Tuesday, October 27, 2009

Tuberculosis pathophysiology and host immunity

Mycobacterium tuberculosis (Gladwin & Trattler, 2006)
• Gram-positive thin rods
• Obligate aerobe
• Slooooow growing
• Posses a class of lipid called mycosides that give it, its virulence

Transmission (Nairn & Helbert, 2007)
· Droplet nuclei containing M. Tuberculosis is breathed into the lungs
· Once inside, the TB bacteria stimulates immune system reaction such as macrophages and neutrophils.
· Some TB bacteria multiplied and survive inside our macrophages while others are destroyed by them.
Formation of Granuloma (Nairn & Helbert, 2007)
• As the infection progress i.e. day 2, another type of immune cells known as T helper 1 cells, which has received signals from the macrophages of the infection, arrived to the infection site to help fight TB bacteria
• T helper 1 cells secretes potent inflammatory chemicals known as cytokines specially Interferon gamma (IFN-gamma) and tumor necrosis factor (TNF) aiming to kill and contain TB bacteria
• In the process of doing so, a granuloma made of calcium shell is formed around dead tissue that resulted from TNF destroying the host tissues along with the TB bacteria
Primary Tuberculosis Infection a.k.a first infection (Nairn & Helbert, 2007)
• 90% of those infected with TB do not have any symptoms
• Less than 10% develop TB disease or widespread infection.
• Even when infection is contained and controlled, many mycobacteria survive inside macrophages or other cells for several years. This is latent TB.
• On the other hand, if your immune system is “over zealous” and fights TB infection with excessive production of TNF, local tissue damage occurs and infectiousness develops
Secondary or Reactivation Tuberculosis (Nairn & Helbert, 2007)
• Occurs in about 10% of patients; usually happens when immune system is compromised or macrophage function is moderately impaired.
• Compromised immune system or moderately impaired macrophage function usually happen with treatment that requires high dose of corticosteroids, malnutrition, or immunosuppression due to HIV/AIDS or anti rejection drugs which are taken by organ transplant patients.
Tuberculosis “Rules of Fives” (Gladwin & Trattler, 2006)
• Droplet nuclei are 5 micrometers and contain 5 Mycobacterium tuberculosis bacilli
• Patients infected with Mycobacterium tuberculosis have a 5% risk of reactivation in the first 2 years and then a 5% lifetime risk
• Patients with “high five” HIV will have a 5 + 5% risk of reactivation per year!

The pathophysiology and disease process of Tuberculosis is highly immunologic. In order for me to understand the disease process thoroughly, there are still a lot to learn and study.

Gladwin, M., & Trattler, B. (2006). Clinical microbiology made ridiculously simple. MedMaster series. Miami: MedMaster.

*Nairn, R., & Helbert, M. (2007). Immunology for medical students. Philadelphia: Mosby.

www.nature.com/.../n7034/fig_tab/434709a_F1.html

*most comprehensive in the explanation of the pathophysiology of TB and its immunology.

Tuesday, October 20, 2009

Epidemiology of TB in foreign-born Asian personals in WA State

Reported Tuberculosis in the United States, 2008
According to this latest report from the CDC, WA state is ranked 14th in the number of TB cases in 2008 with 228 cases. When state population is taken in account, WA State has 23rd highest TB case density. Of the 228 cases, 78 cases (34.2%) are of Asian ethnicity or about 1 out of 3 TB cases.
A Glance at Washington’s Foreign-Born TB Cases
Findings from WA State DOH state that 35.5%, 21.1%, and 19.7% of TB cases in the foreign-born are in the 25-44, 45-64, 65+ age group respectively. When TB cases are diagnosed in foreign-born who is 65+ years old, there is 61% chance that he/she has been living in the United States for more than 10 years.
Implication for health practitioners in WA State
· 1 out of 3 TB cases a health practitioner diagnosed is an Asian American who is likely foreign-born.
· Health practitioners, public health personnel, and social/community workers must be aware that active TB disease is not only prevalent in the foreign-borns who are young (less than 44 years old), and newly arrived (less than 5 years of residency). Indeed, 1 out of 3 cases of TB in the foreign-borns are in those who are 44+ and who have been living in the U.S. for more than 5 years.
· Those who are foreign-born, living 5+ years in U.S., 44+ years old, and displaying any signs and symptoms of TB must be screened for TB and properly followed.

Tuesday, October 13, 2009

HIV factoid gems

In preparation for my EPI 530 class assignment, I discovered several interesting facts about HIV transmission. These interesting facts are from "Viral and Host Factos Affecting HIV-1 Transmission" by Julie Overbaugh. The below are rephrase of the facts mentioned in the article along with my conclusions based on my vague memory of genetics.
#1: It is difficult to create a vaccine for HIV and/or stop multiple drug resistant HIV virus from forming because of HIV reverse transcriptase which renders HIV high genetic variability, continual evolution, and adaptation to host's immune system and drug therapy. HIV reverse transcriptase (and maybe all microbial transcriptase) is highly inaccurate which when coupled with mass production of RNA to DNA leads to mutations left and right.
aside: I remember my genetic professor from undergrad telling us that our DNA transcriptase is quite precise compared to microbe's transcriptase. Ours make only 1 mistake in a million or billion DNA copy and hence we are not constant mutating like the microbes!
#2: Remember the news about a group of people in Europe who are "immune" to HIV transmission? You probably do and the next word that popped into your head is probably "bubonic plague." Yes, that news says something to the gest of, "descendents of survivors of bubonic plague are genetically "immune" to HIV transmission." However, the "real" or molecular reason is this, some individuals of European descent do not express (phenotype) cell-surface CCR5, which is one of the multiple-membrane-spanning chemokine receptor that is needed for HIV-1 entry into cells.

Sunday, October 11, 2009

T cells and B cells

Today in my immunology "class" I was approached with a conflicting information regarding the progenitor(s) of B-cells and T-cells. For those of you who are familiar with hematopoiesis, some textbooks say that B-cells and T-cells are derived from common lymphoid progenitor (CLP); however, upon further inquiry you've no doubt realized that it is more complicated than that. For instance, the jury is still out, so to speak, regarding the true progenitor of T-cells. An article in Nature Immunology by E. Montecino-Rodriguez titled "To T or not to T: reassessing the common lymphoid progenitor" states that T-cells may be derived from early T lineage progenitor rather than CLP.
While posting the above on Moodle as part of my immunology class's assignment, I thought, "Hmmm...is this fact really important or pertinent to nursing?" and all I could came up with was, "I think so," for although T-cells and B-cells make up our adaptive immune system, I don't know if knowing whether or not they come from a different progenitor will affect the way I care for my patients. This thinking, though, is a work in progress for I still have a whole quarter of immunology, infectious disease, and epidemiology ahead of me!