Month: September 2017

From our anonymous insider…

Virus week. Long days of lectures followed by three hours of studying old material on infectious bacteria in the evenings.

“The more I study, the less I know,” reflects Gigolo Giorgio, the class alcoholic frequently found on the dance floors of downtown clubs. One classmate asked Giorgio, “Is Campylobacter jejuni gram-positive or negative?” We were all impressed when Giorgio responded, “Gram-negative.” We were stunned: “How did you know that!” He answered, “Well I haven’t heard of it, and I’ve only studied gram-positives.”

This block is particularly challenging because the material doesn’t build on previous lessons. I feel more behind each day. “I’m still on gram-positive bacteria! I have not even started gram-negatives!” wails a classmate as we begin virology.

If you model a physician as an information processor, the result of this block is a database that is indexed in only one direction. For example, we study by investigating the properties of each pathogen one at a time. We can reliably regurgitate information from yesterday about a single bacterial species. However, when we attempt to develop a differential based upon symptoms, we have difficulty identifying potential culprits. For example, both S. pyogenes and an acute HIV infection can lead to sore throat. There were many blank faces when we were asked, “What are the common causes of sore throat?” Fortunately electronically implemented databases can be indexed in multiple ways. This is what gives clinical-assistance programs, e.g., UpToDate.com, their power to boost physician efficiency, especially in regions where ID doctors are scarce.

A 60-year-old internist who specializes in herpes and whose two children are also practicing physicians at the hospital introduces virology to us with four hour-long lectures. The Internist introduced infectious disease: “ID is not rocket science. It’s an approachable field if you have the interest and dedication to learn a lot of diseases.” Jane actually shadows the son and mistakenly thought he would be teaching us.

There are three types of viruses: RNA, DNA, and retrovirus. RNA and DNA viruses hijack host cell machinery to produce proteins of their own design. Retroviruses actually insert their own DNA into host cells.

A basic virus is a small particle containing genetic information (DNA or RNA) that encodes for its infective vector (the proteins that enable the virus to get into cells and reproduce). These proteins include the structural capsid protein(s), the polymerase(s) used to replicate the genome, and critical docking proteins to allow access into the host cell. The mode of transmission is restricted if the virus is enveloped in a lipid bilayer. “Enveloped viruses have an easier way to get into cells, but are much more susceptible to drying out on a surface. Non-enveloped viruses can last for days on a surface.”

The internist asked the class, “What is the difference between herpes and love…? Herpes is forever.” Herpesviridae is a large class of enveloped DNA viruses that include herpes simplex (genital warts and labial cold sores), varicella zoster (chickenpox and shingles), and the college-drag epstein-barr (“mono”). “Sixty to seventy percent of the population is infected with HSV1 [herpes simplex 1, mouth cold sores],” said our lecturer. “Most people do not have reactions, but some people have outbreaks, particularly under stressful conditions. Does anyone want to tell their story about cold sores?” Two students volunteered that they have outbreaks, particularly around exam week. They both have a prescription for the antiviral drug acyclovir, which can reduce symptoms if administered during the beginning of the outbreak (typically a tingling or burning sensation). Herpes viruses remain latent in sensory nerves until the immune system is weakened. Reactivated virus will travel to the skin to cause an outbreak.

Shingles, caused by the latent varicella, will typically infect only a single dermatome (region of skin innervated by a single spinal nerve). We also learned about flaviviridae, which causes several nasty tropical diseases, including Dengue, Zika, and Chikungunya. “Each of these is transmitted through the same Aedes mosquito, so it is possible to get multiple outbreaks simultaneously. I’ve had patients with two at once.”

A number of students thought the viral lectures would have been more effective after a dermatology block (scheduled in two weeks). The early symptoms of viruses are typically nonspecific, with the exception of some characteristic rashes. For example, we looked at pictures for the common rash-causing diseases of childhood (measles, scarlet fever, rubella, slapped cheek and roseola) without having an understanding of what pathophysiological mechanism is causing these lesions.

The ID physician spent about 30 minutes on the hepatitis viruses. “There is now a ninety-five percent cure rate for all genotypes of Hep C. It’s truly unbelievable the surge in drug innovation. Five years ago we had almost nothing. Now there are over 12 drugs.” He commented how the first Hep C drug recently dropped in price to remain competitive as it only covers a few genotypes compared to the newer drugs.

Why are there are so many genotypes and viruses? Some viruses purposefully use an error-prone polymerase (enzyme used to replicate DNA/RNA) to accelerate their mutation rate. For example, influenza pandemics occur when a “genetic shift” arises that is sufficiently different from previous strains so that past exposure provides no immunity. This also means the influenza viruses make up to 10 percent null copies, incapable of infecting, but that is okay for an organism that is expending someone else’s energy.

We also learned that many cancers are thought to be a result of past viral infections. For example, cervical and anorectal cancer are almost entirely attributed to sexually-transmitted human papillomavirus (HPV) infection. This is a DNA virus and the cancer-causing strains are primarily HPV 16,18,31, and 33, which are covered by the Gardasil 9 vaccine (ideally administered to both males and females at age 11-12). Viruses typically induce a cell growth state to increase DNA and RNA replication. Some viruses even encode proteins that suppress growth inhibitors such as tumor-suppressor gene p53.

Wednesday and Thursday featured lectures on HIV led by a quirky, cynical ID physician specializing in HIV patients and speaking in a voice that was a bit like Brian Boitano’s. “Do you think he is gay?” a student asked after lecture. Type-A Anita quickly responded, “Of course he is gay. He treats HIV patients.”

HIV is a retrovirus with machinery to integrate its viral genome into the host genome. HIV’s genome encodes for (can produce) only nine proteins. Gp120 is a glycoprotein inserted into the cell membrane envelope that allows the virus to bind to CD4, a protein found on specific white blood cells. When bound, the hidden Gp41 aggregate to bring the viral envelope closer to the host membrane and eventually fuse allowing access to the host T cell. Other host proteins are necessary for viral fusion, including CCR5. One student sent a case report to the class GroupMe about an HIV-positive individual inadvertently cured of HIV when he received a transplant of bone marrow that lacked this protein. (http://www.nejm.org/doi/full/10.1056/NEJMoa0802905).

