MudPhud20XX

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How come? Kaplan explains this it's b/c the inflammation is taking place in the interstitium not in the alveolar space. Since consolidation is the solidification of the lung due to bacterial agents, shouldn't there also be consolidation in case of atypical pneumonia regardless of the location?

Many thanks in advance.
 

Bojack Horseman

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How come? Kaplan explains this it's b/c the inflammation is taking place in the interstitium not in the alveolar space. Since consolidation is the solidification of the lung due to bacterial agents, shouldn't there also be consolidation in case of atypical pneumonia regardless of the location?

Many thanks in advance.
Isn't the consolidation just pus that fills the alveolar air space? Hence when you percuss a consolidated lung it sounds solid instead of air-filled. If the interstitial thing is correct (I have no idea) then it would make sense that pus doesn't fill the alveoli.
 
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MudPhud20XX

MudPhud20XX

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You're right. Consolidation is the pus and all the junks inside alveoli space. I am trying to understand why you wouldn't get such consolidation in atypical pneumonia. Kaplan is basically saying that you don't see any consolidation in atypical since the infection/inflammation takes place in interstitium not in alveoli space.
 
Jun 11, 2012
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You're right. Consolidation is the pus and all the junks inside alveoli space. I am trying to understand why you wouldn't get such consolidation in atypical pneumonia. Kaplan is basically saying that you don't see any consolidation in atypical since the infection/inflammation takes place in interstitium not in alveoli space.
Atypical is mainly a result of T cell or cell mediated destruction via activation of the T cytotoxic lymphocytes. These cells destroy infected cells by activation of Thelper2 cells that release cytokines when they interact with APC cells of infected normal cells (MHC class 1 cells). This activates the T Helper 2 cells which then stimulate cytotoxic T cells by releasing factors to stimualte them. Wikipedia will tell you that cytotoxic T can be activated by merely binding to MHC class 1 but this is impossible without aid from helper T cells (which also activate B cells).

Anyway, the intracellular damage allows the T cells to initiate cell apoptosis without the need to recruit other material such as neutrophils involved in humoral (adaptive) and first line (innate) immunity.

Consolidation is pus that results from active recruitment of neutrophils. This recruitment is primarily due to bacterial capsular or glycoprotein activation of chemoattractants. Such chemoattractants include LTB4 which activates neutrophils and il-6, il-8 and il-1 which recruit macrophages. The recruitment process is what stimulates the process of entry into target tissues such as diapedesis, entry, and then damage within the tissue via a variety of mechanisms found in innate immunity such as complement mediated lysis (antibody INdependent immunity)- this includes the binding of the complement to the bacteria to enhance opsonization C2b (engulfment by macrophages via phagocytosis) or via MAC complex C5-9.

In any case, the resulting activation and recruitment is what results in pus like presentation.

Atypical- viral, mycoplasma, legionella, chlamydia- all intracellular plus viruses. This is why htey are are afebrile- due to the lack of activation of Il-1, il-6, tnf alpha which are pyrogens involved in macrophage activation that stimulates prostaglandins found in the temperature regulating center of the hypothalamus involved in the set point-PG increases the set point leading to haripulation, contractions (shivering) to increase metabolic rate and resulting heat. This is also why aspirin which blocks prostaglandins at moderate levels can decrease a fever.

typical pneumonia has pus and fever and results in recruitment of macrophages and release in TNF alpha, il1, il6 which cause the fever described above along with pus.

This results in consolidation in the pneumonia wihtin the tissue while atypical remains outside (so to speak) in the interstitium.
 

Transposony

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Good explanation BUT they do have high Fever as well as malaise, headache & chills.
Also what about Klebsiella pneumonia?
 

Transposony

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According to Medscape:
After inhalation of respiratory aerosols, the organism attaches to host epithelial cells in the respiratory tract. The P1 adhesin and other accessory proteins mediate attachment, followed by induction of ciliostasis, local inflammation that consists primarily of perivascular and peribronchial infiltration of mononuclear leukocytes, and tissue destruction that may be mediated by liberation of hydrogen peroxide. Recently, M pneumoniae has been shown to produce an exotoxin that is also believed to play a major role in the damage to the respiratory epithelium that occurs during acute infection.[3] This toxin, named the community-acquired respiratory disease toxin (CARDS) is an ADP-ribosylating and vacuolating cytotoxin similar to pertussis toxin.[4]
Also
The organism has 2 properties that seem to correlate well with its pathogenicity in humans. The first is a selective affinity for respiratory epithelial cells, and the second is the ability to produce hydrogen peroxide, which is thought to be responsible for much of the initial cell disruption in the respiratory tract and for damage to erythrocyte membranes.

The pathogenicity of M pneumoniae has been linked to the activation of inflammatory mediators, including cytokines.
 
Jun 11, 2012
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Good explanation BUT they do have high Fever as well as malaise, headache & chills.
Also what about Klebsiella pneumonia?
I don't think klebsiella is atypical?

Also, thats odd- Kaplan said atypical was associated with low to no fevers. Oh well, I'm sticking with my explanation though- it makes it easier to remember- fits nicely. I think the stuff on mycoplasma is beyond scope of USMLE