Hello Everyone! This is the end of the semester and the final blog for infectious disease. It has been educational to find articles that were related to topics discussed in class and post them accordingly. I have actually enjoyed microbiology the past two semesters and the lab actually has me considering micro as a potential laboratory that I would like to work in. I hope everyone found the articles that I posted interesting. They demonstrated that what we discussed in lecture and performed in lab are everyday things that affect people worldwide. To all my followers and Mrs. Jeff, thanks for reading my blog and commenting!
Sincerely
Sassay
Assay to Assay
Monday, August 1, 2011
Sunday, July 24, 2011
Virology
This week we in Infectious Disease lecture, we discussed viruses. This included viral structure and testing methods for the viruses. One method of testing, NAAT or nucleic acid amplification testing, has always been interesting to me. NAAT testing is performed on deceased donors who are donating organs for transplantation. The NAAT testing results usually take several hours and if results are indeterminant, it take a lot longer. NAAT testing can be qualitative or quantitative. It can be used to screen for HBV, HCV, HIV,CMV, HSV, and other viruses. NAAT testing was developed to shorten the window period or time or the time a patient has been infected and symptoms appear.
Another testing method that was discussed during lecture was Enzyme-linked immunosorbent assay (ELISA) which is solid phase or membrane immunoassays. Most ELISA assays use a labeled antigen to detect a specific antibody and a captured or sandwich method where an antigen/antibody complex is formed. The picture below demonstrates the steps in the assay.
Thursday, July 14, 2011
Outbreak of Campylobacter in Alaska Linked to Raw Milk
The state of Alaska Section of Epidemiology (SOE) is investigating four recent cases of Campylobacter infection associated with drinking raw milk from an Alaska farm. According to a recent epidemiology bulletin, on June 15, 2011, SOE was notified by the Alaska State Public Health Laboratory of four Campylobacter jejuni isolates with identical pulsed-field gel electrophoresis (PFGE) patterns. After conducting interviews of the four individuals, health officials discovered that the consumption of unpasteurized, or raw, milk was the only exposure common to all ill persons.
During their investigation SOE learned the following:
All four persons with matching Campylobacter isolates experienced acute gastroenteritis in May and June 2011. Patient ages ranged from 1 – 81 years. All four persons were living in Southcentral Alaska at the time of their illness, and all reported consuming raw milk from the same cow share farm in the Matanuska-Susitna Valley.Although Alaska state regulations do not permit the sale of raw milk, owning shares of an animal to receive that animal’s milk is permissible. Unlike milk supplied by commercial outlets, there is no testing or pasteurization required of milk before distribution from a cow-share program.
SOE reported that:
With the onset dates for the four confirmed cases scattered over almost a month-long period, it is unlikely that there was a single “bad batch” of milk, but rather multiple batches of contaminated milk. Raw milk outbreaks can be intermittent and protracted, and this outbreak might well be ongoing. Therefore, we strongly encourage health care providers and the general public to report to SOE all cases of acute gastroenteritis following consumption of raw milk. By interviewing ill persons, we are able to better understand the factors associated with this outbreak and thereby provide more specific control measures to prevent future illness from occurring.In light of the potentially ongoing Campylobacter jejuni outbreak, the Alaska Department of Health and Social Services issued a press release today urging anyone who has consumed raw milk and subsequently experienced acute gastrointestinal illness (i.e. diarrhea, vomiting, cramps, fever) since March 2011 to contact the Section of Epidemiology at 907-269-8000.
Dr. Joe McLaughlin, chief of the Alaska SOE, stated, “Raw milk is an ideal substance for the proliferation of bacteria introduced through fecal contamination.” Moreover, he added, “Unpasteurized milk can be infected with a number of pathogens including Listeria, Salmonella, and as we’ve seen in this case, Campylobacter.”
CLSI Publishes Updated Antimicrobial Susceptibility Testing Standard
The Clinical and Laboratory Standards Institute have recently published the annual update of the well-known antimicrobial susceptibility testing standard, Performance Standards for Antimicrobial Susceptibility Testing; Twenty-First Informational Supplement (M100-S21), which is arranged in tabular format and provides updates of the latest recommendations for detecting emerging resistance of aerobic bacteria.