Two lectures were dedicated to managing HIV. The ID physician began: “My patient was diagnosed with HIV around age 40. She was confused until her husband admitted that for decades he would go on business trips and have unprotected sex with men. She got a divorce.” A student whispered, “I wonder if health insurance survives after divorce?” (Answer: depends on the state; see Real World Divorce)

The ID physician continued, “You are now supposed to prescribe antiviral drugs to anyone with HIV as opposed to those below a CD4 count threshold. Europeans still wait for a low CD4 count to develop, probably because of the cost of these drugs.” HIV antivirals, if taken regularly, are able to wipe out detectable virus particles in the blood and return CD4 count to normal. “There was a study conducted in West Africa where married individuals with one HIV-positive partner was treated. They evaluated how many HIV-negative partners contracted HIV over several years. Almost no one who adhered to the medication regiment passed the HIV to their partner. Some partners tested positive for HIV, but it turned out to be a different genetic strain. The partner had to have caught it from someone other than the spouse.”

We also learned about HIV prophylaxis treatment. At-risk individuals, such as healthcare workers in a high-risk region, or high-risk sexually-active individual, are prescribed HIV antivirals to prevent transmission. “If you are stuck with a needle from an HIV-infected patient, TELL SOMEONE. If you get started on prophylaxis drugs within 48 hours, we can basically guarantee a zero percent transmission rate. You have to hit the virus before its genome is integrated into CD4 T-cells.” One classmate asked, “Are there certain regions of the country where all gay people should be on prophylaxis?” The lecturer was slightly confused, but responded, “No. Assess the risk. If someone is having unprotected sex with two-three different partners a week, yes. If they are in a monogamous relationship, no. Also it depends on what insurance they have.”

A few classmates discussed afterwards if medical education weights HIV too much compared to more common viral infections. Less than 1 percent of the world is infected with HIV. In the US, 1.1 million individuals are HIV-positive, about 0.3 percent of our 325 million population.

Our patient case: Taylor, a 41-year-old black female, presents to the ED in respiratory distress. She reports worsening shortness of breath and persistent cough over the past 4 weeks. Chest x-ray shows glassy white highlights on the normally black air-filled lungs. This suggests diffuse intralobular infiltrates (infection in numerous spots within the lungs; a typical pneumonia is just one big spot). She is admitted and placed on antibiotics. However, her pulmonary function continued to deteriorate and she is transferred to the ICU. Her CBC revealed elevated lymphocytes with a CD4 T cell count less than 100. She is immediately started on antifungal medication to address a suspected Pneumocystis jiroveci infection. HIV test is positive.

Her two-week hospital course is challenging. Because of her low immune function from the HIV, she arrived at the hospital coinfected with several viruses. Then once in the hospital she acquired a conventional pneumonia from intubation and urinary tract infection (UTI) from the foley catheter. She makes a full recovery and is discharged for outpatient follow-up.

Taylor, now 55, is energetic and recently became a grandmother. “At the time of the diagnosis, my three children were 14, 16, and 21. I was in complete denial. I went to four doctors in town to get another HIV test. I finally accepted it while talking on the phone with my internist. I dropped the phone and wept. My children came into the kitchen and asked what was wrong. It felt impossible bringing this up with them.” Once Taylor acknowledged her HIV, she quickly began antiviral treatment without serious side effects. Her CD4 count has improved to normal, and she has not been hospitalized since the above episode.

How did your friends and family react? “I was severely depressed for several years. I’ve been on every single antidepressive that you can think of. You never know who will be there when you are most vulnerable. My best friends were the first to flee. Three of my siblings still do not speak with me. My sister will occasionally visit me, but she refuses to hug me, or let me see her children. People, especially in my community, remember the 1980s epidemic. They think if they touch, or even come near someone with HIV they will get infected.”

“I told my oldest son a few months after my diagnosis. He asked, ‘Do you know who did this to you?’ I told him the truth. ‘Yes. The man knew he had HIV, but still slept with me. When I found out and confronted him, he moved far away.’ I was scared my son would search him out and attack him. I fortunately calmed him down.”

How about coworkers? “I do not tell my coworkers about my health. I get my work

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I don’t watch television so most of my news comes from scanning headlines, following links suggested by friends and readers, etc. The impression that I’ve gotten from U.S. media is that North Korea is a starving prison camp. But this Wall Street Journal video shows a clean, organized, and modern city. Having recently returned from trash-strewn Casablanca, I would have guessed that North Korea is wealthier than Morocco (the CIA says otherwise). Presumably the rural areas of North Korea are not as prosperous as the city toured by the WSJ reporters, but that is also true in Morocco and in the U.S. for that matter.

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I checked the news to see what was happening in Puerto Rico, curious to know when the millions of fellow citizens who live there might get electric power back, for example. The leading headlines, however, were all about football players refusing to stand for the national anthem and Donald Trump offering his opinion regarding this behavior. (To Americans who worship their president as a demigod on Earth, of course it was very exciting to receive President Trump’s opinion!)

This leads me to ask… if Americans are going to fight about how to behave during the national anthem at football games, why play the anthem at all? Football is not a governmental ceremony, right? It is plainly possible to play an epic game of football without first hearing the “Star-Spangled Banner” because that’s precisely what happens at the Cleary family’s vacation home in The Wedding Crashers. What happens in other countries? Are national anthems played before European soccer games, for example?

[Separately, folks who refuse to respect the U.S. national anthem as a protest against the treatment of black Americans might be on the right track. Slavery in Europe had ended by 1000. Britain abolished slavery throughout its empire in 1833 (Wikipedia). If the American Revolution had never occurred, in which case we’d not have our own anthem, black Americans would have escaped at least one generation of slavery. On the third hand, do these anti-American football players have a practical plan for re-joining the United Kingdom?]

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From our anonymous insider…

Three marathon 4-hour lecture sessions with infectious disease (ID) specialists. Some would cover over 10 different diseases caused by a specific bacterial strain in a mere hour time. Most of the information went in one ear and out the other, especially with the PhD microbiologists. About two-thirds of students stopped attending lecture after the first session. “I have to study this material on my own over several days to not suffer from information overload. I do not find getting bombarded at lecture is efficient use of my time.” They missed a few clinical pearls from the more lively ID clinicians.

