Week 9: Final Blog of the Semester!

Hello everyone!  It is hard to believe that the semester is nearly over and we are halfway through the program!  Time has flown!  We certainly have covered quite a bit over the last couple of months in Infectious Diseases. We covered everything from infections of sterile body fluids such as CSF and blood to antibiotic susceptibility testing and virology.  In addition, we correlated what was learned in the classroom directly to testing performed in the student laboratory.  We’ve learned quite a bit and hopefully everyone is ready for the ASCP exam!  Good luck on finals!

The following is a link to a site that has a number of quizzes covering essentially all of the material we covered this semester in Infectious Diseases.  Hope you all find it useful in studying for the final!

http://microbiology.jbpub.com/8e/quizzes.cfm 

Week 8: Virology

Hello everyone, I’m sure everyone is happy to have completed the lab practical this afternoon!  This week we discussed viruses and basic methods for detecting viruses in patient specimens.  I will briefly discuss each method of viral detection below.

Cytological and Histological Exam

During a cytological exam, the tissue samples are stained with any of a variety of stains such as PAP, Giemsa, or H & E.  The tissue samples are then examined for synctia (multinucleated cells) and nuclear and cytoplasmic inclusions, which are clusters of viruses or viral materials.  This method is less sensitive than the culture method but safer and easier than culturing dangerous viruses.

Electron Microscopy

Electron microscopy allows for visualization of the actual viruses.  This technique is used more in research laboratories than clinical laboratories.  Electron microscopy can be useful in detecting viruses that can’t be grown using culture techniques.  This method however is labor intensive and relatively insensitive compared to other methods. 

Direct Detection of Viral Ag

Direct detection of viral antigen involves detection of antigens in specimens or after viruses has grown in cell culture.  Antigen detection can be accomplished by either direct fluorescence antibody detection methods which utilize fluorescently labeled antibodies that bind directly to viral antigens in the specimen or indirect fluorescence methods that involves direct labeled anti-human globulin against antibodies attached to corresponding viral antigens in a specimen.  Fluorescence is then measured and observed using a fluorescence microscope.

NA Probes

               

Nucleic acid probes can be useful in viral detection when the amount of virus is abundant.  This technique can be used when culture is not possible or slow. 

Conventional Cell Cultures and Shell Vial Method

The conventional cell culture method is the gold standard for viral detection.  Viruses require cells in order to survive and replicate, so culture by conventional methods is not possible.  A variety of cell lines including primary, low passage, and continuous cell lines are used to facilitate the growth of viruses.  Cultures are then examined for cytopathetic effect (morphological changes to the cells0 using a microscope or tested for hemadsorption/hemagglutination.  The Shell Vial technique is a combination of the conventional cell culture method and fluorescent antibody labeling technique.

Serological Testing

When viruses can not be grown using culture techniques and direct antigen detection is not possible, antibody detection can be performed.  Detection of IgM antibodies to viral antigens indicates an acute stage of infection while detection of IgG antibodies to viral antigens indicates immunity to the virus.

The following article discusses the discovery of a new Ebola virus species and discusses some of the viral detection techniques we discussed in class.  Enjoy!

 http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000212

Week 7 Laboratory: Antibiotic Susceptibility Tests

Hello everyone! This week in the laboratory component of this course we completed antibiotic susceptibility testing on various organisms. I am going to review and summarize the principle of one of the tests performed in the laboratory in order to help everyone have a firmer grasp of the underlying concepts behind the test we performed. How you all find this helpful!

Microdilution Method

The basic principle behind the tube broth dilution method and the microdilution method are the same. In both, two fold dilutions of antimicrobics are tested against a standardized concentration of an organism being tested. The lowest concentration of a drug that will inhibit the growth of a organism is determined (this is the MIC, or minimal inhibitory concentration) by this method. The microdilution method utilizes bacterial broth volumes of 0.05-0.1 ml and microtiter trays with dilutions of antimicrobics dehydrated or frozen in the wells. A standardized suspension of a organism is prepared and poured into a seed tray. A special inoculator device (we used the Renok inoculator device) is used to draw up the broth and dispense a specific amount in each microtiter well. The trays are then incubated in a regular incubator. The results are read after 16-20 hours. Bacterial growth is determined by observing the bottom of the well with a mirror and looking for turbidity. Turbidity indicates growth and clear solution indicates no growth. The MIC can then be determined by observing the amount of drug in the last clear well, going from highest concentration of antimicrobial to the lowest concentration of antimicrobial.

