This one's for you, Teags

This is at the Subway by Sonic in Rexburg. We stopped by to grab a bite to eat, and noticed that they charge for water. 27 cents. Not 25, not 30. 27.

Conference Weekend!

Some of my favourite thoughts from conference this weekend...

Righteousness is measured not by our temptations, but by our resistance to them (Robert D. Hales)

Reverence invites revelation (Margaret S. Lifferth)

The sacrament meeting begins with the prelude music, not the opening prayer (Margaret S. Lifferth)

Don’t underestimate the power and influence that the youth in the church can have (Michael A. Nieder)

This is a great time to be alive (Allan F. Packer)

We can build again (D. Todd Christofferson)

We need to take care of each other (D. Todd Christofferson)

We cannot expect life to always be perfect (Henry B. Eyring)

Life is not meant to be fair or equal (Henry B. Eyring)

Things will work out (Henry B. Eyring)

Tragedy does not have to erode faith – it can strengthen it (Henry B. Eyring)

We need to learn to recognize and help those in need, even when we may need it more than they (Henry B. Eyring)

Our lives are examples to others (Quentin L. Cook)

Our prayers can be enhanced with the use of music, and fasting (Russell M. Nelson)

The road to eternal life is not a sprint, but a path of endurance (Dieter F. Uchtdorf)

Spiritual growth requires participation, not spectatorship (Dieter F. Uchtdorf)

Change is an essential part of life’s experience. (Steven E. Snow)

Be cheerful and optimistic (Steven E. Snow)

Learn to laugh – it will enrich your life, as well as the lives of those around you (Steven E. Snow)

The time is far spent (Barbara Thompson)

We need to take every opportunity to strengthen our families (Barbara Thompson)

Because Jesus walked His path alone, we do not have to walk ours alone (Jeffrey R. Holland)

Part of mortality is to be tried, but another part of it is to have joy (President Monson)

The future is as bright as your faith (President Monson)

Forget yourself and go to work (Dallin H. Oaks)

We cannot do great things, we can only do small things with great love (Mother Theresa, quoted by Dallin H. Oaks)

Turn your homes toward the temple (Gary E. Stevenson)

Everything that leads us to do good is from God (José A. Teixeira)

May your homes be filled with harmony and love (Thomas S. Monson)

Blackberry Dump Cake

I made a very tasty cake this weekend, and I thought I'd share the recipe... and the story...

I got the recipe from Mrs. Oliver in Nachitoches (NACK-uh-tish), Louisiana, when we were there on tour. Grace and I stayed at the Oliver's home one night for homestay. Mr. and Mrs. Oliver, both in their eighties, were not members of the church, but had been meeting with the missionaries for a little while, and agreed to let us stay in their home. Mr. Oliver reminded me a bit of Dad, because as soon as we were settled in their home, he offered us a drink. Of beer. When we declined, he said (with a bit of a twinkle in his eye), "Oh, coffee, then?". He was hilarious. They were both so wonderful and kind.

Nachitoches! It was so beautiful and green, though it was just mid-April.

The chapel in Nachitoches, where we had a musical fireside.

Mrs. Oliver had made some cake for us, and it was so delicious, I had to ask for the recipe. She seemed surprised that I had never heard of dump cake before, so maybe it's a Southern thing. Many tasty foods are....

Breakfast at the Oliver's - biscuits, butter, molasses, sausage, and whole milk.

It's called "Dump Cake" because you really just dump all the ingredients into the pan - no mixing required! I didn't get a picture of the one I made because we ate it before I thought of my camera... which tells you how good it was! :)

2 1/2 cups of crushed pineapple (not drained)
3 cups fresh of frozen blueberries (I used blackberries because that's what I had in my freezer)
3/4 cup of sugar (we decided that this ingredient is probably not necessary... :) )
1 cake mix (yellow cake)
1/2 cup butter, melted
1 cup pecans (I used a mix of walnuts and almonds because, again, that's what I had)

Preheat oven to 350 F. In a buttered 9x13 pan, layer the pineapple, berries, and sugar. Add the powedered cake mix on top, and drizzle the melted butter on top of that. Sprinkle nuts over the top, and bake for about 45 minutes.

