Tuberculosis Skin Test(PPD Skin Test)

The tuberculosis skin test is a skin test which could be used for the detection of immune response to the bacterium(TB). 
This immune response can happen when someone currently has active TB infection, or they were exposed to TB infection in the past, or if they received the had been vacinated TB (such as in China and other asian countries). The WHO estimates that 2 billion people worldwide have latent TB infection, while around 3 million people worldwide die of TB per year. 

The tuberculosis skin test is also known as the tuberculin test or PPD test. PPD is the abbreviation of purified protein derivative. The mechanism of the PPD test is in fact with the infectionof M. tuberculosis bacterium. The bacterium produces a delayed  hypersensitivity skin reaction ( like athma is also a delayed hypersensitive reaction).The components of the organism are added into the extracts of culture filtrates and as the core elements of the tuberculin PPD. Reaction in the skin to tuberculin PPD begins with T cells which have been sensitized by prior infection. These sensitized T cells are recruited by the immune system to the skin site, and then release chemical messengers lymphokines. These lymphokines induce induration through local vasodilation leading to fluid deposition known as edema, fibrin deposition, and recruitment of other types of inflammatory cells to the area.

The incubation period of TB are usually 2 to 12 weeks which is necessary for the PPD test to be positive. Anyone can have a TB test, licluding infants, pregnant women, or HIV-infected people with no danger. It is only dangerous in people who have had a severe reaction to a previous tuberculin skin test.
To perform the PPD test, you will need to see your doctor twice. At the first visit, the health care provider will clean an area of your skin and injecte a small amount of PPD. The needle is gently placed under the top layer of skin, causing a bump (welt) to form which usually goes away in a few hours.
The most important visit is the second visit which is after 48-72 hours of the shot, you must return to your doctor's office to check the area to see if you have had a significant reaction to the PPD test.
And this is done for our international student every year:)

Watch Out These Signs For Heart Attack

Some people finally recognize that they have heart problems until they have a heart attack. Most of the cases, people who have heart attacks have already had coronary artery disease for many years. This causes recurring chest pain called angina or shortness of breath during exercise or exertion.
The most common signs of a heart attack are pain and shortness of breath.
The pain can spread from the chest down the left or right arm, and there can be pain in the back, in the neck or stomach.
The pain can be mild or very strong.
A heart attack often starts with sudden pain in the chest. But the symptoms can often start to be noticeable only slowly. People who have had heart attacks describe the pain as acute, burning or pressing. The pain goes on for more than five minutes and it does not get better when the person rests.
Another sign that it could be a heart attack is if the nitrate medication that a person with coronary artery disease uses for his or her chest pain does not work.
People who have a heart attack are often very afraid, their faces become pale and they break out in sweat. Many people who are having a heart attack have trouble breathing, and have nausea or vomiting. Often these symptoms are much stronger than the chest pain. Particularly for women, these could be the main signs of a heart attack. This is one of the reasons that women more often do not realise they are having a heart attack.
Many women mistakenly believe that heart attacks mostly affect men. But heart attacks are one of the main causes of death in women in industrialised countries. More women die from heart attacks than from breast cancer, for example.
The early signs of a heart attack are not just different from person to person. They can also be different from an earlier heart attack. It is also sometimes possible that a person is not aware of the heart attack. That is called a silent heart attack.
The typical signs of a heart attack that are less frequent than chest pain and shortness of breath include:

• A feeling of tightness or pressure in chest
• Pain or numbness in the upper body that spread to the shoulderblades, the neck and the jaw
• Lightheadedness or fainting
• Dizziness, nausea, vomiting
• Sweating
• Paleness and cold sweating

Important: When someone calls emergency for a heart attack, they should make it clear that it is a heart attack and an emergency doctor is needed.
While waiting for the emergency service to arrive, you can help a person having a heart attack by:

• Helping them keep calm
• Get them comfortable lying on their backs with their upper body a bit elevated
• Loosen any tight clothing
• Make sure they can get fresh air, by opening a window if necessary
• Give them any medication that they have had prescribed for an emergency

If the person passes out, begin CPR - heart-lung resuscitation (cardiopulmonary resuscitation).

