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I have a case study where someone with a gunshot wound mostlikely developed pneumonia and had Staphylococcus aureus enter thebody. I am suppose to define the infection that could occur in thegastrointestinal tract because of this. So, what infection can S.aureus cause in the GI tract and where would it be located?

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Elin Hessel
Elin HesselLv2
28 Sep 2019

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Case Study Section 4 – Nitrogen Metabolism Based on “A Sickeningly Sweet Baby Boy: A Case Study on Autosomal Recessive Inheritance” by Jacqueline Washington and Anne Zayaitz (National Center for Case Study Teaching in Science) The Patient: Mathew Miller is a 7-day-old infant that is rushed to the emergency room by his parents Emma and Jacob Miller, Mennonites from Lancaster County, PA. Emma’s pregnancy and delivery with Mathew was normal but he started having trouble nursing and now has completely stopped feeding. By the time they reach the emergency room Mathew’s limbs were rigid and he had had a seizure. The initial examination showed no infection and his x-rays were normal. The family history collected by the Doctor revealed that Emma and Jacob had had a previous son, Samuel that died at 9 days-of-age. There also is a history of unexplained childhood mortality on both sides of the family; Emma’s mother had two sisters who died in the first year of their lives and Jacob’s father had a sister who died at 7 months of age. Emma also points out to the Doctor that Mathew’s diaper has a funny smell to it. Blood and urine samples were taken for testing and skin biopsies from Mathew, Emma, and Jacob were taken and tested for enzyme activity. The tests results showed that:

• Mathew’s urine had elevated levels of the branched chain amino acids and their α-keto acid derivatives (which caused the sweet smell in his diapers)

• Both Emma and Jacob’s skin biopsies had nearly normal levels of branched chain amino acid metabolism/enzyme activity

• Mathew’s enzyme activity was less than 2% of normal

Question 1: What is the most likely diagnosis for Mathew?

A. Argininemia

B. Diabetes mellitus '

C. Maple syrup urine disease

D. Phenylketonuria

Question2: What enzyme did the skin biopsy test measure?

A. Carbamoyl phosphate synthetase I

B. Alanine aminotransferase

C. Phenylalanine hydroxylase

D. Branched-chain α-keto acid dehydrogenase complex

Question 3: This enzyme functions VERY similarly to two other enzymes that we have discussed, what are they?

A. Phosphofructokinase-1 and fructose 1,6-bisphosphatase (FBPAse-1)

B. Pyruvate dehydrogenase complex and α-ketoglutarate dehydrogenase complex

C. Urease and arginase

D. Isocitrate dehydrogenase and malate dehydrogenase

Question 4: How did Mathew (and presumably Samuel) inherit the disease if both Emma and Jacob have normal enzyme activity levels?

A. Emma and Jacob must both be carriers for the disease but their one normal gene is enough to maintain enzyme activity levels.

B. The disease can happen spontaneously, there is no genetic link.

C. Jacob is not really the father of the boys.

D. The disease can skip generations.

Question 5: What would be the best diet for Mathew to follow to control his disease?

A. Atkin’s diet (low carbohydrates, high fat, and high protein)

B. Low protein

C. Low fat

D. No special diet will control the disease

Over the next 4 years Mathew’s metabolic disease is controlled by his special diet but he still suffers approximately 3 metabolic crises a year. These occur when amino acids accumulate in his blood leading to the swelling of his brain. Even something as simple as a cold or the flu can affect his amino acid levels and send his metabolism into crisis. Jacob and Emma decide that “We cannot continue to live in constant fear that a minor infection or a simple cold or ear infection could kill our son. Even though we are doing everything we are supposed to, he is still getting sick and we are afraid we may lose Mathew.” They learn that some children with Mathew’s disease have undergone liver transplants and are effectively cured.

Question 6: How/why would a liver transplant effectively cure Mathew’s condition?

A. A new liver would be able to spread it’s genes throughout the body and correct the genetic disorder.

B. A new liver would more effectively respond to metabolic hormonal control.

C. A new liver would express the functional enzyme needed to metabolize the amino acids causing Mathew’s condition.

D. A new liver would produce more hemoglobin to transport oxygen more effectively.

The family is directed to Dr. Morton of Children’s Hospital of Pittsburgh, where transplant experts agree to list Mathew for a liver transplant. Jacob and Emma learn that children who receive a liver transplant have to take strong immunosuppressive drugs for the rest of their lives. It was also clear that there was a 40% possibility that Mathew could reject the liver and need a second transplant (which also might be rejected) or he could die from surgical complications.

