Years like this are rough on blogging. As previously noted, I teach an every-other-year spring course on infection and chronic disease. Well, every summer I also teach an intensive course (basically a semester crammed into a week) on the topic of applied infectious disease epidemiology: taking what’s known about ID epi and learning how to actually “do” it. For this course, which this year was exclusively taken by either DVM students or practicing veterinarians training for their MPH degree, their final assignment is a writing assignment. It’s pretty wide open: they can write about any area of infectious disease epidemiology that interests them, but the posts are supposed to be written for a layman audience. The first of 10 will be up shortly. As always, please keep in mind that these are the students’ posts, and that they’re learning, so feel free to post questions/comments but be respectful.
It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. Second one this round is by Jonathan Yuska.
If you happen to be one of the 46 million individuals who have not been swayed to quit smoking by the countless anti-cigarette ads in print and on television, here is one more piece of evidence that may have you second thinking that next puff. On top of the more than 3,000 chemicals and heavy metals already identified in ordinary cigarettes1, upwards of a million microorganisms per cigarette have also been found to live and thrive in virtually all cigarettes in the United States2. Microbes such as Bacillus (which is linked to the notorious anthrax disease), Clostridium, and Pseudomonas—to name a few—likely contaminate the tobacco leaves early at the farm level and are able to flourish during curing and manufacturing to be viable in the cigarette at the time of the consumer’s use. While some of the bacteria are capable of causing no more than a stomachache, others (and their respective endotoxins) have been linked to pneumonia and chronic lung inflammation—a widely recognized risk factor for cancer1,2. While cigarette smoking is a well-established cause of cancer in and of itself, the role microorganisms have in the toxicity of cigarette smoke should not go underplayed. With increasing evidence supporting the vast illness causing biodiversity found in cigarettes, hopefully more individuals will be aware of the dangerous contaminants they are welcoming into their bodies and call for greater sanitary measures to be taken to potentially create a less harmful cigarette product.
Approximately 23 different species of bacteria have been found in cigarette tobacco, many of which have been linked to serious illness in humans. For example, Pseudomonas aeruginosa—which is the leading cause of nosocomial pneumonia and often found in soil or sand—was found to be present in nearly all cigarettes tested in a study that looked at the presence of cigarette bacteria in the most commonly smoked brands, like Marlboro2. Another study interested in understanding the cause of severe lung inflammation in United States troops during Operation Iraqi Freedom found eight different species of Bacillus (five of which were never seen before) contaminating the soldier’s cigarettes3. Regardless of the actual bacteria within the cigarettes, the endotoxins derived from the bacteria that remain well after the bacteria have died have been shown to be a powerful inducer of lung inflammation (chronic inflammation is recognized as a powerful risk factor for cancer). It is theorized that the bacteria and their respective endotoxins may have an additive or multiplicative effect with tobacco smoke’s natural ability to cause pulmonary inflammation, though the amount of the effect that can be attributed is still up to debate2.
Research has shown that more than 90 percent of cigarettes are contaminated with some form of bacteria, and these bacteria are believed to originate early in the cigarette manufacturing process1. Similar to other crop cultivation, tobacco is grown in large fields where animal manure is used to provide the nutrients needed for a hearty crop. Some of the bacteria from the manure are believed to adhere to the tobacco leaves during the plant’s development. Curing the tobacco, which is essential in the cigarette manufacturing process to develop an ignitable, flavorful product, further facilitates bacterial growth because it is often done in moist, warm conditions3. Unlike other agriculture crops grown for consumption, tobacco has no regulations associated with its sanitation, and as a result, tobacco products can contain soil residues and insecticides in addition to a vast array of deleterious bacteria. Efforts to sanitize tobacco through an antimicrobial wash have been proven to be effective in reducing contaminants; however, since so little mainstream attention has been given to microbes in cigarettes, no sanitation process is currently being used by the cigarette industry2.