I was interested in finding an article concerning drug-resistant bacteria, so I found this interesting article and video concerning MRSA found on bedbugs!  Hope you enjoy it!http://abcnews.go.com/Health/Wellness/bedbugs-carry-drug-resistant-bacteria-study/story?id=13571434

　

Week 7: Antimicrobial Action and Antimicrobial Susceptibility Tests

Hello everyone! I’m sure everyone is happy about completing our second Infectious Diseases exam and is ready for the weekend! However, if you want to get a jump start on studying for our next exam, you have come to the right spot! This week we discussed antimicrobial action and susceptibility tests in lecture. Since this unit involved quite a few new terms and concepts, I decided to create a matching quiz in order to help everyone obtain a firmer grasp on the concepts presented in Tuesday’s lecture. Hope this helps! Match the terms on the left with the definitions on the right.

1. Bactericidal	A. Chemical produced by organism that inhibits growth of other microorganisms
2. Broad-spectrum antibiotics	B. Agents that inhibit the growth of microorganisms
3. Antibiotic	C. Antibiotics that are effective against specific families or even species of microorganisms
4. Bacteriostatic	D. Agents that kill microorganisms
5. Narrow-spectrum antibiotics	E. Plastic strip containing exponential gradient of antibiotic on one side and calibrated MIC reading scale on the other placed on inoculated plate
6. Beta Lactams	F. Antibiotics that act against a wide range of bacteria, both gram positive and gram negative bacteria
7. Transpeptidase enzyme	G. antibiotic agents that act on cell walls, include Penicillin, penicillinase-stable penicillins, broad-spectrum antibiotics, etc
8. Tetracyclines	H. Least amount of that will kill 99.9% of a standardized suspension of organisms
9. Aminoglycosides	I. Antibiotic which blocks formation initiation complex by preventing tRNA binding at acceptor (A) site, preventing addition of new amino acids to peptide
10. Macrolides	J. Antibiotic that binds the 50 S ribosome unit and inhibits translocation of peptidyl tRNA from acceptor site to exit site leading to interruption of transpeptidation or translation
11. MIC	K. Antibiotic which prevents transfer tRNA from A to P site, prevent elongation
12. Turbidity	L. Also called penicillin binding protein, reforms the peptide crosslinks between rows and layers of peptidoglycan
13. Kirby Bauer disk	M. Disk used for agar disk diffusion
14. E-test	N. Lowest concentration of drug that will inhibit growth of organism
15. MBC	O. indicates growth in the microdilution tube method of antibiotic susceptibility testing

　

1 D; 2 F; 3 A; 4 B; 5 C;6 G; 7 L; 8 I; 9 K; 10 J;11 N;12 O;13 M;14 E; 15 H

Week 6: Wounds, Ears, Eyes, and Sinuses

Hello everyone, in honor of our upcoming test, I decided to put together a little quiz of questions concerning wounds, eyes, ears, and sinuses to help everyone study.  Hope you find it helpful! Answer are written below (don’t peek!).

1.)  What is another name for a painful boil filled with pus?

2.) What are three common agents involved with infections of hair follicles?

3.) What type of antibiotics is MRSA resistant to?

4.) Ringworms are due to what organism?

5.) Nonbullous impetigo is caused by what bacteria?

6.) Erysipeloid is due to what organism?

7.) What is the most common organism found in abscesses (think lungs)?

8.) What is myositis?

9.) What is another name for gas gangrene?

10.) A double zone of beta hemolysis is seen with what organism?

11.) Necrotizing fasciitis is associated with what organisms?

12.) What are agents commonly associated with bedsores?

13.) Infections due to trauma and contact with infected saltwater are commonly associated with what group of organisms?

14.) Infections due to contaminated prosthetic devices are associated with what organisms?

15.) What is the preferred specimen for a closed abscess?

16.) What is the preferred specimen for an open or superficial wound?

17.) What media should be used for superficial wounds, burns and bites?

18.) What is keratitis?

19.) What organisms are associated with “swimmer’s ear”?

20.) What media should be used to investigate bacteria collected from an internal ear swab?

