”

from Tips By Frank https://www.sciencenews.org/article/mitochondria-gene-editing-bacterial-toxin-crispr

[thatisprettysmart]

Fuse and Conquer

Hijacking the host cytoskeleton is a popular pathogen trick, but the bacterium Burkholderia thailandensis takes this strategy even further. Once inside a host cell, B. thailandensis (in green) uses the host’s actin fibres (in red) to promote fusion with other cells, forming giant cells in which it rapidly replicates. Studying this behaviour in mouse macrophages, researchers uncovered how the immune system fights back: activated by type I interferon, molecules known as guanylate-binding proteins (GBPs) prevent the bacteria from manipulating actin, ultimately hindering cell fusion. Without GBPs, the macrophages are more likely to fuse when infected by B. thailandensis, and mice lacking GBPs are more susceptible to infection. Closely-related pathogens B. mallei and B. pseudomallei, which cause serious diseases in humans, also rely on cell fusion to spread, so unpicking this process in B. thailandensis is a useful step towards understanding their strategies.

Image from work by David E. Place and colleagues, published on the cover of PLOS Pathogens

Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in PLOS Pathogens, April 2020

from BPoD - Biomedical Picture of the Day https://ift.tt/3cLJ0H1

[juniperpublishers-endocrinology]

Microbe-Endocrine Hormone Interactions- Juniper Publishers

Introduction

The influence of hormones on human cells is very well characterized, yet much less understood is the response to those chemical signals of the 1013-1014 bacteria and fungi that are coresident within the human frame [1]. Microbial Endocrinology is a research area which seeks to understand the role of microbial interactions with mammalian hormones in conditions of health and disease [2-4]. It takes the view that through their long evolutionary relationship with animals microorganisms have evolved systems for sensing hormones which they use as an indicator that they are within the proximity of a potential host. This article considers what happens when the human microbiota Table 1: Hormone responsive microorganisms.come into contact with the chemical signals of their host, and the health significance of this inter-kingdom-encounter.

Hormones can be classified on the basis of their chemical structures: amino acid, peptide and protein and cholesterol based, and the receptor location by which the hormonal signal is transduced. The function of each hormonal type will be described, and the health implications to the host when the hormone is encountered by potentially infectious bacteria and fungi. Structures of the hormones covered and the microbes which recognize them can be found in Table 1, respectively [5-39].

The '+' indicates that the hormone shown, or their metabolites have induced enhancement of growth or virulence of the bacterial species shown. Key: NE, noradrenaline; Adr, adrenaline; Dop, dopamine; Iso, isoprenaline; Dob, dobutamine; DHPG, dihydroxy phenylglycol; DHMA, dihydroxy mandelic acid, ACTH, adrenocorticotrophic hormone.

This table was adapted with permission from Freestone [3].

Amino Acid-Derived Hormones

These are commonly derived from dietary tyrosine and tryptophan, and comprise two main types: thyroid hormone such as thyroxine and the catecholamines dopamine, noradrenaline and adrenaline [5]. Catecholamines are well studied as they possess a diversity of signaling functions and are widely distributed throughout the tissues and organs of the human body [5]. Noradrenaline and adrenaline are neurotransmitters but also play an integral role in the flight or fight response. In terms of the infection significance of catecholamine release, the field of psychoneuroimmunology has long reported that stress hormone elevations in humans and animals increases their risk of developing an infection. This is in part due to stress-released catecholamine and glucocorticoid hormones reducing the functionality of the immune system [6,7]. More recently, Microbial Endocrinology studies have shown that like immune cells many bacteria involved in human infections recognize catecholamines which they appear to use as an indicator that their host is stressed, and possibly less able to mount a defense to the invading microbe [3,4]. Table 1 shows the catecholamine-responsive microbes that have been identified so far. Most analyses of bacterial stress hormone interactions have looked at growth effects using serum- or blood-based culture media, chosen to more closely reflect the host environment in which the hormone will be encountered [40]. Blood or serum containing media is iron limited due to the presence of ferric iron sequestering proteins such as transferrin or lactoferrin which inhibits the growth of most bacterial pathogens [41]. Because iron is so essential for the in-vivo growth of bacteria [42], its limitation by transferrin and lactoferrin represents a key immune defense against infection. However, bacteria can directly use catecholamines as a kind of siderophore to steal transferrin and lactoferrin Fe which enables up to 100,000-fold increases in bacterial cell numbers in what normally should be highly bacteriostatic host tissue fluids [14,15,18,23].