One ID doctor delved into the disease-filled, gram-positive, spore-forming, anaerobic genus Clostridium. Spores enable a bacterium to lay dormant, surviving external pressures such as extreme temperatures, pH, and sanitation chemicals. C. difficile is able to survive hand sanitizer and many hospital disinfectants. “Only thorough hand washing will get C diff off your hands. Hand sanitizer does nothing to it.” C diff jumps from bed to bed in hospitals, causing terrible gastroenteritis. Although C. diff is not able to thrive against normal gut flora, after a broad-spectrum antibiotic that decimates the normal flora, C diff will overtake the gut leading to pseudomembranous colitis and the release of toxins that cause life-threatening rice-water diarrhea similar to cholera. The genus Clostridium also contains C. tetani and C. botulinum two related species that cause tetanus and botulism, respectively. C. tetani produces a neurotoxin that destroys inhibitory neuron activity producing a spastic paralysis, typified by lock-jaw. Why are rusty nails and dog bites associated with tetanus? The skin typically seals over a deep penetrating wound before it is fully repaired. Sealed off from the destructive power of oxygen, anaerobic bacteria such as Clostridium tetani thrive. C. botulinum produces a similar neurotoxin, classified as a Tier I bioterrorism agent, that destroys neuromuscular junction activity, producing a flaccid paralysis. Otto Warmbier, the University of Virginia student imprisoned by North Korea, contracted botulism, which lead to respiratory arrest and coma. (The same Botulinum Toxin, “Botox,” can be harnessed to extend the expiration date of the Hollywood elite.)

A 35-year-old overweight unkempt ID pharmacist and an internal medicine resident led a highly effective two-hour lecture and workshop. Unlike the pharmacist at your local Walgreens, pharmacists who work in hospitals must complete a residency. Our lecturer said that his job was to eliminate any bug that comes into his hospital. He went over the clinical impact of antibiotic resistance: “the never-ending arms race.” “My job is to make you good stewards of antibiotics. Now, this can seem like a daunting task, especially when Cipro [broad-spectrum antibiotic] is OTC in Mexico, but let’s give it a shot.” The ID pharmacist added his opinion that there are few new antibiotic classes in the pharmaceutical pipeline because it is difficult to make a profit: “In addition to costing millions to bring a new drug to market, once it is in market, bacteria develop resistance so fast that it doesn’t have a long shelf-life. Further, the medical system reserves new antibiotics as a last line defense.” A student shared a Harvard-Technion experiment on the class GroupMe illustrating the rapid generation of antibacterial resistant genes. Escherichia coli with a fluorescence probe was plated on one end of a giant agar plate with steps of increasing concentrations of the antibiotics trimethoprim (Bactrim) or ciprofloxacin A time-lapse video depicts bacterial colonies traversing onto each step and completely covering the sheet by 12 days.

The 27-year-old internal medicine resident, reminded us that Group A Strep (strepococcal pyogenes) is one-hundred percent sensitive to penicillin. “Don’t be a jerk and give your poor patient a Z-pack,” she cautioned. [Azithromycin is a broader-spectrum antibiotic.] We were also informed that hospitals in different regions have different antibiotic schedules: “MRSA is much more rare in rural Idaho than in NYC. I would be terrified to get hospitalized in NYC.”

The workshop culminated in using iPads to play “Heads Up”. One student would put the iPad on his or her head and, based on hints from other group members, try to guess the bacterium or antibiotic displayed on the screen, e.g., 1st-generation cephalosporin or Clostridium tetani.

My favorite lecture was by a 35-year-old emergency medicine physician on the management of sepsis, a systemic immune response to infection. The immune response causes blood vessels to dilate, thus reducing blood pressure (hypotension), leading to multiple organ failures (“septic shock”). Patients who show up in the ED with septic shock have a mortality rate of twenty-five percent. “I like how he made you feel like you were in the ED. He gave so many different clinical cases,” commented a student after class.

The physician explained, “If a patient is in shock, I immediately conduct a RUSH (Rapid Ultrasound for Shock and Hypotension) exam. I am looking for what is causing the shock. Is it an internal bleed causing blood to pool in Morison’s Pouch [between kidney and liver] or around the rectum? Is it cardiac tamponade [fluid in the sac of the heart restricting its motion]?” Once he has determined septic shock, he starts the patient on antibiotics even without any confirmation of bacterial infection. He then determines if the patient is fluid-sensitive, i.e., if cardiac output would improve with IV saline. The Starling Curve describes cardiac output as a function of End Diastolic Volume (blood volume) for a given heart contractility and vascular tone. The physician continued, “We used to just give the standard 30mL/kg. [2 L for a 70 kg person.] Now electrical engineers have given us the NICOM [Non-invasive cardiac output monitoring] device to determine if someone is fluid-sensitive or insensitive.” NICOM device uses two pairs of electrodes to measure the change in impedance across the chest to the abdomen as a bolus of fluid is injected into the patient. He concluded, “No idea how it works, but we use it everyday. It is pretty neat to see the Frank Starling Curve appear on the NICOM screen and watch the physiology we learn in medical school actually be applied.”

Our patient case: A young ED physician describes his treatment of Abigail, a 26-year-old waitress attending community college for interior design. She presents to the ED for a worsening blood-tinged productive cough, fever, syncope (fainting episodes), and back pain. Over two months she has been to the ED twice and been prescribed different antibiotics for a productive cough and myalgia. With blood pressure of 80 over 55 and heart rate of 110, she is immediately recognized to be in shock and is transferred to the ICU. The RUSH exam reveals left ventricular dysfunction suggestive of distributive shock (leaky blood vessels from suspected sepsis infection decreasing blood volume). Even after a total of two liters of IV saline, she requires pressors (norepinephrine) to maintain a MAP (mean arterial pressure) above 65 mmHg.

“Her entire course changed from a simple question: ‘Do you use drugs?’,” explained the ED physician. Abigail confirmed she regularly injects oxycodone into her veins. “We immediately suspected septic shock with endocarditis [infection of heart tissue] likely from Staph aureus, which has a proclivity to infect the tricuspid valve after getting injected into the blood.” Blood and sputum cultures grew methicillin-resistant Staphylococcus aureus (MRSA). She is immediately started on IV vancomycin (a non-penicillin-based antibiotic reserved for serious gram-positive hospital infections). Echocardiography reveals substantial vegetation on the tricuspid valve. The colonies were releasing small particles into her pulmonary circulation causing septic pulmonary emboli. In addition to heart and lung colonization, she developed osteomyelitis (bone infection) in her vertebrae. The immense immune response due to the bacteremia (infection in blood) and Staph aureus toxins caused glomerulonephritis (kidney inflammation) and hematuria (blood in urine).