Acquired Antimicrobial Resistance Genes

Antimicrobial agents for treatment of infectious diseases is a wonderful achievements in the 20th century. However, soon after their introduction, acquired resistance emerged and this new condition had to be followed with the introduction of  new antimicrobial agents.
A large number of different genes in different loci should be responsible for antimicrobial resistance. Identification of these genes is important to understand resistance epidemiology, for verification of nonsusceptible phenotypes and for identification of resistant strains, and then advanced to guide the usage in clinics.
Normally, the detection of resistance genes has been performed by PCR or microarrays. However, in several cases, it is necessary to perform supplementary sequencing of the amplified PCR products. As a result, it is expensive andtime-consuming to performacomplete identification of resistance genes present in a strain collection.
The cost of DNA sequencing has been reduced, almost 10-fold reduction in every five years. As a consequence, DNA sequencing is becoming increasingly affordable for routine use and was recently utilized for complete characterization of antimicrobial resistance and virulence gene content during the safety evaluation of 28 strains intended for use in human nutrition. The challenge is, however, to extract the relevant
information from the large amount of data that is generated by these techniques.
ResFinder is a web server which providing a convenient way of identifying acquired antimicrobial resistance genes in completely sequenced isolates, it can be accessed at www.genomicepidemiology.org. Continuously updation give us new information as new resistance genes are identified.

Myocardial Infarction Redefined

Myocardial infarction (MI) can be defined from a number of different perspectives related to clinical, electrocardiographic (ECG), biochemical and pathologic characteristics. The term MI also has social and psychological implications, both as an indicator of a major health problem and as a measure of disease prevalence in population statistics and outcomes of clinical trials.

In the distant past, a general consensus existed for the clinical entity designated as MI. In studies of disease
prevalence by the World Health Organization (WHO), MI was defined by a combination of two of three characteristics: typical symptoms (i.e., chest discomfort), enzyme rise and a typical ECG pattern involving the development of Q waves. However, current clinical practice, health care delivery systems, as well as epidemiologic studies and clinical trials, all require a more precise definition of MI.

It is accepted that the term MI reflects a loss of cardiac myocytes (necrosis) caused by prolonged ischemia. Ischemia is the result of a perfusion-dependent imbalance between supply and demand. Ischemia in a clinical setting can be identified from the patient’s history and from the ECG. Possible ischemic symptoms include chest, epigastric, arm, wrist or jaw discomfort with exertion or at rest. The discomfort associated with acute MI usually lasts at least 20 min, but may be shorter in duration. The discomfort may develop in the central or left chest and then radiate to the arm, jaw, back or shoulder.

The presence or absence and the amount of myocardial damage resulting from prolonged ischemia can be assessed by a number of different means, including pathologic examination, measurement of myocardial proteins in the blood, ECG recordings (ST-T segment wave changes, Q waves), imaging modalities such as myocardial perfusion imaging, echocardiography and contrast ventriculography.

Myocardial necrosis results in and can be recognized by the appearance in the blood of different proteins released into the circulation due to the damaged myocytes: myoglobin, cardiac troponins T and I, creatine kinase, lactate dehydrogenase, as well as many others (Fig. 2). Myocardial infarction is diagnosed when blood levels of sensitive and specific biomarkers, such as cardiac troponin and the MB fraction of creatine kinase (CK-MB), are increased in the clinical setting of acute ischemia. These biomarkers reflect myocardial damage but do not indicate its mechanism. Thus, an elevated value in the absence of clinical evidence of ischemia should prompt a search for other causes of cardiac damage, such as myocarditis.

OTITIS MEDIA

Last week we discussed ear infections in infectious disease class, I am interested in otitis media since it is second common infection in Childs around 1-6 year old. 

Otitis media is inflammation of the middle ear, or a middle ear infection. It occurs in the area between the tympanic membrane and the inner ear, including a duct known as the Eustachian Tube. Sometimes present as non-purulent fluid within the middle ear cavity. It affects more boys than girls, occurs more in cold weather. 1/3 of children will have 3 or more infections by age 3, 90% of children will have at least one infection by age 6.

Most common bacteria cause otitis media are: Streptococcus pneumonia, Haemophilus influenzae(non-typeable), Moraxella catarrhalis, Group A Streptococcus, Staph aureus, Pseudomonas aeruginosa, RSV assoc. with Acute Otitis Media. Most common pathogenesis is following an URI in which there is edema of the Eustachian Tube, leading to blockage. Stasis of these middle ear secretions leads to infection and irritation. Other factors include allergic rhinitis, nasal polyps, and adenoidal hypertrophy. 

