The patient walked barefoot on the beach and had cirrhosis, which makes him vulnerable for V. vulnificus bacteremia. V. vulnificus bacteremia has a very poor prognosis.

From Uptodate: "[V. vulnificus] is the leading cause of shellfish-associated deaths in the United States. Infections due to V. vulnificus are most common in individuals who have chronic, underlying illness; individuals with liver disease or hemochromatosis are at greatest risk."

It seems like Staph aureus UTI's are almost exclusively nosocomial, esp. w/ patients with urinary catheters: "We identified and entered into the study 102 consecutive patients for whom at least 1 urine culture was positive for S. aureus...82% had a urinary catheter of some type in place"

Here's the link to the study

Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

The question stem is asking what features led to the ineffectiveness of pharmacotherapy. Patient's presentation is consistent with Mycoplasma pneumoniae infection, which doesn't have a cell wall and therefore peptidoglycan, which is the site of action for penicillins. It does require sterols for growth, but that wouldn't explain why amoxicillin is ineffective.

Overview of Saliva production:

1. Acinar cells secrete initial saliva, which is isotonic to plasma.
2. Ductal cells modify initial saliva, causing reabsorption of Na+, Cl- and secretion of K+ and HCO-. -> higher K+ and HCO- concentrations, lower Na+ Cl- concentrations in saliva. In this process, MORE NaCl is reabsorbed, meaning that saliva ends up being hypotonic to plasma.

Ductal reabsorption process is hindered in high-flow states, which causes isotonic saliva