“Although the bacteria is the cause of her sepsis, the infection was not the immediate concern,” explained the EM physician. Intensive support therapy including blood/plasma transfusions, fluids, mechanical ventilation, and vasopressors were given throughout her two-week ICU stay. “I’ve rarely seen someone recover completely in medicine after septic shock with tricuspid valve endocarditis. It truly amazes me. Heart, lung, kidney—all fully recovered except for lower back pain.” Abigail was transferred to a “step down” unit [in between the ICU and the general ward] and discharged to rehab.

When we returned to lecture, an ID physician introduced diseases of the spirochetes such as Syphilis and Lyme Disease. “Always note the presence of rash on the palms or soles.” This can help narrow down a broad differential as not many diseases cause a rash there. Syphilis, caused by Treponema pallidum, begins with formation of a chancre, a characteristic painless ulcer, on the penis or in the vagina that lasts for four-six weeks. “I can never understand how some males do nothing about this quite obvious lesion.” Patients then develop a generalized lymphadenopathy (enlarged or sensitive lymph nodes) with a diffuse rash on the palms and soles that resolves. After a multi-year latency period (typically within 5 years of primary infection or 15-20 years after primary infection), some patients enter a serious tertiary phase that involve syphilitic aortitis (inflammation of the aorta potentially causing an aortic aneurysm ), neurosyphilis and gummas (red protrusions of the skin with a necrotic core).

Lyme disease, caused by Borrelia burgdorferi, requires an infected tick to be feeding on the human for at least 48 hours for the bacteria to change membrane proteins in preparation for human cell infection. The feeding ticks are typically less than two millimeters in size, so they are easier to miss than a syphilis chancre. Lyme-infected ticks and diseased humans are most common in the Northeast and upper Midwest, coinciding with large deer populations.

Statistics for the week… Study: 12 hours. Sleep: 8 hours/night; Fun: 2 days. Example fun: Our class held a Game-of-Thrones watch party. Straight-Shooter Sally: “Game of Thrones unites multiple generations under one roof. My parents love this show just as much as I do!”

More: http://fifthchance.com/MedicalSchool2020

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A relative has purchased a house that is under construction so she and her husband have the opportunity to specify the communications wiring. This being the U.S., the builder wants to run 6 coaxial TV connections and let everything else be wireless (what else does one need after a government-funded OxyContin supply, an Obamaphone, and cable TV in every room?).

I’m skeptical of the wireless idea due to the fact that spectrum seems to be scarce already and the U.S. population is growing. The U.S. population could reach 1 billion before this house reaches the end of its design life. What happens where there are 1 billion people all trying to use same spectrum for WiFi?

My first idea is two “CAT 5” runs to every room, starting from a central closet in which the cable modem lives. (Of course, CAT 5 is now up to CAT 7 or CAT 8, though Monoprice seems to be stuck at CAT 6A for bulk cable.) If a legacy phone connection is desired it can be done by putting the RJ11 plug into the center of the RJ45 jack. Then add one additional CAT 5/6A to the forecast location of any TV. HDMI can run over Ethernet, right? So if the future is just to drive the video from the closet to the TV then the single CAT 5 wire will suffice.

Is there any long-term value in coax cables? Is it already possible to use a CAT 6 connection for the in-home wiring to a cable TV box?

My second idea would be wiring up ceiling speakers for background music (see my article on whole-house music). Since most people aren’t audiophiles, just run all the wires back to the same central closet where it will be possible to use Sonos AMPs or a conventional multi-channel amplifier.

Readers: thoughts? Also, how to specify this precisely to a builder?

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From our anonymous insider…

We gathered at a Sunday barbecue before our first day of the second year. We won’t expect to see too much of Awkward Allen because he married a business consultant who works two hours away and moved in with his wife. Although several students toiled away in our research labs over the break, most people took at least a short vacation. The young father whose wife is in law school jetted off to Europe: “our first vacation since the baby was born eight months ago.” Baby was parked with the grandparents for two weeks. Two classmates coincidentally were both on separate vacations with parents and siblings to Peru. They took different approaches to anthropology. One camped in the mountains among the Inca ruins. The other reported, “the alcohol is so cheap there. Our family’s whole tab for a week was seventy bucks!”

We’re nervous about this block, covering clinical microbiology (everything that can cause an infection: bacteria, viruses, fungi, parasites, autoimmune disorders). All of last year’s blocks were centered around a single physiology textbook. We’ll be using a diversity of materials, many self-selected, for microbiology. About a fourth of students started researching textbooks and studying during the break. The general consensus of upperclassmen, based on the class Facebook and Group-Me chat, is to use Sketchy Micro. These are a video series of narrated progressive illustrations. For example, they will draw a cat for bacteria that are catalase-positive, or draw a van for bacteria that the recommended antibiotic treatment is vancomycin. In our new small-groups, some students close their eyes to imagine the illustration. It seems odd, but it works for them. So far I’m just using a textbook: Medical Microbiology by Murray.

Reflecting modern education’s prioritization of bureaucracy over academics, M2 opened with an hour-long orientation led by two deans, experts on paperwork for the LCME. This year will be clinically-focused in comparison to last year’s emphasis on basic science. This will prepare us for the rotations of M3 and M4, our “clerkship years.” We need to be able to conduct a full history and targeted physical exam, then present this to our attending or resident with our differential diagnoses. Most lectures will be conducted by practicing clinicians, instead of PhDs, requiring scheduling flexibility on our part.

Our first lecture began on Monday at 9:00 am, right after the orientation. An Emergency Medicine physician in his mid-thirties specializing in the management of sepsis kicked off what promises to be a jam-packed two weeks of bacteriology. Our textbooks give the illusion that the moment you send a sample (e.g., blood, stool, urine, or sputum) off to the “Lab”, the identity of the bacteria is immediately ascertained. “When I have a potential septic patient in the ED, I do not have two days to wait to grow a culture. Instead, I will get back a few key findings in maybe two hours before the full report. The prelim report will give me Gram-staining. If the identified bacteria is Gram-positive they will also run a quick catalase enzyme activity.” I was excited to check the Google Calendar and see that he is returning for two more lecture this week. My female classmates were also excited, characterizing our lecturer as “dreamy.”