It's so good, and really easy. The only thing that I might change is that some of the cake mix didn't get "wet" with either butter or berry juice, so there were some dry spots. So next time I think I'll try mixing the ingredients a little in the pan, though that might disrupt the awesome cake layer that forms on top. We'll see... :)

Mr. and Mrs. Oliver (yes, I have forgotten their first names... sorry!)

Because I know your weekend won't be complete without it...

Here is the study guide from my most recent medical microbiology exam. And yes, it's 12 pages long. :)

Chapter 19 - Mechanisms of Bacterial Pathogenesis

1. Define each of the following terms: pathology, etiology, etiological agent, pathogenesis, colonization, disease, infection, pathogen, pathogenic, bacteremia, septicemia, toxemia, viremia, and reservoir.
Pathology – study of disease
Etiology – the cause of the disease (eg. The organism)
Colonization – bacteria growing in the body
Disease – change from a state of health
Infection – colonization with a pathogenic bacterium
Pathogen – disease-causing agent
Pathogenic – adj. for pathogen
Bacteremia – bacteria in the blood
Septicemia – bacteria growing in the blood
Toxemia – toxins in the blood
Viremia – viruses in the blood
Reservoir – where the pathogen “hangs out” naturally.

2. What is normal flora? Explain how normal flora could be categorized as: mutualistic, commensal, or opportunistic. What is a parasite?
Normal flora is the colonization of bacteria in out body that is normal and not harmful. They contribute to microbial antagonism, and may synthesize nutrients such as vitamins that help us.
Mutualistic – both benefit
Commensal – one benefits
Opportunistic – NF takes advantage of suppressed immune system to cause infection in an unusual location
Parasite – one benefits, other is harmed

3. What is the germ theory of disease? What are Koch’s Postulates? What are they used for?
Germ theory – germs cause disease. One germ, one disease.
Koch – to prove which microorganism is the causative agent of the disease
Isolate sample from infected individual
Culture
Infect new individual
When signs and symptoms develop that are the same as the first infected individual, the organism is the same, and can be concluded to be the causative agent.

4. Describe how each of the following is used to describe a disease (and explain what the term means): communicable, contagious, noncommunicable, endemic, epidemic, pandemic, acute, chronic, and latent.
Communicable – can spread from person to person (HIV)
Contagious – spreads easily from person to person (rhinovirus)
Non-communicable – cannot be spread from person to person (tetanus)
Endemic – at a consistent rate of infection
Epidemic – spike of infection rate in a given area
Pandemic – disease is worldwide
Acute – rapid onset, severe, then finishes
Chronic – slow onset, prolonged illness
Latent – person is a carrier, but shows no symptoms. Can flare up (varicella)

5. What is the difference between a local infection and a systemic infection?
Local – confined to one area
Systemic – whole body

6. What is the difference between a primary infection and a secondary infection? What is a subclinical infection?
1ary – first infection
2ary – infection after the 1ary, more susceptible to it bc of weakened immune system
Subclinical – no symptoms

7. Describe the following mechanisms of disease transmission: contact transmission (direct, indirect, and droplet), vehicle transmission, and vector transmission.
Contact:
Direct – person-to-person
Indirect – through an inanimate object
Droplet – cough, sneeze
Vehicle – food and water
Vector – insect bite

8. What is a fomite? What is a nosocomial infection?
Fomite – for indirect transmission
Nosocomial – acquired in a healthcare setting

9. What is epidemiology?
Study of frequency and distribution of disease.

10. What is the Center for Disease Control and Prevention (CDC)? What types of things does this agency do?
National Epidemiology Center (USA). Tracks infectious diseases, helps local health agencies during outbreaks. Publishes monthly reports.

11. Describe the sequence of events successful pathogens carry out.
Transmission to host, entry into tissue, adherence to target tissue, invasion/evasion, host damage, exit, transmission.

12. What are portals of entry? What are the possible portals of entry for pathogens?
PofE are where the pathogen gains entry to the host. Usually: mucous membranes (GI, GU, respiratory), parenteral, skin.

13. What are virulence factors? How does each of the following function as a virulence factor: adhesions, fimbriae, biofilms, capsule, cell walls of mycobacteria, toxins, and enzymes?
Adhesins – help bacteria stick to host tissue. Fimbriae and pili.
Fimbrie – “ “
Biofilms – glue to surfaces
Capsule – evade phagocytosis, poorly antigenic
Mycolic acid – evade phagocytosis
Toxins – host damage, direct (exo) and indirect (endo)
Enzymes – kinase, coagulase, hyaluronidase, collagenase, IgA protease.