Question 7: Assuming the liver transplant was successful and Mathew did not reject the new liver, what type of diet would Mathew be able to/need to eat?

A. He would still need to eat his special diet but he would be at less risk of a metabolic crisis

B. He could eat a normal diet

C. He would need to change to a high protein diet like Atkin’s

D. He would be on an all liquid diet

Question 8: Emma and Jacob decide they want to try to have another child. What would be the chance that this child would also have the disorder that Mathew and Samuel have/had?

A. 0 %

B. 25%

C. 50%

D. 75%

E. 100%

Question 9: If Mathew grew up, got married, and decided to have children, what would be the chance that his children would have the disorder? A. 0%, the liver transplant would have cured him

B. 25%

C. 50%

D. 100%

E. It would depend on his wife, if she was normal than there would be a 0% chance of his children having the disorder but 100% would be carriers, if she was a carrier than there would be a 50% chance of his children having the disorder and a 50% chance that they would be a carrier.

Question 10: The disorder is found in 1 in 200,000 infants throughout the US but 1 in 200 in the Amish and Mennonites of Lancaster County, PA. Why is there such a difference in the prevalence of the disease?

A. There are environmental factors associated with being Amish or Mennonites that increase the prevalence.

B. There is a large amount of genetic similarity within these populations because they tend to marry within the population so recessive disorders such as this are more likely.

C. The gene mutation is preferentially carried in Caucasians so when you average the prevalence across all races in the US the prevalence drops.

D. It is unknown why the prevalence is so much greater in Amish and Mennonites.

First of all I am not endorsing Intelligent Design (Wikipedialink); I'm asking this because I (someone who does not have abackground in biology, organic chemistry, or philosophy) got into aconversation with someone who does endorse it, and I'm trying tosee his point of view as far as rationality can allow. Second ofall, I apologize for any vagueness; Intelligent Design isn't wellenough defined as a theory for me to help that. I also apologize ifthis is rehashing content already plentiful on the Internet, butfor my purposes I can't simply depend on the likes of Wikipedia orTalk Origins, so what I'm looking for here instead is to take theopposite approach and see, based on your informed minds, if therecould possibly be any reasonable likelihood of an ideal ID theorybeing adopted.

I'm looking for the most favorable consideration for what IDmight be if it were best developed as a viable hypothesis or theoryto get an idea of how far such a discussion is worth taking. Anunbiased, informed Devil's advocate, if you will.

My cursory investigation of what Stephen Meyers (video link) andMichael Behe (video link) say (correct me if I'm wrong) seems to bethat either the first cell was likely designed intelligentlyjudging by the complex code of DNA and that evolution took coursefrom there, or that the first cells were made and many instances ofevolution were from some kind of intelligently guided mutations aswas needed to make "irreducibly complex" cells or body functions(whether the guidance stops after the Cambrian or continued even tothe point of making different types of new bacteria and differenttypes of apes/humans or whether every single mutation and adaptiveability is being guided, I'm not sure if they're at any consensus,and that's why I don't know if I should stop my question atabiogenesis or include evolution). The person I spoke with alsobrought up some specific claims (everything looks designed, DNA hasordered, complex information, blood clotting is irreduciblycomplex, ID can and has make predictions like decades ago that"Junk DNA" wasn't junk) that I don't need you to debunk (I haveGoogle).

But if there could be any possible support or truth to any ofthe above, I would appreciate knowing about that. (Again, Devil'sadvocate so I can be informed and understand where the points comefrom.) Reading an ID book alone, it would be in places hard to knowwhere they differ from actual scientific conclusions. After all,when someone who seems to know what they're talking about and canexplain something in technical detail says that something isimpossible or extremely unlikely, it's hard for me to know why theywould be wrong (are they ignoring other possibilities?misrepresenting facts? are they really right and just getting thecold shoulder from an atheistic scientific community because itimplies a deity?). So I focus on mainstream sources, even if theydon't bother entertaining ID and leave me ignorant of its possiblevirtues. And thus I'm hoping someone from this informed communitymight enlighten me to what those possible virtues might be.

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