Afterwards, a 45-year-old lab technician from Quest Diagnostics came in with three boxes of samples to lead a workshop. He explained how he runs 10 of the tests that we might order. He opened with a colony of methicillin-resistant staphylococcus aureus (MRSA), the bacteria that causes pneumonia, sepsis, endocarditis, and skin infections, and ran a quick catalase test. The petri dish had small transparencies in the agar gel demonstrating MRSA’s ability to lyse red blood cells. He took a swab, swiped a colony on the petri dish and put some hydrogen peroxide on the swab. We saw it start bubbling up. “Now you know it is MRSA, and not Strep.” He showed us two McConkey growth plates where a colony of pink lactose-fermenting, harmless E Coli contrasted with a dull-yellow strain of Salmonellae. Students afterwards commented, “He knew a lot, and this was a perfect complement to the theory, but I wish he would stop waving that swab around. I don’t want to catch MRSA!”

Lectures afterwards delved into the main categories of bacteria defined by the Gram stain. Gram-positive bacteria have a thick outer peptidoglycan (sugars cross-linked with short peptide bridges) cell wall outside its cell membrane; Gram-negative bacteria have an additional outer lipid membrane covering its thinner cell wall. This key difference, specifically the presence or absence of a second cell membrane, will affect the virulence (ability to cause disease) and susceptibility to various antibiotics.

We learned that there is a fine line between hosting normal bacterial flora and being on the verge of death from infection. For example, Streptococcus pneumoniae, the most common cause of bacterial pneumonia, is a normal component of the oropharynx and throat. Pneumonia ensues when oropharynx secretions are aspirated (entry into larynx and respiratory tract) and the protective mucous lining of the upper respiratory tract is diminished by IgA protease secretion. The “flesh-eating” bacteria, Streptococcus pyogenes is also the culprit of the common strep throat in children. S. pyogenes produces many virulent proteins that enable its spread but induce a strong immune response. M-protein on its cell wall prevent phagocytosis, but elicits a strong antibody response. Sometimes, S. pyogenes release streptolysins and pyrogenic exotoxins that lead to Scarlet Fever or potentially Toxic Shock Syndrome from systemic activation of the immune system. The surge of antibodies produced during a S. pyogenes infection can lead to Rheumatic Fever (involving heart inflammation) and Post-Strep Glomeuruloar Nephritis (inflmmation of kidney from small immune deposits). According to the American Academy of Family Physicians, “Although antibiotics have been shown to reduce the severity of acute symptoms and shorten the duration of the illness by about one day, more than 90 percent of treated and untreated patients with acute pharyngitis are symptom-free by day 7. Therefore, the primary reason for treating uncomplicated streptococcal pharyngitis is to markedly reduce the incidence of subsequent rheumatic fever” and other serious complications. Many people, especially if they work in healthcare, host Staphylococcus aureus in peaceful colonies on their skin. A small cut or abrasion in the skin can let Staph in where it will usually cause a benign skin infection, but sometimes can lead to release of Staphylococcal Toxic Shock Syndrome Toxin. This toxin, called a superantigen because it can lead to activation of twenty percent of T-cells, endothelial cell dysfunction, and shock. If the strain is methicillin-resistant (MRSA), treatment is vancomycin to kill the bacteria, and fluids, vasopressors, and blood transfusions to address the life-threatening symptoms of shock.

Our best defense against harmful bacteria seems to be other bacteria. Our body realized that we cannot beat them, so instead our immune system attempts to supervise the ecosystem. Numerous surfaces – skin, oral cavity, gut, urogenital canal – are colonized with competing bacteria that prevent any single one from domination (most antibiotics are copies of compounds secreted by one bacteria to inhibit the growth of another). Some of the worst infections occur when the entire ecosystem is wiped out after administration of a broad-spectrum antibiotic. Babies are vulnerable due to immature flora and immune systems, which is why women in the 35th week of pregnancy are screened for vaginal colonization of Streptococcal agalactiae (group B strep). If the baby picks up S. agalactiae during delivery, it could lead to bacteremia (bacteria in the blood), pneumonia, and meningitis.

The EM physician emphasized that the physiological response to an infection is not necessarily indicative of the degree of colonization. “Infection is just one component of septic shock.” Septic shock occurs from the immune system’s overreaction to an unwelcome guest. In fact, gastroenteritis can even be caused without eating a food infected with staphylococcus. If staphylococcus had ever been colonized in the food, it could deposit toxins that are resistant to heat and cold. “The bacteria could be long gone from a contained piece of food and cause severe gastroenteritis even if nothing is colonizing the gut. Simply the immune system reaction is enough.” Antibiotics do not help against toxins.

Our patient case: Ellie, a 30-year-old female, was vacationing with a group in the Caribbean a year earlier. Ten group members got diarrhea after eating ice cream. After three days of symptoms, she and her husband went to a clinic where they waited briefly until the doctor showed up on a moped. The doctor explained that they didn’t normally give meds for these symptoms, but the husband insisted and Ellie received a single dose of an unknown antibiotic. Her GI symptoms improved after three days, but four days later she developed general malaise, 102-degree fever, myalgia (muscle pain), petechiae (small diffuse red specks on the skin) and hemoptysis (coughing up blood). Ellie made it home, but these symptoms persisted for two weeks. Her primary care doctor referred her to an infectious disease (ID) specialist for further evaluation.

The ID physician, who did his residency in Ghana seeing nasty infections every day, explained, “This case really perplexed me. It was not a typical presentation nor clinical course.” She was put on a seven-day course of levofloxacin for suspected Typhoid fever. A blood culture came back normal, but her stool sample revealed a non-typhoid fever strain of salmonella, a bacteria that infects the gut immune system. Typhoid-causing salmonella is distinguished by a short DNA piece. This gene island allows the bacteria to hitch a ride with macrophages to infect organs beyond the gut. Despite the antibiotic treatment covering salmonella, her symptoms did not improve. “I was convinced I had dengue fever. There was a CDC warning about it,” explained Ellie. This fear was compounded because the ID doctor was uncertain about his diagnosis. “It can take up to a week after this treatment for symptoms to get better. Throughout the whole experience I was not sure her constitutional symptoms were due to the salmonella infection. Typically a non-typhoidal strain would be constrained to gastroenteritis which according to HPI [history of present illness] resolved quickly.” On day seven, when he was going to re-evaluate her diagnosis and start her on another antibiotic treatment, her fever resolved. The ID physician hypothesized that the initial antibiotic dose may have caused Ellie’s more serious problems by disrupting her ordinary bacterial flora.