Misperceptions about how much risk the bacteria pose to the smoker is one reason so little attention has been given to microbes in cigarettes. Some critics believe that bacteria in cigarettes pose no harm because the cigarette flakes are prevented from entering the lungs because of the built-in filter within the cigarette. Some further argue that the viable bacteria found in the tobacco are destroyed or heavily reduced in number by the heat of the cigarette. Though, the validity of these observations are derailed by the fact in the process of transportation, or even minor jostling, tobacco flakes are often seen lying freely on the mouth end of the filter. Thus, loose tobacco on filters could transfer bacteria to the mouths and lungs of smokers before the cigarette is even lit. Additionally, some extremely fine tobacco microparticulates are able to pass through the cigarette filters currently being used and can be inhaled deep into the lungs to cause inflammation2,5. The harsh, high temperature conditions of cigarette smoking also does little in eliminating the bacteria that are able to produce robust heat resistant endospores such as the bacterial species Bacillus and Clostridium1. It is clear that more attention should be given to dismiss the misperceptions of bacterial risk associated with cigarettes so that effective sanitary regulations can be applied to tobacco similar to other widely consumed foodstuffs.
If the more than 3,000 chemicals and heavy metals that have been identified in ordinary cigarettes have not influenced you to quit smoking, hopefully the realization that one cigarette can contain roughly 1,000,000 microorganisms will have you second thinking the habit the next time you light up. Microorganisms that have been linked to serious illness in humans like pneumonia and chronic inflammation are thought to contaminate tobacco leaves early in the manufacturing process, and these organisms thrive and multiply to be viable bacteria in the consumer cigarette. While cigarettes themselves are recognized as a serious cause of ill health, the role microorganisms have in their toxicity should not be underplayed. With a better understanding of the vast bacterial biodiversity within cigarettes, sanitary regulations that eliminate bacterial contamination should be mandated to potentially make a less harmful tobacco product. Though until then, people should recognize the dangerous bacterial contaminants they are welcoming into their bodies every time they light up.
1. Sapkota, Amy R., Sibel Berger, and Timothy M. Vogel. “Human Pathogens
Abundant in the Bacterial Metagenome of Cigarettes.” National Center for Biotechnology Information. 22 Oct. 2009. U.S. National Library of Medicine. 13 Apr. 2013 <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854762/>.
2. Pauly, J. L., J. D. Waight, and G. M. Paszkiewicz. “Tobacco flakes on cigarette filters
grow bacteria: A potential health risk to the smoker?” Tobacco Control. 18 Oct. 2007. 13 Apr. 2013 <http://tobaccocontrol.bmj.com/content/17/Suppl_1/i49.long>.
3. Rooney, Alejandro P., James L. Swezey, Donald T. Wicklow, and Matthew J. McAtee.
“Bacterial Species Diversity in Cigarettes Linked to an Investigation of Severe Pneumonitis in U.S. Military Personnel Deployed in Operation Iraqi Freedom.” Current Microbiology 51 (2005): 46-52.
4. “How to Grow Tobacco.” How To Grow Stuff. 23 Nov. 2007. 13 Apr. 2013
5. Pauly, John L., and Geraldine Paszkiewicz. “Cigarette Smoke, Bacteria, Mold,
Microbial Toxins, and Chronic Lung Inflammation.” National Center for Biotechnology Information. 09 July 2011. U.S. National Library of Medicine. 13 Apr. 2013 <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136185/>.
It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. First one this year is by Dana Lowry.
Humans have a long history of illness and death from infectious diseases. It wasn’t until the 1790s that we had a solution. Edward Jenner recognized that milkmaids never contracted smallpox but suffered from a more mild disease, cowpox. Jenner took pus from a cowpox lesion on a milkmaid’s hand and placed it in an incision he made in an eight year-old boy’s arm. He then exposed the boy to smallpox; the boy didn’t contract the disease, proving he was immune. Jenner experimented on several other children, including his own 11-month old son, and his theory of passing on immunity proved to be successful. The Latin term for cow is vacca, which is where Jenner coined the term “vaccine”. Jenner’s discovery eventually led to the eradication of smallpox from the U.S. in 1949 and from the world in 1979. For over a century, vaccines were limited to preventing smallpox but as we know today, vaccines prevent a large number of diseases.