1-furnucle; 2-S. aureus, Enterobacteriaceae, Pseudomonas; 3- beta-lactam antibiotics; 4 – dermatophytes; 5- S. pyogenes; 6- Erysipelothrix rhusiophathiae; 7- S aureus; 8- inflammation of the muscle tissue; 9- clostridial myonecrosis; 10- C. perfringens; 11- S. pyogenes, S. aureus, anaerobes; 12- B. fragilis, E. coli, S. aureus, P. aeruginosa; 13- Vibrio spp; 14- S. epidermidis, other CNS, diptheroids, and P. acnes; 15- aspirate fluid; 16- deep swab; 17- SBA, MAC, Thio broth, gram stain; 18- inflammation of the cornea

19- P. aeruginosa; 20- SBA, CHOC, MAC, Thio broth, and anaerobic 

Week 6: Mycobacteria

Hello everyone, this week in our Infectious Disease lecture we discussed Mycobacteria.  We spent a great deal of time discussing Mycobacterium tuberculosis, the etiological agent responsible for most case of tuberculosis in humans.  In the United States 4,495 cases of tuberculosis were documented in 2009, 126 of which were in Alabama.  According to the World Health Organization, there are 8.4 million new cases of tuberculosis each year worldwide.  Tuberculosis tends to be most prevalent among immigrants, drug or alcohol abusers, the homeless, and the immunocompromised, particularly those infected with HIV.  Risk factors associated with tuberculosis infection include crowded living conditions, health status of the individual, behavioral risks, environmental and social factors, poverty level, and the fact that the organism is found everywhere.  M. tuberculosis is transmitted primarily through inhalation of droplet nuclei expelled through talking, sneezing, and singing, although it may also be contracted via aerosols due to contact with wounds and tissue of an infected individual.  The spectrum of the diseases associated with M. tuberculosis range from asymptomatic to the typical pulmonary condition, to military tuberculosis in which the disease presents in areas other than the lungs including the spleen, liver, bone marrow and kidneys, to name a few.  Symptoms of typical pulmonary tuberculosis include a productive, prolonged cough, chest pain, and hemoptysis.  Systemic symptoms include fever, chill, night sweats, appetite loss, weight loss, and easy fatigability.

The following is an interesting article I found regarding tuberculosis in ancient Egypt.  Scientists have been able to utilize molecular techniques in order to identify M. tuberculosis in mummies.  Hope you enjoy it!

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)65185-9/fulltext

Week 5 Laboratory: Gastrointestinal Infections

Hello everyone, today I am going to discuss the experiments performed in the laboratory on Thursday and Wednesday.  Specifically, I am going to discuss my rectal sample, since most people in the class did not receive this particular bacterial species on their pre-prepared plates.  For the rectal samples, we received four prepared plates, an SBA, a MAC, an XLD, and a CVA.  My pathogenic isolate appeared as a clear colony on MAC, a gray colony on SBA, yellow colonies on XLD, and showed no growth on CVA.  No growth on CVA revealed that my isolate was not Campylobacter since this plate is specific for Campylobacter.  Clear growth on MAC revealed that my isolate was a non-lactose fermenting gram negative rod.  The yellow colonies on the XLD confused me slightly at, since normal GI flora typically appear yellow on XLD.  However, I remembered that Yersinia may appear clear to slightly yellow on XLD, so I began to suspect a possible Yersinia infection.  I performed an API 20 E to confirm this.  My API results yielded a perfect match for Yersinia enterocolitica, which can cause such diseases as mesenteric lymphadenitis, hemorrhagic enterocolitis, and terminal ileitis.  Although I chose to perform an API 20 E to confirm my identification of Yersinia enterocolitica, I could have performed an entirely different set of tests and come to the same conclusion.  If KIA, LIA, and Urea tests had yielded Alk/A, P/Y, and +/- and motility tests had been negative at 35° and positive at room temperature, I would have also come up with an ID of Yersinia. 

Below is a transmission electron microscopic view of Yersinia enterocolitica.  I had never seen an image quite like this, so I thought I would included it!

 

Week 5: Gastrointestinal Infections

Hello everyone, this week we discussed gastrointestinal tract infections.  One of the key points made during this lecture was the mechanisms of pathogenicity of the various bacteria that cause GI infections.  I have decided to make a chart of the different modes of pathogenicity to as study aid for everyone for our upcoming test.  Hope you all find it helpful!