Therapeutic breakpoints included in the supplement are applied to MIC values determined by standard methods in order to assign an interpretation of susceptible, intermediate, or resistant. This essential information assists clinicians with drug selection and interpretation, and provides quality control and troubleshooting guidelines for clinical microbiology laboratories using the procedures standardized in CLSI documents Performance Standards for Antimicrobial Disk Susceptibility Tests; Approved Standard—Tenth Edition (M02-A10) and Methods for Dilution Antimicrobial Susceptibility Tests for Bacteria That Grow Aerobically; Approved Standard—Eighth Edition (M07-A8).
Clinicians depend heavily on information from the clinical microbiology laboratory for treatment of infected patients, especially those that are seriously ill. The clinical importance of antimicrobial susceptibility test results requires that these tests be performed under optimal conditions within laboratories that have the capability to provide results for the newest antimicrobial agents.
Richard B. Thomson, Jr., PhD, D(ABMM), FAAM, Evanston Hospital, NorthShore University HealthSystem, and the member subcommittee and working groups that developed the document says, “We review and use M100 supplements to stay current with methods needed for accurate antimicrobial susceptibility testing and result interpretation. Clinical microbiologists like myself realize that susceptibility values and interpretive criteria accompanying the culture report are the most important components of the microbiology report. Whether one uses manual or automated susceptibility testing methods, the M100 document is required knowledge for technical, administrative, and medical personnel. In fact, we review content each year with our Infectious Diseases Department and our antimicrobial pharmacist, who refers to our M100 copy so much that we have suggested she get her own!”
Therapeutic breakpoints included in the supplement are applied to MIC values determined by standard methods in order to assign an interpretation of susceptible, intermediate, or resistant. This essential information assists clinicians with drug selection and interpretation, and provides quality control and troubleshooting guidelines for clinical microbiology laboratories using the procedures standardized in CLSI documents Performance Standards for Antimicrobial Disk Susceptibility Tests; Approved Standard—Tenth Edition (M02-A10) and Methods for Dilution Antimicrobial Susceptibility Tests for Bacteria That Grow Aerobically; Approved Standard—Eighth Edition (M07-A8).
Clinicians depend heavily on information from the clinical microbiology laboratory for treatment of infected patients, especially those that are seriously ill. The clinical importance of antimicrobial susceptibility test results requires that these tests be performed under optimal conditions within laboratories that have the capability to provide results for the newest antimicrobial agents.
Richard B. Thomson, Jr., PhD, D(ABMM), FAAM, Evanston Hospital, NorthShore University HealthSystem, and the member subcommittee and working groups that developed the document says, “We review and use M100 supplements to stay current with methods needed for accurate antimicrobial susceptibility testing and result interpretation. Clinical microbiologists like myself realize that susceptibility values and interpretive criteria accompanying the culture report are the most important components of the microbiology report. Whether one uses manual or automated susceptibility testing methods, the M100 document is required knowledge for technical, administrative, and medical personnel. In fact, we review content each year with our Infectious Diseases Department and our antimicrobial pharmacist, who refers to our M100 copy so much that we have suggested she get her own!”
Actinomyces
Actinomyces-Induced Inflammatory Pseudotumor of the Lymph Node Mimicking Scrofula
From University of Chicago, Chicago, IL 60637.
Background: Inflammatory pseudotumor is a rare condition characterized by an aberrant immunologic response that manifests as tumor-like masses in various anatomical locations. Two previous case reports described Actinomyces as a trigger for abdominal inflammatory pseudotumor (1, 2).
Objective: To report what we believe is the first case of Actinomyces-induced inflammatory pseudotumor with primary lymph node involvement.
Case Report: A 34-year-old woman with a history of systemic lupus erythematosus presented to an outpatient clinic with painful swelling on the left side of the neck, a 7-day history of temperatures up to 39.4 °C, and a 3-day history of cough. Her systemic lupus erythematosus was controlled with methotrexate and hydrochloroquine. She received antibiotic therapy for presumed lymphadenitis.