Dopamine, noradrenaline and adrenaline exposure can also induce pathogenic bacteria to become even more virulent by inducing expression of genes in toxin release [43], increasing biofilm formation [18] and enhancing attachment to host epithelial tissues [16,17]. Catecholamines can even catalyze recovery of bacteria severely damaged by antibiotic treatment [18,27], and rapidly promote exchange of genetic material between different bacterial species [44]. In terms of the infection significance of catecholamine-microbe interactions, catecholamines are used therapeutically in acutely ill patients to maintain heart and kidney function [5]. Catecholamines at the levels infused down intravenous catheter lines were found to massively increase staphylococcal biofilm formation on the same plastic, while clinically attainable levels of catecholamines also increased P. aeruginosa biofilm formation on endotracheal tubing (used to maintain an open airway in ventilated patients) as well as enabling the pathogen to resist antibiotic treatment [18].

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Peptide And Protein Hormones

There are reports of peptide-like hormones affecting the infectious potential of pathogenic bacteria. Melioidosis is an infectious disease caused by the Gram-negative bacterium Burkholderia pseudomallei, which tends to be found in soil and water of tropical climates such as Vietnam and parts of Australia. It has been observed that type I diabetes mellitus is an apparent risk factor for the development of the septicemic form of melioidosis [20]. Woods and co-workers found that B. pseudomallei can directly bind human insulin and that each bacterial cell expressed around 5000 surface-associated insulin receptors. Woods et al. [31] showed that insulin inhibited the growth of B. pseudomallei and suggested that the deficiency of the hormone at least in part explained the higher risk of melioidosis in insulin-dependent diabetics [31].

Adrenocorticotropic hormone (ACTH) is a peptide hormone that induces the adrenal cortex to produce corticosteroid hormones such as cortisol which contribute to regulation of systemic glucose levels. It is therefore interesting that Schreiber and Brown found that exposure to ACTH increased attachment of E. coli O157:H7 to gut epithelia, though the underlying mechanism for this response is not clear [39]. Thyrotropin is a pituitary hormone that induces the thyroid gland to produce thyroxine followed by triiodothyronine which stimulates oxidative respiration and organ development. Interestingly, use of radiolabelled thyrotropin has showed the presence of receptor for thyrotropin in Yersinia enterocolitica [45,46]. The thyrotropin specificity of the Y.enterocolitica binding activity was similar to that of the thyrotropin receptor in human thyroid tissue. This binding activity is thought to have implications for Graves' disease, which is an autoimmune disease in which thyroid-stimulating antibodies to the thyroid-stimulating hormone receptor mimic thyroid-stimulating hormone, which activates the receptor leading to hyperthyroidism. Thyrotropin binding sites on have been shown to be recognized by antibodies from humans with Graves' disease, and prior infection by Y. enterocolitica has been implicated in the pathogenesis of Graves' disease [46]. The outer membrane porins Omp A,C and F have been identified as the Y. enterocolitica targets recognized by Graves' patient antibodies, though their role in contributing to development of Graves’ disease remains to be shown [47].

Candida albicans is a dimorphic opportunistic fungal pathogen of females and the immunocompromised which has been shown to interact with several human peptide hormones. Luteinizing hormone is required for ovulation and the formation of a corpus luteum in the female menstrual cycle. C. albicans has been shown to bind human luteinizing hormone and chorionic gonadotropin [36]. Bramley et al. [36] used (125I)-labeled luteinizing hormone and chorionic gonadotropin to demonstrate the presence of specific binding sites for both hormones in C. albicans, and C. tropicalis [36]. The binding activity was found to be highly specific and was not surface associated instead being at greatest levels in microsomes and cytoplasmic fractions. Also, of considerable relevance to C. albicans infectivity, interaction with the luteinizing hormone was found to stimulate germination of Candida spores and germ tube formation [32].