Although many developing countries still suffer from the burden of preventable infectious diseases, the U.S. has greatly increased the life expectancy and quality of life through the use of vaccines. In the 1940s, the U.S. recommended vaccines for diphtheria, pertussis and tetanus; polio was added in the 1950s. In the 1970s, measles, mumps and rubella (MMR) were added to list. Today in the U.S., immunizations are recommended for 17 vaccine-preventable diseases during one’s lifetime and more are available for individuals traveling outside of the U.S. Many of these vaccinations are combined so they can prevent multiple diseases from one series of immunizations. The increase in life expectancy in the 20th century is largely attributable to vaccines. For each birth cohort vaccinated, 33,000 lives are saved, 14 million cases of disease are prevented, healthcare costs are reduced by $9.9 billion and $33.4 billion is saved in indirect costs. The Bill Gates Foundation believes that vaccines are one of the most cost-effective investments in global health, saving about 2.5 million lives each year. One child dies every 20 seconds from vaccine-preventable diseases while tens of thousands of other children suffer from severe illnesses and permanently disabling diseases.
Despite the facts, less and less parents are choosing to vaccinate their children today because of fears that vaccines are unsafe. Much of the controversy started with Dr. Andrew Wakefield, a former British surgeon and medical researcher. Wakefield published a paper in 1998 linking the MMR vaccine to autism and bowel disease. Wakefield’s entire study was found to be fraudulent and the infamous paper was retracted in 2010. But, what got more attention than a retracted science paper was Jenny McCarthy sharing her personal life story of how her son got autism from a vaccine on the Oprah Show. Unfortunately, more moms keep up-to-date with Oprah and popular news rather than science and still do not know the truth behind Wakefield’s falsified study; therefore, the autism myth continues.
Furthermore, parents argue “herd immunity”. If your children are effectively vaccinated then why would I have to worry about mine? First, many vaccine-preventable diseases still exist in other countries and can easily be brought into our country; second, some individuals do not build immunity to the disease even after vaccination. The more and more parents that opt out of vaccinations, the less protection their children have from the rest of the “herd”. Additionally, parents argue that their children should contract diseases “naturally” through the environment to build immunity. Parents don’t fully understand the severity of these diseases because many have been virtually eradicated through the successful use of vaccines. Though some crippling effects of polio still linger, it is rare to come across someone wearing braces or using a wheelchair as a result of a polio infection in the U.S. Many vaccine-preventable diseases can cause death during the initial acute illness and if the individual survives, he or she may be left with chronic effects that last a lifetime. Polio can lead to temporary or permanent paralysis, deformities in the hips, ankles and feet; measles, mumps and varicella can all lead to brain damage and mumps is known to cause deafness; hepatitis B can cause permanent liver damage and even liver cancer. The list of damaging effects goes on and on.
In some areas throughout the U.S., as many as 1 in 20 kindergarteners have not been vaccinated. As the antivaccination fad grows in American so do the infectious disease rates. Measles was said to be eliminated from the U.S. in 2000 but an average of about 60 cases of measles occurs each year, typically from traveling. However, in 2011, there were 17 measles outbreaks in U.S. communities and the number of cases jumped to 222. In 2012, the U.S. had one of the largest pertussis outbreaks in nearly 50 years. Nationwide, over 85,000 vaccine-preventable diseases occur each year. I am not arguing that vaccines have no potential side effects and have never caused adverse effects or even death in children. However, I do think vaccines have done considerably more good than harm. So I urge parents, before deciding to withhold your children from vaccinations, look into the facts and make a decision based on science – not popular news. Although outbreaks of disease have been conquered in the past, many vaccine-preventable diseases remain throughout the world and the U.S. is not immune to future outbreaks.