She returned to the clinic 3 days later with no improvement in her symptoms. At that time, physical examination was notable for a firm, tender left submandibular mass without erythema or fluctuance and decreased breath sounds at the right lung base. Chest computed tomography showed a consolidation in the right lower lobe (Figure, A). Further history revealed that the patient had a positive purified protein derivative test several years earlier but did not begin antituberculous therapy. She was admitted to the hospital for suspected reactivation mycobacterial tuberculosis causing pneumonia and lymphadenopathy (scrofula).
Figure. Actinomyces-induced inflammatory pseudotumor with primary lymph node involvement.
A. Noncontrast coronal computed tomographic scan of the lungs showing right lower-lobe consolidation. B. Biopsy specimen of the lymph node showing broadening of connective tissue framework of the lymph node (pale areas) (hematoxylin–eosin stain; original magnification, × 40). C. Higher-magnification view of panel B showing expansion of sclerosed mesenchymal tissue in the trabeculae of the lymph node with proliferation of spindle cells, vessels, and inflammatory cells (hematoxylin–eosin stain; original magnification, × 400).
Fine-needle aspiration biopsy of the lymph node showed reactive features. Transbronchial biopsy of the lung lesion showed chronic inflammation without granulomas. Neither biopsy culture yielded fungal or bacterial growth, including acid-fast bacilli. Results of tests for legionella, histoplasma, and blastomycosis antigen were negative.
Pathologic examination of an excisional biopsy specimen of the lymph node revealed preserved architecture with focal paracortical hyperplasia and inconspicuous lymphoid follicles. In addition, there was expansion of the capsule, trabeculae, and hilum by sclerosed mesenchymal tissue that contained scattered spindly and polygonal cells; small blood vessels; and inflammatory cells, including plasma cells, histiocytes, and lymphocytes, without evidence of organisms, granulomas, or necrosis (Figure, B and C). Immunohistochemistry revealed no phenotypical abnormalities. These findings were consistent with inflammatory pseudotumor of the lymph node (3).
The patient began methylprednisolone therapy, and her neck swelling decreased substantially. After 12 days, the culture from her biopsy specimen yielded Actinomyces species. She started a 12-month course of amoxicillin therapy. Methylprednisolone therapy was switched to prednisone therapy, and she was discharged receiving a regimen of prednisone with a plan to taper the dosage over 3 months. Three months later, she was asymptomatic and repeated computed tomography showed complete resolution of her lung lesion.
Discussion: Inflammatory pseudotumor is a histologic diagnosis characterized by a proliferation of myofibroblasts with an infiltrate of inflammatory cells, such as lymphocytes, histiocytes, and plasma cells (3, 4). Affected patients commonly present with constitutional symptoms and masses in the lungs, spleen, liver, gastrointestinal tract, bladder, orbit, or lymph nodes (4). Inflammatory pseudotumor encompasses a wide spectrum of conditions, including inflammatory myofibroblastic tumor, plasma cell granuloma, or xanthofibroma (5).
Inflammatory pseudotumor may be a primary immunologic lesion in some cases and a reaction to an infection in others. In rare cases, this condition has been linked to neoplastic processes. Inflammatory pseudotumor of the lymph node is a reactive process centered on the connective tissue framework of the lymph node (3). The disease course is usually benign, and this condition is managed with excision or steroids plus treatment of any underlying cause.
In this patient, actinomycosis was the trigger. Actinomyces are gram-positive, filamentous, commensal bacteria normally found in the human gastrointestinal tract. Actinomyces infection generally occurs in immunosuppressed patients or when the integrity of the gastrointestinal mucosal layer is compromised.