Mechanism of Pathogenicity	Description	Symptoms	Bacterial agents
Toxin production – enterotoxin	No invasion, toxin acts on adenylate cyclase enzyme to catalyze conversion of ATP to cAMP, cells secrete more ions into the lumen of the intestine which is followed by water, causes watery diarrhea	Non-bloody, watery stools, vomiting, abdominal cramps, stool negative for RBCs and PMNs	Enterotoxigenic E. coli, Vibrio cholerae, Vibrio parahemolyticus (other vibrios), Clostridium perfringens, Clostridium difficile (toxin A), Bacillus cereus, others
Toxin production – cytotoxins	Cytotoxins act to disrupt the structure of the intestinal epithelial cells, causing cells to slough off from the mucosa causing inflammation	Dysentery – blood and PMNs in the stool, accompanied by pain, cramps and tenesmus	Enterohemorrhagic E. coli, C. difficile, (toxin B), others
Toxin production – neurotoxins	Usually preformed in food and ingested, emetic toxin causes vomiting indpedent of of other actions on the mucosa, and the neurotoxin produced by Clostridium botulinum prevents the release of acetocholine at nerve junctions, resulting in flaccid paralysis	Vomiting, paralysis	S. aureus, Bacillus cereus, Clostridium botulinum
Invasion	Invasion of GI mucosal cells by bacteria, resulting in inflammation and dysentery	Blood and PMNs in stool	Shigella, Salmonella, Enteroinvasive E. coli, Campylobacter jejuni
Invasion of full bowel wall with lymphatic spread	Diarrhea not often presenting symptom		Salmonella typhi - bacteremia (typhoid fever); Yersinia enterocolitica - mesenteric lymphadenitis
Attachment	Adhere to, destroy, and interfere with normal function of cells of the bowel	Malabsorption problems, diarrhea	Enteropathogenic E. coli, Giardia lamblia

Week 4 Laboratory: Throat and Sputum Samples

This week in lab we did throat swabs and cultures and sputum samples.  An important part of our investigation into the pathogens of the upper and lower respiratory tract is the ability to differentiate between normal flora and potential pathogens.  I have decided to discuss my sputum sample in order to illustrate this point.  I received a plate with two isolates.  Isolate #1 was large to medium in size on SBA, yellow, convex, and beta hemolytic.  Isolate #2 was small, alpha hemolytic, gray and translucent.  I immediately suspected S. aureus for isolate #1 considering the colony morphology.  After performing a catalase test and coagulase test (both of which were positive) I confirmed that this isolate was indeed S. aureus.  S. aureus is considered a pathogen in the lower respiratory tract and is associated with nosocomial pneumonia, aspiration pneumonia, and lung abscesses. I reported isolate #1 as a pathogen.  Isolate #2 was catalase negative, alpha hemolytic, and bile insoluble, which lead me to an ID of viridans streptococcus.  Viridans streptococcus is considered normal flora in the upper respiratory tract and is considered normal flora for sputum samples as well.  Other normal flora found in throat and sputum samples include coagulase negative Staphylococcus, diptheroids, and Neisseria spp.  I reported the viridans streptococcus as normal flora for this sample.

After this lab however, I was curious about my viridans streptococcus isolate.  I knew I had been correct to report this isolate as normal flora for the area of the body in which it was isolated, but I wondered if viridans streptococcus was ever considered a pathogen in the lower respiratory tract.  I did some investigation online and found this interesting article on Pubmed concerning viridans streptococcus and cases in which it was associated with a diagnosis of pneumonia.  I suppose there is always an exception to every rule!

http://www.ncbi.nlm.nih.gov/pubmed/1465696 

Week 4: Lower Respiratory Infections

Hello everyone, this week in lecture we discussed lower respiratory infections.  I was particularly interested in the discussion of Legionella and Legionnaires’ disease.  Legionella pneumophila is responsible for roughly 90% of cases of Legionnaires’ disease.  Legionella is found primarily in water sources such as lakes, rivers, water distribution centers, cooling centers, fountains and potable water.  Legionella is contracted via inhalation of infectious aerosols.  There are 15 different serotypes of Legionella, serotype one being the most common serotype seen in infections.  Serotypes 4 and 6 are the next most common serotypes seen.  This bacterium is not spread by person to person contact.  The first symptoms of Legionnaires’ disease are non-specific.  Initial symptoms include fever, chills, cough, muscle pain, headache, chest pain, and diarrhea.  Pneumonia follows as well as possible renal failure, additional gastrointestinal problems, liver function abnormality, and central nervous system problems such as delirium, disorientation, confusion, and rare seizures. 