14. Give the function of each of the following enzymes and explain how they can aid pathogens in causing disease: hemolysins (both α and β hemolysins), leukocidins, streptokinase, staphylokinase, coagulase, collagenase, proteases, hyaluronidase, and phospholipase C.
Hemolysins – lyse RBCs
α – complete lysis
β – partial lysis
Leukocidins – lyse WBCs
Strepto/staphylokinase – break down blood clots, gain entry
Coagulase – formation of blood clots, wall off from WBCs
Collagenase – break collagen, get deeper into tissues
Protease – break down specific proteins, eg. IgA protease.
Hyaluronidase – break down hyaluronic acid, get deeper into tissues
Phospholipase C – hydrolyses lecithin (in tissues)

15. What are exotoxins? List the examples of the following types of exotoxins discussed in class and explain how they affect the host: cytotoxins, enterotoxins, and neurotoxins.
Exotoxins – released by the cell. Usually G(+), but can be G(-).
Cytotoxins – damage cells
Erythrotoxins – damage to capillary cells, cause blood to leak out (S. pyogenes)
Enterotoxins – damage to GI -> diarrhea, vomiting, etc. (Cholera, S. food poisoning, bacterial dystentery)
Neurotoxins – inhibit normal NT flow (Tetanus, Botulinum)

16. What is endotoxin? How does it affect humans?
Made by G(-) cells, is the LPS in the outer membrane. Once ingested by phagocytes, LPS is relased, stimulating cell to release cytokine IL-1, which reaches hypothalamus. Resets the “thermostat”, h-thal. Releases prostaglandins to initiate the fever response (vasodilation, vasopermeability, high temp.). Can lead to shock due to decrease in BP from vasodilation.

17. How do the following help bacteria evade the immune system: antigenic variation and inactivation of antibodies or complement?
AV – evade immune system’s antibodies
Inactivation – cascade/signaling system is disrupted

18. What are cross-reactive antibodies? How are they involved in damage to host cells?
Antibodies produced in response to an antigen, that undergo slight variation in the final differentiation process, that are similar enough to our own proteins to elicit an inflammatory response against our own tissues. Strep throat -> rheumatic fever, glomerulonephritis. Heart valves & strep. Antibiotics are prescribed with Strep. Infections not to help clear up the infection (which will subside in a few days), but to prevent the formation of antibodies that could attack our own cells.

19. What are superantigens? How are they involved in damage to host cells?
Antigens that are repeating polysaccharide units, stimulate non-T-cell-specific activation of the immune system, large cytokine release -> shock. Can get out of hand quickly, lead to death. Toxic shock syndrome (S. aureus).

Chapter 20 - Antibacterial Agents

1. Briefly describe the history of the antibacterial agents Protosil (sulfanilamide) and penicillin.
Protosil (sulfas) – 1935, used first in mice to treat systemic strep. Protosil is cleaved in the body to produce sulfanilamide, the active agent.
Penicillin – Alexander Fleming – Penicillium mold prevented bacterial growth on a plate.

2. Are all antibacterial agents antibiotics? Why or why not?
No – antibiotics are, by definition, made by other microorganisms. Some antibacterial agents, like the sulfa drugs, are made in the lab.

3. Describe the property of selective toxicity. Why is this an important property of antibacterial agents?
Selective toxicity means that the drug is selectively harmful toward the pathogen, and not our own cells. This is important because we want to maximize damage to pathogens while minimizing damage to our cells.