Conclusion: Inflammatory pseudotumor represents a diagnostic conundrum, because its clinical features can be consistent with cancer, infectious disease, or primary immunologic disease. No radiologic or laboratory tests are specific for this condition. This case highlights the diagnostic importance of biopsy and cultures in patients who present with fever and unexplained lymphadenopathy
Tuesday, July 12, 2011
Attack of the hyperbugs
Attack of the hyperbugs: We've had superbugs, but now there are strains so resilient that no drugs will kill them
By Alice GrebotLast updated at 10:00 PM on 9th July 2011
The term superbug has become frighteningly familiar over the past decade. These bacteria, which have become resistant to the antibiotics
used to treat them – in other words, the medicines no longer work – are a major cause of hospital-acquired infections and cost the NHS £1billion a year to tackle.An estimated 25,000 patients die of drug-resistant infections each year,
with the most common, MRSA, slowly being superseded by a raft of new, even more deadly strains.
These have been dubbed hyperbugs and are partly fuelled by the growth
of health tourism with patients bringing back new strains from hospitals
abroad.
Earlier this year, the World Health Organisation warned that the situation
had reached a critical point and said that if no action was taken, 'the
world is heading towards a postantibiotic era, in which many common
infections will no longer have a cure and, once again, kill unabated.'
So what are these bugs, how do you catch them and, more importantly,
how can they be avoided? Here, DR KIM HARDIE, associate
professor in molecular microbiology at Nottingham University, explains what you need to know.
THE EVOLUTION OF A KILLER
Some superbugs are naturally resistant to antibiotics, but in other cases they have undergone changes to enable them to survive.
Mutations (changes) in the genetic code of all cells – ours and the bacteria – happen all the time. If a mutation occurs that prevents a bacterium from
being killed by an antibiotic, this bacterium will live while the others around it are killed when the antibiotic treatment is given.
The resistant bacterium will then reproduce.
Superbugs have evolved in hospitals where there are lots of antibiotics.
The resistant bacteria multiply and share their new genes with other bacteria, which can lead to a set of anti-biotic resistance genes
in a single bacterial cell, and a superbug is born.
WHO IS MOST AT RISK?
Many superbugs live harmlessly on or in the body and only cause problems when the immune system becomes weakened by other illness,
or if they enter a wound.
Those who are already ill are most susceptible as their immune systems
are already busy fighting something else. This also applies to people who have been weakened by surgery, childbirth, old age or drug treatments,for example.
The young are also at risk, especially babies.
HOW DO THEY SPREAD?
In the same way as any other bacteria – through touching contaminated
surfaces and then touching a vulnerable person.
The bacteria may lurk on a surface, someone's hand or be moving from a part of the body where they do no harm to another part where they can cause an infection.
You can catch superbugs anywhere, but you're more likely to find them in a hospital as this is where a high concentration of those susceptible to infection are found.
Alongside wounds, superbugs can enter the body via a device such as a catheter or intravenous line. Others enter through the mouth, nose or urinary tract directly.
HOW TO AVOID THEM
Superbugs are no easier to catch than other germs, so if you practise good hygiene, you can avoid them.
Wash hands well after going to the toilet, before touching wounds or a sick
person, before eating and so on.
There are kits available to protect patients from superbugs, usually containing antibacterial surface wipes, body washes and sprays for fabric.
There is no harm buying one if you or a relative is going into hospital. But
there is soap and alcohol hand gel at the hospital already.
If healthcare workers don't wash their hands when you ask, having a
kit nearby would enable a patient to do something if they were worried,
and reducing stress is a good way to speed recovery from illness.
WHAT ARE THE MOST COMMON TYPES?
Methicillin-resistant Staphylococcus aureus (MRSA) and Clostridium
difficile (C.diff) are the most frequently reported. Staphylococcus aureus (S.aureus) is a common skin bacterium, which has become resistant
to methicillin, a type of penicillin that used to be able to kill it, as
well as other antibiotics.
One in three people have S.aureus living harmlessly on their skin and
in their nose, and a proportion carry MRSA harmlessly. It is only when
bacteria get into a wound that they cause problems. Infection causes
abscesses and boils and can be fatal if it enters the bloodstream.
NHS patients going into hospital for a relevant planned procedure should now be screened for MRSA in advance. If not, you could ask to be, or insist everyone washes their hands before touching you as the MRSA may
come from someone else rather than yourself.