The most surprising aspect of the case was that Ellie told us that she’d just returned from the same Caribbean island: “I did not go to the same ice-cream shop.”

Statistics for the week… Study: 10 hours. Sleep: 8 hours/night; Fun: 2 days. Example fun: Jane and I joined Lanky Luke and his PA wife Sarcastic Samantha for a late afternoon beach-music concert followed by burgers at their pristine apartment. Samantha, in her final rotations at PA school, recently returned from her eight-week ED rotation in two nearby counties. “What shocked me about my ER rotation was that the docs are paid per patient and PAs are salaried. To maximize profit, all time-consuming procedures (e.g., central lines) are done by PAs. The result is that doctors tend to see the green triage patients [the least serious cases] while the PA is working with the yellow triage group. It just didn’t make sense.”

More: http://fifthchance.com/MedicalSchool2020

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Before starting the publication of Medical School 2020, Year 2 entries, here are some Year 1 wrap-up thoughts from our anonymous insider:

Nearly every answer in medical school spurred another question until finally the answer wasn’t known or wasn’t answerable in the limited time for each subject. I eventually got used to the frustration that the system at-hand was too complex for a simple generalization. The every-two-month exam cycle gives students a sprint mentality, but I came to realize that it was okay to not know everything. Medical school is a marathon, not a sprint.

One year done and I’m more excited about working in healthcare, but disillusioned about the trajectory of American health. Diabetes, drug abuse, premature heart disease, psychosis. These are not typically driven by genetics, but rather symptoms of the society that we’ve built. Americans expect the healthcare system to clean up the mess, but seldom are doctors able to provide a complete cure for these ills of modern society.

I have also become disillusioned about our ability to formulate health care policy. We learned about ongoing clinical trials that pay diabetics to exercise and eat better, similar to the classic “A behavioral approach to achieving initial cocaine abstinence” (Higgins, et al. Am J Psychiatry, 1991), in which patients were given $1,000 to stay clean for 12 weeks rather than being put into rehab ($1,000 per day?). This could be much cheaper than Medicaid and Medicare paying to treat the inevitable complications. Politicians make beautiful speeches taking credit for providing insurance to millions of Americans, but where are these people who have purportedly been helped? Some of the hardest working people I met in the clinic made too much to qualify for Medicaid, but not enough to afford an Obamacare policy. They eventually have to stop work and show up in clinic with a far worse prognosis, e.g., half a foot that needs to be amputated, and the bill is paid by Medicaid or absorbed by the hospital’s charity care fund.

At least in our university-run, mostly Medicaid/Medicare-funded, health care system, I didn’t see obvious examples of what Jack Wennberg, the founder of clinical evaluative sciences, called “supplier-induced demand.” However, my attendings would nearly always refer patients to specialists out of fear of “missing something,” and every stubbed toe got an X-ray. Perhaps Wennberg’s estimate that 30 percent of healthcare expenditures are unnecessary or harmful is correct, but it wasn’t obvious which 30 percent we should have cut.

As a child I associated healthcare with doctors and nurses. One trip to the most popular restaurant across from the hospital campus and Jane and I realized that it was really more about administrators, lawyers, IT, and Human Resources staffers. I’m no longer surprised to see a hospital employee badge reading “business development officer” pinned to a business suit.

Classmates often wonder “Why does medical school cost so much?” Our conclusion is that the enemy may be us. Administrators and deans have proliferated along with LCME requirements in the name of creating an fair and equitable learning environment. Is it helpful to have lectures recorded? Yes, but it requires a huge IT department and expensive software. Our gym was just upgraded, which seems to have been a marketing decision because most classmates didn’t know that we had an in-school gym within the school in addition to the membership at a comprehensive fitness center (with pool!) that is covered by our tuition. The Wellness Committee and the Office of Inclusion and Diversity, led by a Ph.D. psychologist, seem to have unlimited funding to hold seminars on self-defense and microaggressions (I try never to miss one due to the great catering from local restaurants); funding for student-organized events on medical topics, such as a suture workshop, is limited to $2.50 per attendee and can be challenging to obtain. Waste is noted, but seldom criticized, due to the free-flowing Federal spigot of student loan funds.

I conducted an informal survey of classmates towards the end of the year. Some of their responses are below.

What has surprised you?

“The amount of independence. You hear about all these learning environment resources, different subjects, supplemental materials for purchase like Anki and Firecracker. It is pretty overwhelming at first. I eventually realized that if I just study the exact the same way [as in undergraduate courses] then I do well. It is just school.” [Jane]

“That I could actually be interested in surgery.” [Disinterested Dorothy, originally planning to follow her father into internal medicine]

“People like talking about their health problems.” [He obviously hadn’t met my grandfather!]

Is it more or less studying than you expected?

“Less overall but exam week is brutal. It’s the way it is, not the way it should be. I regret not being as organized and dedicated as some students. I would study more spread out instead of cramming before.” [Jane]

What did you wish you knew about healthcare that you know now?

“I always thought doctors were unquestionable. Doctors are human. Ask them questions. If they are not explaining the reason, they are not doing their job right. I now know there are good doctors and bad doctors.” [let’s hope that she doesn’t practice these sorting skills at home; she’s the daughter of a physician]

“Healthcare is challenging but it is more accessible than people would think. I approach healthcare as a field in which if you work hard enough or study long enough you can succeed. Compare this to, for example, computer programming or engineering. No matter how hard I worked at that, I just could not do it.” [she majored in biology as an undergrad]

What do you like about the class and what do you not like about the class?

“I like how our class is fun and likes to hang out with each other. We have a good sense of humor. What do I not like? Our class will complain about anything. They can also be quite disrespectful.” [Jane]

Do you wish you took time off before medical school. Gap year or no?