            Legionnaires’ disease occurs as sporadic cases, epidemic outbreaks, and as nosocomial infections.  Legionnaires’ disease has an incidence of roughly 8,000-18,000 cases per year in the United States.  The mortality rate is 10%-15% in healthy individuals and up to 75% in the immunocompromised.  Individuals predisposed to Legionnaires’ include cigarette smokers, the elderly, individuals with chronic lung disease, and people of immunosuppressive drugs.

            The following is a video from the BBC concerning windshield-wiper fluid contaminated with Legionella in the United Kingdom.  It was found that professional drivers in the UK are five times more likely to contract Legionnaires’ due to increased likelihood of contact with contaminated windshield wiper fluid.  

http://www.bbc.co.uk/news/10306411

Week 3: Upper Respiratory Infections

Hello everyone, this week we discussed upper respiratory infections.  One of the primary infections we discussed was pharyngitis, an infection characterized by pain, swelling, erythrema, gray-white exudate on the throat, fever and cervical lymphadenopathy.  The primary cause of bacterial pharyngitis is Streptococcus pyogenes.  I have decided to discuss Streptococcus pyogenes and its various clinical manifestations since the possible resulting conditions of an infection with Streptococcus pyogenes vary so greatly as far as clinical manifestations and severity of the conditions.  As previously mentioned, S. pyogenes can cause pharyngitis as a primary infection with such suppurative sequelae as sinusitis and otitis media.  Non-suppurative sequelae of S. pyogenes include Acute Rheumatic Fever and Acute Glomerular Nephritis.  Both of these conditions are immunological in nature.  ARF is believed to be autoimmune in nature and AGN is an immune complex issue.  Infections with Streptococcus pyogenes can also cause such cutaneous and soft tissue infections such as impetigo, erysipelas, and cellulitis.  Streptococcus pyogenes can also cause severe invasive syndromes such as severe scarlet fever, septicemia, severe pneumonia, streptococcal toxin shock-like syndrome and necrotizing fasciitis.  Necrotizing fasciitis is a deep seated infection of subcutaneous tissue involving progressive destruction of tissue, fascia, and fat.  This condition is associated with such streptococcal pyrogenic exotoxins as SPE A, B, and C.  Underlying conditions such as cancer, renal failure, diabetes, immunosuppression, peripheral vascular disease, skin trauma, burns, and skin infections can increase the risk of developing necrotizing fasciitis as a result of infection with Streptococcus pyogenes.  Treatment of necrotizing fasciitis includes antibiotic treatment, surgery, and amputation. 

            I have attached a video concerning necrotizing fasciitis that I found interesting.  Enjoy!

Week 3: Urine and CSF Cultures

Hello everyone, today I am going to discuss the process I went through to ID the bacteria present in my urine culture.  I received MAC, SBA and CHROMagar plates already plated with the urine specimen.  The specimen appeared as medium white-gray convex colonies on SBA, and nothing grew on MAC or CHROMagar.  No growth on MAC led me to deduce that the isolate was not a gram negative rod, but since my isolate failed to grow on the CHROMagar, I had no way of knowing what the possible microscopic morphology of the isolate was or the possible ID of the organism.  I was unable to proceed with any further biochemical testing since I didn’t know the microscopic morphology, so I decided to perform a gram stain.  The gram stain revealed gram positive cocci in clusters.  Knowing the microscopic morphology allowed me to proceed with testing.  I performed a catalase test which was positive, a coagulase test which was negative, and a Novobiocin susceptibility test which revealed resistance.  The results of these tests brought me to a final ID of Staphylococcus saprophyticus.  The next day, after reincubating my CHROMagar, colonies grew.  The colonies were pink and opaque.  Pink opaque colonies correspond with Staphylococcus saprophyticus.  Both pathways taken to identifying the organism brought me to the same conclusion.  The lesson to be learned here is that there are multiple ways to arrive at the same ID, and if one method of identifying an organism fails, another can be used.

The middle colony growth is Staphylococcus saprophyticus .   The picture at the very top is a gram stain of  Staphylococcus.