Fifth of five student guest posts by Jonathan Yuska
The saying, “The more you know, the more you can control,” is no more meaningful than when used in the context of HIV detection and prevention. Public health advocates endlessly stress the need for knowing one’s status; and one would assume that any way in which the most amount of people can be tested would be beneficial for the population1. The Food and Drug Administration shared this same idea when they overwhelmingly approved the first ever over-the-counter (OTC) HIV testing kit in 20052; which in theory, sounds like a promising way to reduce the possible 350,000 HIV cases that remain undiagnosed in this country3. Though, some medical staff are still weary of this type of diagnostic method for reasons such that it breaks the linkage between the patient and long-term care. The debate on whether HIV testing should be—shall we say—left only to the professionals or put in the hands of everyday citizens is only just beginning; though, here are some points you may want to consider when making your own opinion on HIV home testing.
The OraQuick ADVANCE is one example of an in-home testing kit that provides the user with an accurate (sensitivity of 99.3% and specificity of 99.8%) and rapid means of HIV detection with nearly no invasiveness. In just 20 minutes and a swab of the mouth, individuals who may have been living their entire life unaware they are HIV positive, now can take that knowledge as empowerment to manage their health safely and finally receive the appropriate care they may desperately have needed. Supporters of in-home kits believe it offers a choice of what to do with the knowledge of being diagnosed and dismisses possible stigmatizations associated with being tested since testing can be done in the privacy of one’s own home. Proponents also feel that HIV home testing may become the new norm before engaging in intimacy and suggest testing kits come in boxes of two so partners can test each other4. The OTC HIV testing kits are hoped to slow down the more than 40,000 new infections3 that occur every year in the United States; though, some that believe kits such as OraQuick will make little difference in reducing the HIV infection crisis in the populations that need it most.
The HIV home testing kit is hoped to attract those at highest risk including young, low-income and education, non-white males who neither frequent medical care facilities nor are tested regularly on their HIV status5. Surveys conducted by the National Center for Health Statistics have shown that 79% of persons in these types of populations would indeed use home HIV tests if available; though, when participants in the survey were told the price of testing kits was $40, the approval rate of the kits dropped to 40%2. This raises some speculation on whether OTC kits will actually access these sorts of populations without first lowering the price to purchase them.
Rather than accessing those at highest risk, some naysayers anticipate the tests will predominantly appeal only to those “worry well” or hypochondriac individuals who continually test negative or new couples that want to verify their HIV statuses before sexual intimacy begins. Though, what one does with the knowledge of having tested negative for HIV is still under question. It may be seen that negative results actually promotes more risky sexual behaviors—since they were able to “get away” with it in the past—such as having intercourse without protection. This sort of risky behavior may expose the individual to a whole host of other sexually transmitted diseases2.
Issues with the proper usage of kits may also pose a problem in accurately diagnosing those who have been recently infected with HIV which could lead to false-negative results. Individuals participating in unsafe practices may be unaware of the 8-week “window period” needed for in-home tests to detect HIV antibodies (human antibody component is needed to determine HIV status in at-home tests [RNA tests commonly used by clinics can detect HIV within 9 to 11 days post infection]) and unwittingly spread their infection to others6.
False-positive results from in-home tests may also cause a great deal of damage to the validity of proven HIV detection methods as well as the likelihood of individuals to repeat HIV testing after receiving highly upsetting untrue news. False positive outcomes from tests are most common in populations with a low occurrence of disease in the first place—like in HIV—where the occurrence of unknown cases is roughly 0.2%. The ability to perfectly detect such a small percentage of people infected even with a test that is highly sensitive and specific is extremely unlikely and the predictive value of the test will be noticeably low2.