If a patient is found to be carrying MRSA, treatment involves using an antibacterial wash or powder and a special cream in their nose. MRSA infections have also been identified in healthy individuals who haven't
been hospitalised, which is called Community- acquired MRSA.
Methicillinsensitive Staphylococcus aureus (MSSA) is the same bacterium
and produces the same symptoms as MRSA but it is not resistant tomethicillin.
Actress Leslie Ash was awarded a record £5 million in compensation
in 2008 after contracting MSSA while receiving treatment for broken ribs and a punctured lung at Chelsea and Westminster Hospital four years earlier. A spinal infection almost paralysed her and she continues to use a walking stick.
C.diff is a bacterium carried naturally in the gut of around two thirds of children and three per cent of adults. It rarely causes problems in healthy people.
However, some antibiotics can upset the balance of 'good' bacteria
in the gut, allowing C.diff to multiply and attack the body. Symptoms
include diarrhoea and severe inflammation of the bowel which can be fatal.
C.diff is spread through contact from faeces and isn't killed by alcohol
gels, so one should use warm water and soap to wash hands.
RISE OF THE HYPERBUGS
Perhaps the most alarming superbugs around at the moment are S.
aureus strains, which produce a toxin called Panton-Valentine
Leukocidin (PVL). PVL kills white blood cells and skin tissue. Infections
have increased ten-fold in the past six years.
As well as being hard to kill, it is able to infect healthy people. Some strains can't be killed by methicillin.
In 2010, there were 2,227 cases of PVL in England, up from 224 in 2005.
New Delhi metallo-beta-lactamose (NDM-1) is also a concern. NDM-1 is
a gene that can jump between bacteria, making the strain resistant to
some of the most powerful antibiotics that are often used as a last resort
– hence the moniker hyperbug.
Two types of bacteria have been host to NDM-1: the gut bacterium
E.coli and lunginfecting Klebsiella pneumonia. It was brought to the UK by
patients who had travelled to countries such as India or Pakistan for
medical treatment.
There are only two antibiotics left that can kill these bacteria.
According to the Health Protection Agency, 109 cases of bacteria with
NDM-1 have been recorded in the UK to date.
WHAT DOES THE FUTURE HOLD?
Once resistant strains evolve, the number of infections will remain similar (or fall, hopefully, due to improved hygiene).
However, deaths will increase. Since 2005, there have been only two new antibiotics that have been put through trials.
It is essential that procedures and money are put in place to look for and test novel anti-biotics or other forms of drug treatment that will kill bacteria.
In the meantime, the public (and doctors) must learn not to use antibiotics unless they are absolutely necessary.
Unless drastic steps are taken now, a post-antibiotic era is a matter of when, not if.
Read more: http://www.dailymail.co.uk/health/article-2012905/Attack-hyperbugs-Weve-superbugs-strains-resilient-drugs-kill-them.html#ixzz1RuaF1UZ8
used to treat them – in other words, the medicines no longer work – are a major cause of hospital-acquired infections and cost the NHS £1billion a year to tackle.An estimated 25,000 patients die of drug-resistant infections each year,
with the most common, MRSA, slowly being superseded by a raft of new, even more deadly strains.
These have been dubbed hyperbugs and are partly fuelled by the growth
of health tourism with patients bringing back new strains from hospitals
abroad.
New threat: The New Delhi metallo-beta-lactamose (NDM-1) is resistant to most antibiotics
had reached a critical point and said that if no action was taken, 'the
world is heading towards a postantibiotic era, in which many common
infections will no longer have a cure and, once again, kill unabated.'
So what are these bugs, how do you catch them and, more importantly,
how can they be avoided? Here, DR KIM HARDIE, associate
professor in molecular microbiology at Nottingham University, explains what you need to know.
THE EVOLUTION OF A KILLER
Some superbugs are naturally resistant to antibiotics, but in other cases they have undergone changes to enable them to survive.
Mutations (changes) in the genetic code of all cells – ours and the bacteria – happen all the time. If a mutation occurs that prevents a bacterium from
being killed by an antibiotic, this bacterium will live while the others around it are killed when the antibiotic treatment is given.