4. What is the difference between broad-spectrum and narrow-spectrum drugs? Under what conditions would each type of drug be used?
Broad – affects all, used when ID in unknown
Narrow – affects some, used when ID known, to protect NF

5. List the various targets of antimicrobial drugs and give which types of drugs have each type of target. (Those listed in Figure 20-1 and those discussed in class).
Cell wall synthesis
Penicillins
Cephalosporins
Beta-lactams
Isoniazid
Ethambutol
Cycloserine
Ethionamide
Bacitracin
Polymixin
Protein Synthesis
30S:
Aminoglycosides
Tetracyclines
50S:
Chloramphenicol
Macrolides
Clindamycin
Linezolid
Quinupristindalfopristin
DNA replication
Quinolones
Metronidazole
Clofazimine
RNA synthesis
Rifampin
Rifabutin
Antimetabolites
Sulfanamides
Dapsone
Trimethoprim
Para-aminosalycylic acid

6. What are Beta-lactams? What do they do to kill bacterial cells?
Β-lactams are rings in the structure of antibiotics in the penicillin and cephalosporin families. They inactivate bacterial enzymes used in the synthesis of peptidoglycan. Without p-glycan, the cells cannot replicate.

7. What would be a problem with drugs used to fight fungal infections?
How about those used to fight viral infections?
Fungal – harder to crate drugs with selective toxicity as fungi are eukaryotic cells. More in common structurally, so harder to target.
Viruses – spend little time outside of host cells, hard to detect and target. Don’t carry out metabolism, so not “cell” processes to target.

8. List and describe the mechanisms of antibiotic resistance. What are beta-lactamases?
Destroy the drug (lactamases)
Altering drug target site
Increase drug elimination from cell, host
Alter permeability to drug (more impermeable)
β-lactamases are enzymes that break the β-lactam ring of antibiotics in the penicillin and cephalosporin families.

9. How is resistance to a drug acquired?
Begins with spontaneous mutation, and spreads through plasmid transfer (pili, phage conversion).

10. What human practices lead to antibiotic resistance in bacteria?
Overuse of antibiotics
Use by immunosuppressed individuals
Patient noncompliance
Animal feed

Chapter 22 –

Staphylococcus organisms

G(+) coccus. Facultative anaerobes. Tolerate high salt (resistance to osmotic pressure).
S. AUREUS – COAGULASE+

Virulence – capsule, peptidoglycan, teichoic acid, protein A, cytoplasmic membrane, toxins – exfolitoxins, enterotoxins, TSS superantigen, cytotoxins; enzymes: coagulase, catalase, hyalurondiase, fibrinolysin, lipases, nucleases, penicillinase

Epidemiology – NF skin, nares. Survive on dry surfaces, fomite spread.

Diseases
Staph. Scalded Skin Syndrome (Ritter’s) (destroy connective tissue between dermis and epidermis, epidermis falls off. Exfolitoxins).
Bullous Impetigo – blisters on skin
Food Poisoning – heat stable toxin
TSS – high mortality
Folliculitis – hair follicles infected (“ingrown hairs”?)
Furuncle (boil) (site of draining pus, must be drained (will not clear up))
Carbuncle (several sites of draining pus)
Pustular Impetigo
Bacteremia
Endocarditis
Pneumonia
Osteomyelitis – infection in bone, from bacteremia or spread of wound
Septic Arthritis

ID: Gram stain, catalase, coagulase, mannitol fermentation.
Treatment – penicillin resistance is common


Chapter 23 – Streptococcus
G(+), chains, fac. Anaerobes, some are aerotolerants. Produce lactic acid. Catalase (-). Complex nutritional requirements.

Virulence –
Capsule – mimics hyaluronic acid
M proteins
Heart valve protein (rheumatic fever protein)
Blocks C3B
Toxins – erythrogenic
Streptolysin
Type S – aerobic conditions
Type O – anaerobic conditions
Streptokinase
Breaks down blood clots

Epidemiology
Oropharynx and skin – children and Young adults
Transmitted through direct contact (infected mucus, body secretions)
Asymptomatic patients, pts on antibiotics are less contagious
Noninvasive disease is common
Over 10 million cases, underreported
Most common : pharyngitis, pyoderma

Diseases –
Suppurative (development of pus)
Pharyngitis (strep throat)
2-4/365 incubation
cannot diagnose visually
Complication : Scarlet fever
Pyoderma (Impetigo)
S. aureus
Erysipelas
Acute skin infection
Systemis signs (fever, chills…)
Cellulitis
Inflammation of connective tissue
Bacteremia
40% mortality
Necrotizing Fasciitis
Streptococcal gangrene
Destroy muscle, fat, skin
25% mortality
Streptococcal toxic shock syndrome (STSS)
Superantigens
Often accompanies NF
45% mortality

Non-suppurative (no pus)
Rheumatic Fever
Complication of pharyngitis or skin infections, may have had asymptomatic infection
Prevented with antibiotics
Cross-reactive antibodies
Inflammation in heart, joints, blood vessels, skin
Affected individuals are more susceptible to further infection/damage
Actue glomerulonephritis – damage to glomerulus, causes blood in the urine

ID –
S.pyogenes :
Group A
G(+)
blood agar
PYR enzymes (differentiate b/t S. pyogenes, S. anginosus)
Antigen detection – rapid strep test

Treatment –
Penicillin
Macrolides
NF – surgery
Rheumatic Fever – preventative antibiotics
Wash hands, etc.