Lastly and most obviously is the disconnect from care that occurs from in-home diagnostic kits. Public testing focuses on linking HIV-positive patients with counseling and treatment; though, when this diagnosis is done in private, a person’s anxiety may force them to exile where they never seek treatment and may even contemplate suicide1. It is important to note that diagnosing patients is only half of the battle, linking them to the appropriate care is the other half—something home testing inherently does not do.
“The more you know, the more you can control” is a saying that is at the heart of reducing the amount of HIV transmissions person-to-person by knowing one’s status. HIV home testing kits such as OraQuick sounds like a promising way to reduce the number of transmissions since they are quick and convenient for the user, but whether these tests will actually reach those individuals who are at greatest risk is doubtful. At home kits may also promote risky behaviors, increase the numbers of false-positives and –negatives, and deteriorate the linkage to care that is vital to those with new diagnoses.
Will in-home HIV testing kits be the assistance needed in decreasing the HIV transmission concern—some professionals are questionable. Now after reviewing the facts on HIV home testing, what is your stance on the subject?
1. Chesney, Margaret A., and Ashley W. Smith. “Critical Delays in HIV Testing and
Care.” American Behavioral Scientist. Apr. 1999. 17 Feb. 2013 <http://abs.sagepub.com/content/42/7/1162.short>.
2. Walensky, Rochelle P., and David Paltiel. “Rapid HIV Testing at Home: Does It Solve
a Problem or Create One?” Annals of Internal Medicine (2006): 459-562.
3. Fleming, P. L. “HIV Prevalence in the United States, 2000.” Feb. 2002. 18 Feb. 2013
4. McNeil, Donald G. “Another Use for Rapid Home H.I.V. Test: Screening Sexual
Partners.” The New York Times. 5 Oct. 2012. 18 Feb. 2013 <file:///Users/ska020/Desktop/Another%20Use%20for%20Home%20H.I.V.%20Test%20-%20Screening%20Partners%20-%20NYTimes.com.webarchive>.
5. Phillips, Kathryn A. “Potential Use of Home HIV Testing.” The New England Journal
of Medicine. 11 May 1995. 18 Feb. 2013 <http://www.nejm.org/doi/full/10.1056/NEJM199505113321918>.
6. “Possible Exposure to HIV?” How long it takes to test HIV positive after infection.
Stop AIDS Project. 18 Feb. 2013 <http://stopaids.org/resources/possible-exposure-hiv/time-it-takes-test-positive>.
Third of five student guest posts by Dana Lowry
In 1911, Peyton Rous first discovered viruses can cause cancer. A chicken with a lump in her breast had been brought to Rous by a farmer. Rous prepared an extract that eliminated bacteria and tumor cells and injected this extract into other chickens—tumors grew. Rous suggested “a minute parasitic organism” was causing the tumor growth, which is now known to be a virus. However, Rous’ discovery remained very controversial, and it wasn’t until 1966 that he was awarded a Nobel Prize for his discovery. Since Rous’s discovery, researchers have found an estimated 15 percent of all cancers worldwide are associated with viruses. Some common virus and cancer associations are: human papilloma virus (HPV) and cervical cancer, hepatitis B and liver cancer and human T lymphotropic virus type 1 (HTLV-1) and T-cell leukemia.
Epstein-Barr virus (EBV), a member of the herpesvirus family, is one of the most common viruses worldwide. Among 35 to 40 year olds in the U.S., up to 95% have been infected with EBV. Oftentimes, children infected with EBV have no clinical signs or symptoms; however, 30% to 50% of adolescents and young adults exposed to EBV for the first time will develop infectious mononucleosis, commonly known as mono. In the U.S., individuals are usually exposed to EBV in adolescence or young adulthood compared to developing countries, where oftentimes individuals are exposed as infants or young children. EBV usually remains dormant in the body throughout an individual’s lifetime, similar to the varicella-zoster virus, the virus responsible for the chicken pox. EBV is known to play a role in Burkitt ’s lymphoma (cancer of the immune cells), nasopharyngeal cancer (cancer of the upper throat) and Hodgkin’s lymphoma (cancer of the lymphatic system), but can EBV also play a role in breast cancer?
