In medical school, we started learning about pathology in the second half of the third year and we did a solid year in the fourth year. The University of Queensland had an amazing Department of Pathology in the School of Medicine. I loved it. I almost loved pathology as much as I loved studying microbiology and zoölogy.
One of my favourite pathologists was Professor Richard Steele, everyone though, knew him as Dick.
Prof. Steele was a pulmonary pathologist and his teaching load was focused on inflammation. I can still remember him saying, “Calor, Dolor, Rubor, Tumor, and Penuria”, which roughly translates as heat, pain, redness or erythema, swelling and loss of function. These are the cardinal signs of inflammation.
One of the classic Dick Steele lecture series was on pneumonia, and while I mentioned pneumococcal pneumonia in episode 11, Dick taught us about Friedlander’s bacillus as a cause of a very nasty type of often fatal consolidating pneumonia.
The Friedlander’s bacillus is Klebsiella pneumoniæ. Prior to Friedlander’s description of pneumonia, Edwin Klebs reported seeing bacteria in the airways of deceased pneumonia victims. It was Friedlander though who noted the bacteria were present in the airways of patients dying of pneumonia and made a bold statement that pneumonia was caused by this particular bacterium. It’s not sure if the Friedlander’s bacillus described in the late 1800s is really the Klebsiella pneumoniæ we know today. Certainly, the Klebsiella pneumoniæ we see today doesn’t cause large numbers of severe bacterial pneumonia. Ironically and very sadly, Friedlander died when he was about 40 of a respiratory illness. It’s possible he died from an infection caused by Friedlander’s bacillus which some have also called pneumobacillus as opposed to pneumococcus which is Streptococcus pneumoniæ.
Klebsiella pneumoniæ is quite pretty when seen microscopically in a Gram’s stain, especially if it’s from a blood culture bottle. Quite often the bacilli are short and plump suggesting the bacteria are in a log phase of growth and metabolically very active.
All that said and done, Klebsiella pneumoniæ has hit the news again this year with outbreaks of carbapenemase elaborating Klebsiella pneumoniæ in hospitals and the community. So what are carbapenemases I hear you ask? Carbapenemases are enzymes that catalyse the hydrolysis of carbapenem antimicrobials as well as monobactams, cephalosporins and penicillins. So in effect, basically all the b-lactam antimicrobials. In addition, many enteric bacteria like Klebsiella pneumoniæ also harbour resistance genes to enable resistance to aminoglycosides like gentamicin, resistance to fluoroquinolones like norfloxacin and ciprofloxacin as well as agents like trimethoprim and trimethoprim-sulphamethoxazole. Infections with KPCs as they’re known can be very difficult to treat. Because of this, they are very important infection prevention and control agents of concern. Can you imagine an aged-care facility with an outbreak of KPC? A place where quite a few patients would have indwelling catheters, whose lungs would be prime targets for pneumonia, and in which good IPC can be a real challenge. In Australia, most AGFs do not have resident medical personnel and residents have their own GPs so standardisation of care can be difficult.
Again, I raise the issue of antimicrobial resistance on Medical Fun Facts. It’s one of the most important human catastrophes of our time and yet I still come across medical practitioners who fail to appreciate they are contributing to the mess with inappropriate prescribing. Worse still I’ve heard alternative integrative GPs claim we’ve missed the boat and they’re not contributing to the problem if they use multiple long-term antimicrobials to treat their patients.
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