Ch 23 b

Strep. agalactiae

Group B strep

Characteristics-
G(+) streptococci
Facultative anaerobe
Beta-hemolytic (Small percentage non-hemolytic)
B antigen

Virulence –

Epidemiology –
Site : lower GI tract, GU tract
10-30% of pregnant women are carriers
60% of infants born to infected mothers become infected
In men and non-pregnant women :
Skin and soft tissue
Bacteremia
UTI/urosepsis
Pneumonia
Predisposing factors :
Diabetes mellitus
Cancer
Alcoholism

Diseases –
Puerperal sepsis (childbed fever)
In newborns : Septicemia, Pneumonia, Meningitis
Early-onset neonatal disease (1/52)
Acquired in utero or at birth
Bacteremia, pneumonia, meningitis
Must examine CSF
5% mortality
15-30% of survivors have permanent neurological damage –
blindness, deafness, severe mental retardation
Late Onset Neonatal disease(1-12/52)
Source : mother, other infants
Bacteremia, meningitis
Pregnant Women – UTIs
Men and non-pregnant women
In immunocompromised individuals
Bacteremia
Pneumonia
Bone and joint infections
Skin and soft tissue infection
15-32% mortality

ID –
Culture
Antigen detection
PCR

Treatment –
Penicillin G
Pregnant women – IV of antibiotics before delivery, can cross placenta, offers defense if colonized by bacteria

Viridans Streptococci

Characteristics –
Heterogenous collection of alpha-hemolytic and non-hemolytic strep. Spp.
20 spp. In 6 groups
Req. complex media, blood products, 5-10% CO2

Colonize
Oropharynx (NF)
GI (NF), GU

Diseases
Dental caries
Subacute endocarditis
Not from Ig, but from bacteria. The viridans bind to damaged (congenital, superantigen) heart valves. Transmitted during dental work.
Suppurative intraabdominal infections

Treatment
Penicillin
Some resistant strains

Strep. pnuemoniae

Characteristics -
G(+) coccus, large cells, oval/lancet shape
Also called diplococcus, pneumococcus
Fastidious requirements
Alpha-hemolytic in aerobic
Beta-hemolytic in anaerobic
Catalase (-)
Poor growth in high glucose
Prominent capsule

Virulence factors
CAPSULE

Epidemiology
Enodgenous (NF)
Direct transmission is rare
Often a SECONDARY infection
Young and old at higher risk (meningitis)
More common in cool months

Diseases
Sinusitis & Otitis media
Over 7 million cases/year
Paranasal sinuses and middle ear
2ary to viral infection in upper respiratory tract
Sinus – all ages
Otitis media – young children
Eustacian tube is shorter, bacteria can travel more easily to middle ear. Opening more narrow, closes off more easily. Closes off, fluid accumulates, puts pressure on tympanic memrane, can rupture eardrum (can heal), break malleus/incus/stapes -> hearing loss.
Meningitis
6000 cases/year
Mostly in children
More damage than other types of meningitis

Bacteremia
55000 cases/year
Endocarditis, even with previously undamaged heart valves

Identification

Treatment
Penicillins and others
Immunization


Ch 24 – Enterococcus

Characteristics
Originally group D strep
E. faecalis
E. faecium
Catalase (-)
Fermentation
Tolerates high salt, bile salts
Commensal organism in large intestine
High antibiotic resistance
Infections : endogenous source

Transmission
Person-to-person
Contaminated food

Virulence Factors:
Multi-drug resistance
Colonization
Secreted factors

Diseases
Risk factors:
Catheterization
Long-term hospitalization
UTI (especially w/ catheter)
10% of all nosocomial infections
Vancomycin- Resistant Enterococcus (VRE) 35-50% mortality
Peritonitis (after surgery)
Endocarditis (5-15%)
Bacteremia
Wound infections, abcesses

Treatment
Highly resistant
25% resist aminoglycoside
50% resist ampicillin
25% resist vancomycin

I saw this sign today as I walked up from the Hart toward the MC. There have been quite a few problems recently at crosswalks (both drivers not paying attention and pedestrians wandering all over the place). The school has been working with the city to try to remedy this (including drumroll..... fixing the crosswalk signals on 2nd South!! I thought I would never live to see the day! Especially the way the cars barrel through that intersection).