Physical exams will find an erythematic, opaque, bulging tympanic membrane with loss of anatomic landmarks including a dull/absent light reflex. Pneumatic Otoscopy reveals that decreased tympanic membrane mobility and is the gold standard for the diagnosis. 

Complications of otitis media are serious such as hearing loss, acute mastoiditis, cholesteatoma, bacterial meningitis, epidural abscess, subdural empyema, brain abscess, otitic hydrocephalus, Lateral sinus thrombosis, etc. Earlier treatment makes better prognosis. Teatment often use Amoxicillin: 20-40 mg/kg/day tid for 10-14 days.

Myocarditis

Myocarditis could be caused by varieties of different disorders, many of which are infectious antigens. In Western countries, viral infections are by far the most common cause of myocarditis. Bacterial myocarditis is less common but should always be considered in patients with sepsis and ventricular dysfunction. The prevalence of bacterial myocarditis is difficult to estimate. The few published studies describe a post-mortem prevalence ranging from 0.2% to 1.5%. However, several of these studies included patients with bacterial myocarditis secondary to endocarditis.

Here I will be more focus on bacteria since we learned much more in bacteria. 

Bacterial myocarditis can develop by direct bacterial invasion or by toxins elaborated by the pathogen. The latter is a prominent feature of diphtheric and clostridial infections. Causes of ventricular dysfunction include: (1) myocardial inflammation and necrosis; (2) toxin-induced ventricular dysfunction; (3) sepsis-induced myocardial dysfunction; and (4) ventricular remodeling. Myocardial dysfunction is commonly associated with severe sepsis. Approximately 50%of patients with severe sepsis and septic shock can present with left ventricular systolic dysfunction.Right ventricular dysfunction is also common and usually follows the pattern of left ventricular dysfunction. The mechanisms involved in myocardial depression are most probably mediated by circulating cytokines such as tumor necrosis factor, interleukin-1 and interleukin-6. The subset of patients with sepsis-induced myocardial dysfunction that might have undiagnosed bacterial myocarditis is not known.

The definitive diagnosis of BM requires endomyocardial biopsy (EMB) or morphologically proven active myocarditis with evidence of bacterial invasion or positive tissue cultures. According to the Dallas criteria, active myocarditis is defined as”an inflammatory infiltrate of the myocardium with necrosis and/or degeneration of adjacent myocytes not typical of the ischemic damage associated with coronary heart disease.” EMB is highly specific for the diagnosis of myocarditis, but its sensitivity is low. Factors such as disease distribution (focal vs diffuse), stage of the disease process and sampling error influence the sensitivity of EMB. A clinical diagnosis of bacterial myocarditis may be reasonable when blood cultures are positive and there is proven active myocarditis on biopsy as long as other diagnoses have been excluded.

Campylobacter spp

Last week we learned several bacteria which could cause gastrointestinal infection. In the lab, I have been assigned a case study for campylobacter jejuni. Now I would like to share more info about Campylobacter spp.

Campylobacter spp could cause both diarrheal and systemic diseases, and the most common specie is Campylobacter jejuni. 

Campylobacter spp are Gram-negative rods with comma, S, or “gull-wing” shapes. They are motile, with a single polar flagellum, no spore or capsule. 

They could be cultured in an atmosphere with reduced O₂ (5% O₂) with added CO₂ (10% CO₂), at 42 ℃. Several selective media can be used, for eample, Skirrow’s medium. The colonies appear as watery and spreading, round and convex. 

Virulence factors are lipopolysaccharides (LPS) with endotoxic activity, cytopathic extracellular toxins and enterotoxins. 

The pathogenesis of the infection are: 1) The infection by oral route from food, drink, or contact with infected animals or animal products (Milk, meat products ); 2) Susceptible to gastric acid (about 10⁴ organisums); 3) Multiply in the small intestine invade the epithium produce inflammation  cause bloody stools. Occasionally, the bloodstream is invaded.

The symptoms for the infection usually are diarrhea, malaise, fever, abdominal pain. 

The diagnostic laboratory test is diarrheal stool specimen smears and culture. Smears: Gram-stained smears of stool may show the typical “gull-shaped” rods. Culture: (have been described above).

The control of the infection would be to control the source of infection which may be food (eg, milk, under-cooked fowl) or contract with infected animals or humans and their excreta.