The resistant bacterium will then reproduce.
Superbugs have evolved in hospitals where there are lots of antibiotics.
The resistant bacteria multiply and share their new genes with other bacteria, which can lead to a set of anti-biotic resistance genes
in a single bacterial cell, and a superbug is born.
WHO IS MOST AT RISK?
Many superbugs live harmlessly on or in the body and only cause problems when the immune system becomes weakened by other illness,
or if they enter a wound.
Those who are already ill are most susceptible as their immune systems
are already busy fighting something else. This also applies to people who have been weakened by surgery, childbirth, old age or drug treatments,for example.
The young are also at risk, especially babies.
HOW DO THEY SPREAD?
In the same way as any other bacteria – through touching contaminated
surfaces and then touching a vulnerable person.
The bacteria may lurk on a surface, someone's hand or be moving from a part of the body where they do no harm to another part where they can cause an infection.
You can catch superbugs anywhere, but you're more likely to find them in a hospital as this is where a high concentration of those susceptible to infection are found.
Alongside wounds, superbugs can enter the body via a device such as a catheter or intravenous line. Others enter through the mouth, nose or urinary tract directly.
HOW TO AVOID THEM
Superbugs are no easier to catch than other germs, so if you practise good hygiene, you can avoid them.
Wash hands well after going to the toilet, before touching wounds or a sick
person, before eating and so on.
There are kits available to protect patients from superbugs, usually containing antibacterial surface wipes, body washes and sprays for fabric.
There is no harm buying one if you or a relative is going into hospital. But
there is soap and alcohol hand gel at the hospital already.
If healthcare workers don't wash their hands when you ask, having a
kit nearby would enable a patient to do something if they were worried,
and reducing stress is a good way to speed recovery from illness.
WHAT ARE THE MOST COMMON TYPES?
Methicillin-resistant Staphylococcus aureus (MRSA) and Clostridium
difficile (C.diff) are the most frequently reported. Staphylococcus aureus (S.aureus) is a common skin bacterium, which has become resistant
to methicillin, a type of penicillin that used to be able to kill it, as
well as other antibiotics.
One in three people have S.aureus living harmlessly on their skin and
in their nose, and a proportion carry MRSA harmlessly. It is only when
bacteria get into a wound that they cause problems. Infection causes
abscesses and boils and can be fatal if it enters the bloodstream.
Struck down: Leslie Ash won £5m damages after catching MRSA
come from someone else rather than yourself.
If a patient is found to be carrying MRSA, treatment involves using an antibacterial wash or powder and a special cream in their nose. MRSA infections have also been identified in healthy individuals who haven't
been hospitalised, which is called Community- acquired MRSA.
Methicillinsensitive Staphylococcus aureus (MSSA) is the same bacterium
and produces the same symptoms as MRSA but it is not resistant tomethicillin.
Actress Leslie Ash was awarded a record £5 million in compensation
in 2008 after contracting MSSA while receiving treatment for broken ribs and a punctured lung at Chelsea and Westminster Hospital four years earlier. A spinal infection almost paralysed her and she continues to use a walking stick.
C.diff is a bacterium carried naturally in the gut of around two thirds of children and three per cent of adults. It rarely causes problems in healthy people.
However, some antibiotics can upset the balance of 'good' bacteria
in the gut, allowing C.diff to multiply and attack the body. Symptoms
include diarrhoea and severe inflammation of the bowel which can be fatal.
C.diff is spread through contact from faeces and isn't killed by alcohol
gels, so one should use warm water and soap to wash hands.
RISE OF THE HYPERBUGS
Perhaps the most alarming superbugs around at the moment are S.
aureus strains, which produce a toxin called Panton-Valentine
Leukocidin (PVL). PVL kills white blood cells and skin tissue. Infections
have increased ten-fold in the past six years.
As well as being hard to kill, it is able to infect healthy people. Some strains can't be killed by methicillin.
In 2010, there were 2,227 cases of PVL in England, up from 224 in 2005.