I guess this sign is one of the other ways they are increasing awareness. I read it as I walked by, thought about it while walking, started to laugh nearly out loud, and turned around to take a picture. "Use crosswalks!" "Share the Road!" But it's the caption at the bottom that gets me "think of the impact you can make". Um... I thought the idea was to NOT make an impact.

Hehe.

It's Saturday!!

I was so excited to wake up this morning and to not have to be anywhere any time soon. It's nice. I spent the night at Katie's again, and am convinced that she has the Best Couch in the World. Really! Today was the first day since Wednesday that I haven't woken up with a migraine (which is weird, because I really haven't gotten them lately at all - the last one before this week was on tour with the Symphony Band in April). So, I am giving credit to the couch. :) I met Katie at her work last night so we could head over to her apartment together. She works at Hogi Yogi, which is a bit of a Utah-Idaho institution... but is basically a fast-food type place, but a little higher up than McDonald's. Anyway, they had some drama there last night - someone graffitied one of their booths. They have security cameras, though, so they'll be able to figure out who did it (only a few people sat at that bench last night). We were talking about it afterward, and just thought it was a little funny - the graffiti was a gang tag (which in and of itself isn't funny), but... a gang tag in Rexburg? Borderline hilarious. What, are they having drug territory wars? It was probably just some 14-year-old who was trying to be cool. Anyway.

I've been thinking of what to do next year... I know I'll be home for a while, but I'm trying to figure out a more long-term plan. I still think that med school is the way to go for me, but I just may have to take a different route to get there. So I'm starting to think of what I need to do to make myself a stronger applicant for next year, and also thinking about possible master's programs. It's a little hard, because I don't have a strong interest in research (last summer cured me of that, haha... sigh), but many programs focus on that. I really just want something that will help me gain a better understanding and perspective in medicine and prepare me for med school. I started thinking about bioethics, which I think would be really neat. The only catch is that there seems to be only one program in all of Canada, at the U of T. And Toronto is a nice city, but... I guess it would just be nice to have a few more options. There are some online master's programs, but I'm pretty wary of those and how useful they would prove to be in further studies and jobs. Another program is a master's of public health, which would be really cool. BYU (Provo) has a great MPH program, and for part of it you get to work in an underdeveloped area of the country or the world and implement a program that you help design (eg. stop smoking program, patient education programs, etc). Which I think would be an A-M-A-Z-I-N-G opportunity! But let's be honest... I'm not sure I could handle Provo! Haha... I guess I'll have to think about things a bit more.

Sometimes I just want to forget about it all and go to law school instead. Sometimes I want to forget it all and be a bum on the street, but of those two options, I'm pretty sure my parents would disapprove of the latter.

Or maybe the former. ;)

So things have settled down a little... the two roommates who were kicked finally *moved* out this week. It was pretty tense until they did, but things have been ok since then. And by "ok", what I really mean is "no one is openly hostile". Which is a nice change, but... still a far cry from what would be nice. Anyway, I am glad things are a little better.

I had a good day in the ceramics studio, I was able to get some work done and am really happy with hoe it turned out. We did a Raku firing in class today, which was a lot of fun. With Raku, when the pieces are fired and really hot, you pull them out of the kiln and then set them in bins that are full of sawdust, newspaper, and other combustibles. The pieces are so hot that they ignite the material, and the ash produced gives the piece a cool finish. I'm hoping to Raku fire a piece next week. The ones done today were really beautiful. The only drawback is that the pieces don't get hot enough to vitrify, and they remain porous, so you can't use them to hold food or water. But I think I'll still give it a shot. I'm hoping to find a ceramics studio in Winnipeg so I can keep up with it after graduation.