“No stigma either way. Straight in or five years out doesn’t matter. Once you are here, you are here.” [Youngest classmate]

“It took me three application cycles to get into a school.” [Straight-Shooter Sally]

“I am glad I took a gap year. I don’t think I was intellectually mature enough to go straight through. I think I would have fooled around with all the free time in medical school if I didn’t learn some discipline working in the real world.” [Male classmate who worked for pharmaceutical company]

“I am glad I am here, but certain specialities are off the table for me. I’m too old!” [Upperclassman who started medical school at 35]

What do you think about our teachers?

“Passion is infectious. When someone is passionate you can’t help but listen to them. M.D.s are more fun than Ph.D.s. Teachers talk about what they know. They know their patients. That’s why we are here.” [undergraduate physicist major known as the class gunner]

“About a third of the instructors are great. I give an instructor one chance. If I don’t like them, I no longer show up for lecture.” [Classmate notoriously late for the few lectures he does attend. If the class gives him the heads up it was worthwhile, he might watch the recorded lecture online.]

What do you think about anatomy?

“I liked MSK (musculocutaneous) dissections. It was satisfying using your hands to isolate muscle and fascia layers. Reproductive was pretty cool too. I literally cut a penis in half and took the fascia layers apart. Not many people can say that! Oh, and that bone saw was sick!” [Disinterested Dorothy]

“I hate anatomy. You cannot see anything in a cadaver. So excited to be done with it.” [Pinterest Penelope apparently has better things to do]

“Anatomy is the best part of medical school. It is the unique topic for medical school. All the other material a lot of us have have been to exposed to in various undergraduate majors. No one gets exposed to anatomy, at least at this level.”

Anatomy Advice for M1?

“Get in there to get over. Thinking about it is bigger issue. I never had issue. Doesn’t feel real because the cadavers are cold.”

“It is pretty rare to have surgeons take time out of their day to spend two hours helping you dissect. Take advantage of it. You get out what you put in. Be interested in what you are doing. It looks bad when half the class leaves early from lab.” [Jane]

“Buy a pair of scrubs. You look badass and that way you won’t get your normal clothes smelling like the lab.” [Class Orthopod]

What are you excited about?

“Being a doctor allows you to make a decent living wherever you want to live. You don’t have to live in a big city where all the jobs are for young people.” [Classmate from Kansas]

“All my friends and family ask me about their health problems. It is fun to play doctor. We can now understand what is wrong with them. Ask us what to do about it? We are no better than the internet. Patient care comes from experience, not from education. I’m excited to eventually be able to answer their questions with action.”

What is something you would change?

“Administration treats us as kids, not adults. There is a resource for everything.” [Classmate who juggles a newborn and toddler with medical school studies]

“The cost of tuition. The founding of for-profit medical schools tells you all you need to know.” [Classmate with PA-student wife]

“Just tell me what is going to be on Step I. I do not have time nor the brain space for anything else.” [Type-A Anita…]

“Residency match. If you want to do a speciality, it has become so competitive. The Match is in a death spiral.” [Class Orthopod]

---

Following the curriculum isn’t enough if you want to be a good doctor. Friends at other schools, a few classmates, and a physician mentor agree that the focus of medical school is ensuring that the lowest denominator passes, not challenging each student to reach his or her highest potential. The resources are there for anyone who wants to take the initiative, but peer pressure works in the opposite direction. The most vocal students echo each other’s complaints that the curriculum isn’t sufficiently test-focused.

First year for most students serves a reminder that not all of us are special. Most medical students were near the top of their undergraduate class, but that was partly because their fear of failure (failure = less than an A) was so great they didn’t take challenging courses. Classmates’ first reaction to getting a question wrong may be to assert that the question was unfair, poorly worded, or that the answer was not worth cramming into our already crammed brains. We expect to be the discoverer of a new drug or the manager of a big project. One of my bosses during my gap year said, “What we really need are great employees. Leadership comes afterwards.” The more that I shed the entitlement mentality, the more I was able to focus on my strengths.

One thing that I learned is that medical students don’t relax until a few months prior to graduation. Classmates traded their fear of not getting into their first-choice medical school for three years of anxiety of not doing well enough on Step I (end of second year) and in rotations (third year) to get into their first-choice residency. One of our clerkship directors sent us an article about the surgery residency match process: “This leaves the 163 orthopedic residencies that participate in the Match in the unenviable position of having to sort through 88,169 applications for 717 total positions from just over 1,000 total applicants.” (Scott E. Porter, JAAOS, 2017) I.e., a typical applicant applied to 88 programs, more than half of the total programs nationwide.

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One of my neighbors (no longer a Millionaire for Obama; now a Millionaire Against Trump) posted the following on Facebook:

Thanks for your service and your leadership Senator McCain.

One of his female friends responded with

Amen. Always a hero, again and again and again!

Another friend, whose profile picture shows an overweight woman past middle age:

Thank God he has a heart.

Another older woman:

He’s a good man

I think that they’re all excited because McCain opposed an ostensible Obamacare repeal (I don’t bother to read the details on these anymore since the last “repeal” that I looked at was almost exactly the same as Obamacare).

It doesn’t surprise me that Massachusetts Democrats like this particular position that McCain has taken. But the unqualified love for McCain from these middle-aged-and-older women baffles me. Why would these women celebrate a guy who divorced his crippled-by-a-car-accident wife to marry a rich woman 18 years his junior?

(McCain sued his wife in 1980, which made him a relatively early adopter of the no-fault divorce law in Arizona (1973). The rich young intended protected herself from a potential second lawsuit by McCain with a prenuptial agreement (NPR) and continued residence in a jurisdiction where prenups will be enforced (see Arizona family law).)

Related:

• “The wife U.S. Republican John McCain callously left behind” (Daily Mail 2008)

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I just finished a couple of interesting books on Amazon Kindle Unlimited:

• D DAY Through German Eyes – The Hidden Story of June 6th 1944
• D DAY Through German Eyes – Book 2

These books are transcripts of interviews conducted 10 years after D-Day. One question that they answer is “Why were German soldiers fighting?” If they saw the war in the same way that we did, for example, why not simply surrender and walk over to the side with both Might and Right?

Here’s one example:

Helmut Voigt was a Grenadier (Rifleman) with the 716th Static Infantry Division, based in the Saint Aubin area, inland of Juno Beach.