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Cholesterol-Derived Hormones

Cholesterol is the chemical basis of steroid hormones such as oestrogen, progesterone and testosterone which regulate aspects of the metabolism, tissue differentiation and reproductive cycles of females and males. Investigations from a variety of researchers have shown that exposure of some bacteria and fungi to steroid hormones can elevate infection risk in certain patient groups. For instance oestrogen have been shown to increase the likelihood of urogenital infections, particularly during pregnancy, or in women taking high oestrogen contraceptives or hormone replacement therapy [38]. Chlamydia trachomatis is an important sexually transmitted pathogen, especially in young women; Sonnex [38] reported that treatment of C. trachomatis with physiological levels of oestrogen increased infection of human endometrial cells, and enhanced Chlamydia colonisation of female mice. C. trachomatis infection of female mice was also increased following pre-treatment with progesterone. C. albicans is a major source of fungal infections in women of reproductive age [38] which has been shown to possess an oestrogen binding protein of high affinity and specificity [32,33,34]. Contact with oestrogen has been reported to increase C. albicans growth as well as its infectivity, causing the yeast to shift into to a more invasive hyphal morphology [33]. Tarry et al. [34] showed that C. albicans vaginal colonization in a rat model of infection was increased over 8-fold when a physiological level of oestrogen was present [38]. Banerjee et al. [35] investigated the effects of progesterone on C. albicans gene expression and found that expression of 99 genes was differentially affected by the hormone. Most changes were metabolism associated such as protein synthesis and cellular transport. Of relevance to infection risk was the finding that expression of virulence associated genes such as those involved in hyphal induction, pathogenesis and multi-drug resistance genes were significantly increased in progesterone-treated Candida [48-50].

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Conclusion

The effects of endogenous hormones on mammalian cell are well understood, yet although microbes within the human body will repeatedly encounter their host hormones the biological significance to the host of these interactions is only now becoming apparent. This review examined only a few of the many hormones within the human body, but still revealed that there are considerable health implication for some of the microbe- hormone encounters. Table 1 revealed that the most extensively studied area of microbial endocrinology is catecholamine- related, largely because of the long held view of stress increasing infection risk. However it is clear that other types of contact the human microbiota may have with mammalian hormones has health implications. It will be interesting to discover if additional signals within our hormonal milieu are being sensed by the thousands of other species of microbes we host.

For more Journals in Juniper Publishers please click on https://juniperpublishers.com/journals.php

For more articles in Journal of Thyroid Research please click on: https://juniperpublishers.com/jetr/index.php

[caitlinmargaritareads]

Book 5- Five Feet Apart by Rachael Lippincott

[Originally posted March 3, 2019]

I intended for my Book 5 review to be Toni Morrison’s “The Bluest Eye,” but as you can see from the header that didn’t go as planned.. Turns out that Morrison, while absolutely brilliant, is super depressing and difficult to read. TBD on the review for that one.

Fast forward to me perusing the library and being sucked in by another teen title, and that’s where we get to “Five Feet Apart.” I had a seen a trailer for this one featuring former Disney child-star, Cole Sprouse [I have garbage taste sometimes, and I’m not afraid to admit it], so of course I felt compelled to read the book before dragging Ryan out to see the movie with me.

The story centers primarily on two teens, Will and Stella, who both have cystic fibrosis. Stella is a lifelong patient at the hospital, seeking treatment for a sore throat and fever, when she meets Will, who has come to the hospital for a new, experimental treatment for B. [Burkholderia] cepacia. The title of the book comes from the fact that CFer’s [as they’re nicknamed in the book] cannot be closer than five feet apart, or else they run the risk of spreading illnesses which could be fatal to someone with CF. To make the story more dramatic, B. cepacia is a bacteria which cuts a CFer’s already short life expectancy in half, making contact between Will and Stella much more dangerous.

The character profiles are nothing original- a typical “goody two shoes” who follows the rules and her medicine regimens to the T, clashes with the rebel bad-boy who only wants to live the remainder of his life to the fullest- but the alternating first-person narratives and the unfortunate circumstances of the couple make it a unique and enjoyable read. I laughed, I cried, and I felt like I was able to truly empathize and understand the characters’ emotions. I recommend this book to anyone who enjoys a good YA novel, and if you don't feel compelled to read it then go see the movie!

3.5 out of 5 stars