In 2010, James Lawson and Benjamin Heng reviewed 27 papers concerning EBV and breast cancer associations. EBV infections are universal in high and low risk breast cancer groups, making it unlikely that EBV is the sole contributor to forms of breast cancer . However, the age at which EBV is contracted seems to play a role in the risk of developing breast cancer. Women in Western countries are at higher risk of developing breast cancer and tend to be infected with EBV during adolescence or young adulthood, whereas women from non-Western countries have a lower risk for developing breast cancer and tend be infected during infancy or early childhood. Hodgkin’s lymphoma shares a similar correlation with higher rates in Western countries . Although there seems to be a relationship between age of EBV infections and risk of breast cancer, potential confounders need to be considered. Women in developing countries tend to have more children, have children at a younger age and breastfeed their children for longer periods of time. Breastfeeding, having more children and having children earlier in life all seem to be protective factors against breast cancer.
Beyond epidemiological evidence, lies biological evidence. Twenty two of the studies Lawson and Heng reviewed were based on polymerase chain reaction (PCR) techniques. Issues have been found with standard PCR procedures, but it is becoming widely accepted that EBV can be identified in breast cancer tissue through specific PCR techniques . EBV genes have been found in breast cancers through polymerase chain reaction (PCR) analyses. EBV has not only been shown to shed in human breast milk , but it has also been shown to stimulate growth of human breast-milk cells . The mechanism by which EBV actually causes cell alterations is not known, but it is thought to be different from the mechanisms used in lymphomas and nasopharyngeal cancer .
It is unlikely that we can actually “catch” breast cancer, as EBV doesn’t seem to be the sole cause of breast cancer. EBV may contribute to breast cancer by altering genes in the breast cells which eventually leads the uncontrolled cell division, known as cancer. More importantly, it seems the age an individual is infected with EBV may play an even bigger role in the outcome of disease. An EBV vaccination is in the works that will hopefully prevent infectious mononucleosis and EBV-associated cancers. However, the vaccination may not prevent the EBV infection itself; it is targeted towards the most abundant protein on the virus and on virus-infected cells. If the vaccination proves to be successful, it will be interesting to see if a reduction in breast cancer rates will follow, along with the known cancers associated with EBV. Only time will tell.
- Lawson, J. and Heng, B. (2010). Viruses and Breast Cancer. Cancers 2010, 2(2), 752-772; doi: 10.3390/cancers2020752.
- Yasui et al. (2001). Breast cancer risk and “delayed” primary Epstein-Barr virus infection. Cancer Epidemiology, Biomarkers & Prevention, 10:9-16. http://cebp.aacrjournals.org/content/ 10/1/9.long.
- Junker et al. Epstein-Barr virus shedding in breast milk. (1991). The American Journal of the Medical Sciences, 302: 220–223. http://www.ncbi.nlm.nih.gov/pubmed/1656752.
- Xue et al. (2003). Epstein-Barr virus gene expression in human breast cancer: protagonist or passenger?. British Journal of Cancer, 89:113–119. http://www.nature.com/bjc/journal/ v89/n1/full/6601027a.html
Second of five student guest posts by Nai-Chung N. Chang
Tuberculosis (TB) is a major disease burden in many areas of the world. As such, it was declared a global public health emergency in 1993 by the World Health Organization (WHO). It is a bacterial disease that is transmitted through the air when an infected individual coughs, sneezes, speaks, or sings. However, not all individuals who contract the disease will display symptoms. This separates the infected into two categories, latent and active. Latent individuals are non-infectious and will not transmit the disease, whereas active individuals are able to transmit the disease.