My father, being in the banking profession, had affected my thinking about the war completely. My father was very sympathetic to the National Socialist (Nazi Party) view of the world. In this view, a United Europe was trying to assert its independence and its very right to exist, against certain powerful international forces. America and the English were in an unholy alliance with the Bolsheviks, and it was these Russians who were orchestrating world events from Moscow. Moscow –that word! During the war, so many bad things were explained by saying that ‘Moscow arranged it’ or ‘Moscow has done this to us.’ Even when the Americans and the English bombed our cities, when they began destroying whole towns, the newspapers would often say this was done ‘at the command of Moscow.’

Russia actually was responsible for the German defense strategy, according to one interviewee:

Gert Hoffmann was a Festungswerkmeister (Fortification Development Officer) attached to the 352nd Artillery Regiment, 352nd Infantry Division, in the sector of Carentan on the Southern Cotentin peninsula, inland from the American Omaha beach.

I must first clarify that the phrase ‘Atlantic Wall’ is itself rather misleading. There certainly was a ‘wall’ along the North East coast of France, around the Pas de Calais, where there were enormous concrete bunkers and gun emplacements, … But the further West you went, the less substantial the fortifications became, because the Western area, including Normandy and Brittany, was not originally considered a likely site for an invasion. Up until the autumn of 1943, the Normandy defences were quite simple, being mostly small bunkers, minefields, anti-tank barricades and so on, with a few larger concrete emplacements. Many of the smaller bunkers were actually civilian stone barns or houses, which had been reinforced and fortified, not at all like those massive concrete blockhouses of the Pas de Calais zone. It was when General Rommel was put in charge of the Atlantic Wall that the Normandy area began to be more heavily reinforced with more barricades, anti-tank ditches, much bigger bunker structures and so on. But this process was not finished when the invasion came, which was very fortunate for the Allies. We had many other plans for the Normandy coast which were only just coming to fruition.

I was a Fortress Officer of the Divisional artillery. Our role was vitally important, although today it is largely forgotten. We humble Wehrmacht engineers and builders have been eclipsed by the panzer men and the infantry and all the rest.

My role was in the creation of zones of fire on a large scale. This meant that we found ways of altering the landscape of the battlefield, using mounds, ditches and other means, in order to influence the way that an enemy attack, especially an armoured attack, would progress inland. We have to be honest today and say that the function of the coastal defences, I mean the emplacements on the shoreline itself, on the sea wall, was only to slow down an attack and give time for the alert to be sounded and a counterattack to be implemented. Of course, the infantry men inside those sea wall emplacements didn’t know this! On the contrary, they were told repeatedly that their mission was to drive the enemy back into the sea, to prevent them moving off the beaches, that not one enemy boot must step past the shore line, and so on. But this was purely to motivate them. We could hardly tell those boys on the sand, ‘You’re only there to slow the Allies down.’ It was expected that, at least in the first few hours, a determined Allied attack using armour would progress inland. In fact, it would be better if it did progress some small distance: this would bring large volumes of troops and armour into a prepared zone where they could be surrounded and ground down. This would destroy the enemy’s capability and also, very importantly, deter future attacks.

this was a bitter lesson which we learned in several places, but above all at the battle of Kursk in Russia in 1943. You may know the story of Kursk? Well, at Kursk we made the dreadful mistake of allowing the Soviets enough time to prepare a defence in depth against our panzer formations. Those Russian engineers took over a zone of ten thousand square kilometres, and they built a huge series of traps for our armour, with endless ditches, forts, traps, minefields and so on. None of these defences was insurmountable by itself, and over several days they were finally overcome, but the cumulative effect was to bog down our panzers, and turn them from a thrusting attack force into a slow or static target. The Russians showed us how to defeat an armoured attack properly! Not with a single line of fortifications, as the French tried to do with their absurd Maginot Line in 1940, but by taking a whole geographic zone and making it into a swamp for panzer forces, a swamp for men and vehicles. Making the entire landscape into a swamp for the invaders. That was what we planned to do in Normandy, in the absence of a true shoreline ‘Atlantic Wall.’

an example would be the landscape we created around the base of the Cotentin Peninsula. There, we opened the canal sluices and we flooded a wide area of fields to a depth of two metres, which panzers cannot cope with. Then, we placed a series of incendiary barges along one side; these were river craft fitted with burning material which would explode as the enemy approached, deterring them from trying to ford the water. We created a lane around one side which could be used to cross the floods, defended lightly so that the enemy would think they were fighting their way through. As the enemy came out of this, they would be faced with an anti-tank ramp system camouflaged by nets, which would hold up their panzers as they broke through. Onto this zone, we had Nebelwerfer (rocket mortar) batteries calibrated to fire on the stranded vehicles. Any panzers that finally crossed the ramps would become caught up in a system of bunkers armed with PAK guns, firing down a slope. And so on, and so on. The enemy would find himself with a long, thinly spread spearhead of armour which grew less powerful with each phase, very vulnerable to being isolated and ground down. This was all very closely based on what the Russians had done to us at Kursk.

Related:

• “Fake Russian Facebook Accounts Bought $100,000 in Political Ads” (nytimes on how Russians spent enough to reach one third of Americans for 0.6 seconds via a Super Bowl ad)

More: Read

• D DAY Through German Eyes – The Hidden Story of June 6th 1944
• D DAY Through German Eyes – Book 2

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The Pilatus PC-12 has a single engine and therefore in theory it is worth practicing what to do when the engine quits. Harrison Ford’s landing on a golf course shortly after taking off from Santa Monica is a good example of the value of proficiency. In practice, though, the PC-12’s engine is extremely unlikely to quit. This is a PT-6A turboprop (jet engine that spins a propeller), which is statistically far more reliable than piston engines or human pilots.

This investigation into the crash of an Air Force PC-12 shows that the training cure can be worse than the engine failure disease. Two Air Force pilots, presumably both more proficient than the average civilian pilot, wrecked a perfectly functional PC-12 while practicing getting back to the runway in the event of an engine failure shortly after takeoff. This is confusing because the PC-12 has a stick pusher to prevent pilots from aerodynamically stalling the plane. It is sad because FlightSafety has built Level D simulators in which this maneuver can be practiced without risk to any body part other than ego.

Fellow instructors and pilots: What do we take away from this?

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