Week 2 Laboratory: Blood Cultures

Hello everyone, it is me again.  Today in the laboratory we read the plates prepared yesterday and completed additional testing in order to come up with a final ID for our blood culture sample.  I am going to discuss the process I went through to identify the pathogen in my blood culture specimen.  The purpose of this discussion is to show how easily one pathogen can be mistaken for another and the importance of complete and thorough testing on a specimen.

I began by making a gram stain of my specimen using the blood from the blood culture bottle.  After allowing the stained slide to dry, I examined the slide under oil immersion.  I quickly identified the morphology of the bacteria as gram positive cocci in chains.  Having determined the morphology and gram stain, I then plated the specimen on the appropriate media, in this case SBA with a “P” disk.  I then incubated the plate overnight in CO2.  

The next day I retrieved my specimen and examined the macroscopic morphology of the bacterial colonies.  The colonies were small, white to gray in color, convex and semi-opaque.  The specimen also displayed beta-hemolysis.  The gram stain and colony morphology lead me to declare the preliminary ID to be beta-hemolytic Streptococcus.  I believed my specimen specifically to be S. pyogenes; the macroscopic and microscopic morphology fit that of S. pyogenes perfectly.  I performed two additional tests in order to come up with a final ID: a catalase test and a PathoDX Strep grouping testing.  As expected the catalase was negative and I believed I saw agglutination for Group A strep on the PathoDX card.  This supported my ID of S. pyogenes.  However, Mrs. Jeff told me this was incorrect.  I performed the PathoDX test again, this time inoculating the reagent broth with more colonies from my plate.  This time there was clear visual agglutination for Group G Strep, making my final ID Streptococcus dysgalactiae subsp. equisimilis, a Group C or G strep species.  The colony morphology for Group C and G strep is almost identical to that of Group A strep, making it fairly easy to confuse the two as I originally did.  So the lesson here is to always complete all necessary testing, never make a final ID on the colony morphology alone!

Which is which???  Pretty similar huh?  The specimen below is  Group G  Strep and the specimen above is Group A Strep.

Week 2: Bloodstream Infections

Hello everyone, hope you are all having a nice week.  In Tuesday’s Infectious Diseases lecture we discussed bloodstream infections.  Endocarditis is an important topic when discussing bloodstream infections, so I have decided to devote more attention to the subject.  Endocarditis is defined as the inflammation of the heart’s inner lining which can lead to damage of the heart valves.  The duration of this condition is less than six weeks.  Endocarditis is the classic example of intravascular bacteremia and can involve normal or prosthetic valves.  If endocarditis is suspected, two to three cultures should be collected over one to two hours.  Endocarditis is treated with Penicillin, aminoglycoside, antifungal agents (should a fungal species such as Candida or Aspergillus be the root cause of the endocarditis), and surgery. 

Many different bacterial agents may involved in endocarditis, including the HACEK organisms, opportunistic organisms found as normal flora in the oral cavity but may become involved in periodontal disease, endocarditis and other diseases.  Haemophilus, the “H” in HACEK, is the most prevalent HACEK agent involved in endocarditis.  Other HACEK organisms involved in endocarditis include Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella.  Capnocytophaga, Bartonella, S. aureus, S. epidermidis, S. pneumoniae, S. pyogenes, N. gonorrhoeae, and P. aeruginosa are additional bacteria that may be involved in endocarditis.  Viridans streptococci, Enterococcus (other group D strep), anaerobic and microaerophilic strep, as well as the HACEK organisms may be involved in subacute bacterial endocarditis, a condition that lasts six weeks or longer.  Like endocarditis, subacute endocarditis is treated with Penicillin and aminoglycoside.

           The following is an entertaining yet informational video concerning endocarditis.  Enjoy! http://www.youtube.com/watch?v=Udgbbz1_qe0&feature=related

Welcome!

Welcome to my blog about big bad bugs and infectious diseases!  I am writing this blog as part of my graduate infectious disease course at the University of Alabama at Birmingham.  I'll be posting once a week about topics discussed in class and the laboratory.  I am hoping to find interesting articles and links concerning microbiology and infectious diseases to post here, articles that will move a bit beyond what is discussed in class.  I am also going to try to find some relevant biology fun facts, ones that can be dropped causally in conversations at parties and what not.  Facts to impress your friends with!  Anyway, thats all for now!