It's not end of sem 5 which I am going to graduate. It's about the end of semester 4, better known as "honey moon" sem for any IMU student. (Well some perceive it as honey moon while some don't, you know what i mean;-))
It's the second day of my Gombak Hospital attachment, not that interesting case, just some infectious cases here and then. (Yeah, don't get me wrong, it is infectious cases, cases like leprosy and TB) The aborigines are well known of getting malaria, TB or leprosy, you just can't get away from them. This is rainforest and Malaysia anyways. It is interesting to note that what type of organisms will infect the patients. Klebsiella pneumoniae, Haemophilus parainfluenzae etc. These two bacteria are rather rare (to me) in terms of explaining what type of organism which is responsible for pneumonia. Normally we always think of the trio in talking about pneumonia or any famous bacteria involved in bacterial respiratory tract infection i.e. Haemophilus influenzae, Streptococcus influenzae and Moraxella catarrhalis. It is a must know for any medical student if ask about the bacterial infection of the respiratory tract. Prof Victor teach us well about this. Klebsiella sp. is rather for immunocompromised, malnutrition cases, ALCOHOLICS, otherwise it's is rather not significant for us to relate them into pneumonia cases. They are just too minute and not that common (so far of what I know, since this country is Malaysia, you rarely see alcoholics right?)
It is interesting to note some leprosy cases. They are important, that's one, in terms of knowledge, also for your exam. The culprit for leprosy is Mr. Mycobacterium leprae. Yes, it is mycobacterium which means it is of the same family as the culprit of TB. They are aerobic, acid-fast bacilli (rods), they neither stain G(+) nor G(-). Virtually they are the only bacteria that are acid-fast except Nocardia asteroides. "Acid-fast" menas the organism ability to retain the carbolfuchsin stain despite subsequent treatment with an ethanol-hydrochloric acid mixture. The high lipid content of their cell wall makes them able to take up the stain.
Mycobacterium leprae infection is acquired by prolonged contact with patients. Keyword here is "prolonged". Therefore, you won't get the infection just because you just happen to stand in front of the patient and touched his wound or via his nasal secretions. Humans are natural hosts although armadillo may be a reservoir for human infection. They replicate intracellularly, which most mycobacterium will do and there are two distinct forms of leprosy--tuberculoid and lepromatous. To briefly tell about the key clinical findings, they include hypopigmented macular or plaque-like skin lesions, thickened superficial nerves and significant anesthesia of skin lesions. This is the horror that is created by the culprit. Treatment? Dapsone (diaminodiphenylsulfone) and resistance strains tend to come about quite frequent, it is combined with other drugs in the form of combination therapy in which dapson, rifampin and clofazimine for lepromatous leprosy and dapsone and rifampin for tuberculoid form.
Feeling a bit tired now. Really a tiring day if you are working in a hospital, luckily it's not as busy or as crowded as any other major hospitals. Good to take a look at the culture of the aborigines and we have to really admire their skills on building and to live in the wilds.
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