New Delhi metallo-beta-lactamose (NDM-1) is also a concern. NDM-1 is
a gene that can jump between bacteria, making the strain resistant to
some of the most powerful antibiotics that are often used as a last resort
– hence the moniker hyperbug.
Two types of bacteria have been host to NDM-1: the gut bacterium
E.coli and lunginfecting Klebsiella pneumonia. It was brought to the UK by
patients who had travelled to countries such as India or Pakistan for
medical treatment.
There are only two antibiotics left that can kill these bacteria.
According to the Health Protection Agency, 109 cases of bacteria with
NDM-1 have been recorded in the UK to date.
WHAT DOES THE FUTURE HOLD?
Once resistant strains evolve, the number of infections will remain similar (or fall, hopefully, due to improved hygiene).
However, deaths will increase. Since 2005, there have been only two new antibiotics that have been put through trials.
It is essential that procedures and money are put in place to look for and test novel anti-biotics or other forms of drug treatment that will kill bacteria.
In the meantime, the public (and doctors) must learn not to use antibiotics unless they are absolutely necessary.
Unless drastic steps are taken now, a post-antibiotic era is a matter of when, not if.
Read more: http://www.dailymail.co.uk/health/article-2012905/Attack-hyperbugs-Weve-superbugs-strains-resilient-drugs-kill-them.html#ixzz1RuaF1UZ8
Tuberculosis in Jefferson County Alabama
Tuberculosis (TB) ![]()
Tuberculosis is caused by the bacterium, Mycobacterium tuberculosis. It is spread through the air by a person with an active case of TB located in the lungs when coughing, sneezing or speaking. While TB commonly involves the lungs, TB can develop in other organs including the kidneys, brain, spine, and bone. Not all individuals infected with Mycobacterium tuberculosis will develop an active case of the disease. TB skin and blood testing only indicates if an individual is infected with the organism that causes the disease; the diagnosis of active or latent TB requires additional testing including chest x-rays and sputum cultures. The risk of exposure to TB is increased in high population density settings such as prisons, homeless shelters, and hospitals. Latent TB Infection
In
![]()
In
Individuals with
In 2010, the national rate of tuberculosis (TB) was 3.6 cases per 100,000 population, representing a 3.9% decline in the rate from 2009.
(LTBI) occurs when an individual becomes infected with Mycobacterium tuberculosis, but the immune system is able to contain the bacteria, and the person never develops signs or symptoms of the disease. In this situation, the bacteria are not growing, and the individual with Latent TB cannot transmit the disease to another person. The disease may lie dormant of years, or even a life time, in an individual with Latent TB. TB Disease, the immune system is compromised, and the bacteria begin to grow. If the growth is occurring in the lungs, the individual is capable of transmitting the disease. Individuals with a compromised immune system, such as HIV and transplant patients, are at increased risk for developing the active disease. Active TB generally develop a cough accompanied by chest pain lasting at least three weeks. The coughing may produce blood or sputum in which Mycobacterium tuberculosis can be found. The individual may also experience loss of appetite, weight loss, weakness or fatigue, fever, chills, and/or night sweats. These individuals need to undergo a six to twelve month course of treatment. Failure to comply and complete the course of treatment increases the risk that the TB bacteria develop resistance to the drugs of choice and that the disease remains active. 4 Tuberculosis rates in Jefferson County have also declined, as illustrated in Figure 4.1. Twenty-nine cases of tuberculosis were diagnosed in Jefferson County in 2010, resulting in a rate of 4.4 cases per 100,000 population. During 2010, only 3 of the diagnosed cases were among the homeless, a decrease to 10.3% of all cases from 16.2% (6 cases) in 2009. While the increase in multi-drug resistant (MDR) tuberculosis has been of increasing concern at the national level, there have been no cases of MDR tuberculosis reported in Jefferson County since 2006. 4 Centers for Disease Control and Prevention; Trends in Tuberculosis --- United States, 20109; MMWR 60(11);333-337 (
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6011a2.htm?s_cid=mm6011a2_e%0d%0a ) 
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