TB is a significant concern in patients diagnosed with HIV, since individuals diagnosed with HIV and latent forms of TB infection is more likely to develop the disease, then the HIV negative individuals. In addition, in people living with HIV, TB is one of the leading causes of death. (CDC, 2012) The fact that latent forms of the disease are capable of becoming fully active forms given the right stimulus represents a high risk to individuals living in poor conditions, which is widely present in developing nations. It is of even greater concern to individuals who have immune system diseases, such as HIV. Individuals with latent TB infection depend on robust immune system responses to prevent the infection from going into active form. HIV and similar diseases targets and weakens immune systems so that the response to infections becomes weaker, providing increased risk of TB infections and the activation of latent forms.
TB is a major concern not only because of its status as a global epidemic. While there are many forms of prevention and treatment for the disease, such as antibiotics and vaccine, these treatments are not overly effective in combating and controlling the spread of the disease. TB is widespread and has a high chance of becoming resistant to any treatment that it is exposed to, especially antibiotics and other chemotherapeutic drugs such as isoniazid. Several of these strains already exist and each has varying levels of resistance, including Multidrug-Resistant (MDR) and Extensively Drug-Resistant (XDR). MDR is a strain that is resistant to two of the most often used and potent TB drugs, isoniazid and rifampin; whereas XDR is MDR strains that have developed resistance to any fluoroquinolone and at least one of three second-line drugs such as kanamycin or capreomycin. Also, the vaccine that has been developed for preventing TB is not overly protective, and sometimes fails to protect against infection. (CDC, 2012) The vaccine is not designed to prevent the infection of TB; instead, it is aimed towards boosting and speeding up the immune system response to any new infection so that the infected individual remains in latent forms. (Russell, et al., 2010)
The increasing trends in the resistance of TB to various treatments is a serious concern as it have major impacts in controlling the spread of the disease in many regions. This condition worsens with MDR and XDR TB. With regular, normal strains of TB, latent and early infections could be combated and controlled by a successful chemotherapeutic treatment even in patients with immune system diseases. However, with MDR and XDR TB, the strains are able to fully develop in an individual with weakened immune system, as evident in areas where incidence of TB and HIV is high, such as South Africa. (O’Donnell, et al., 2013) For cases with MDR and XDR strains, the weakened immune systems are not potent enough to prevent infections or keep them in latent form. Additionally, the active forms of these strains are resistant to common, and in some cases, advanced treatments.
With the increasing development of drug-resistant TB, the most effective way to combat TB is not only through vaccines and treatments. Instead, strict public health policy is needed to properly maintain control and combat the spread of TB. With a well-structured public health system, we can ensure that the long treatment of TB is complete, since most of the increase in the resistance to treatment often results from issues during treatment. Events such as patient non-compliance to the treatment and inadequate health-care supervision can all result in the development of new strains of the bacteria that have developed resistance to the treatments that was used. (Russell, et al., 2010) Also, a well-structured public health system can maintain better supply and quality of drugs throughout the treatment process, as well as the prevention and detection of possible new drug resistant strains. More importantly, it can maintain better surveillance and ensure patient compliance during the treatment process, which would help in reducing the development of drug resistant strains. The surveillance systems can also target comorbid diseases such as HIV to reduce risk factors for activating latent forms of the disease in patients with HIV and similar diseases.
CDC, 2012. Tuberculosis (TB). [Online]
Available at: http://www.cdc.gov/tb/topic/basics/default.htm
[Accessed 13 2 2013].
O’Donnell, M. R. et al., 2013. Treatment Outcomes for Extensively Drug-Resistant Tuberculosis and HIV Co-infection. Emerging Infectious Disease [Internet], 19(3).
Russell, D. G., Barry 3rd, C. E. & Flynn, J. L., 2010. Tuberculosis: What We Don’t Know Can, and Does, Hurt Us. Science, 328(5980), pp. 852-856.