Course: Microbiology
Series: Staphylococcus

Staphylococcal gastroenteritis is an exotoxin mediated pathology with sudden onset of nausea, vomiting, diarrhea, and abdominal pain. 

​​Dr. Mobeen discusses the transmission, growth, toxin production, pathology, clinical presentation, and management of staphylococcal gastroenteritis.

In this lecture, Dr. Zaafran discusses the etiology of syphilis as an infectious disease, the diagnosis of treponema pallidum, the clinical manifestations at different stages of the disease, and the clinical management used to treat the disease.

Dr. Amr Madkour presents atypical cases of the urinary tract infections, diagnosis, treatment approach, and cases.

What 3 categories of diseases are caused by streptococcus pyogenes?
What are the CDC's recommendations for managing strep throat? 
How does the flesh eating disease pathogen (streptococcus pyogenes) cause the tissue to die?
Why most of the post-streptococcal glomerulonephritis patients may not need hospitalization?
What is the role of clindamycin while managing streptococcal diseases?

Dr. Mobeen dicusses the following diseases in this lecture:

• Pyogenic (tissue invasion)
  • Sore Throat
  • Skin Infections
    • Folliculitis
    • Pyoderma/Pustules
    • Cellulitis
    • Erysipelas
    • Impetigo
• Toxigenic (exotoxin mediated)
  • Scarlet Fever
  • Toxic Shock Like Syndrome
  • Necrotizing Fasciitis
• Immunogenic (immune response mediated)
  • Rheumatic Fever
  • Post-streptococcal glomerulonephritis

Notes to be posted soon.

Mechanism of action of Penicillin and Vancomycin. Complete pharmacology of these drugs will follow later. 

Dr. Mobeen covers the following topics in this brief video: 
Penicillin-binding proteins 
Cell wall's N-acetylmuramic Acid N-Acetylglucosamine 
Bacterial defense against Penicillin
 

We are sure that strep/sore throat is a routine presentation in your clinic. In the US only streptococci pyogenes cause millions of yearly visits to healthcare facilities. Streptococci cause disease by direct organ invasion, by their enzymes, and by releasing exotoxins. Understanding streptococci thoroughly and then wielding a great command over the management approach will help you continue to be amazing for your patients. In this two-part series, we will talk about the streptococcal foundations necessary to understand and manage the disease, and then various diseases and their management. Let's start with the first part here. Make sure that you have understood this before the second part about the diseases and their management.

In this lecture we will discuss the following topics:

• Virulence potential
• Habitat
  • Throat
  • Skin
• Tests
  • Erythrogenic/Pyogenic exotoxin
  • Gram +
  • PYR +
  • RAD
  • Catalase -
  • Bacitracin sensitive
• Antigenic components of the cell wall
  • Hyaluronic acid
  • C carbs
  • M Proteins
  • Exotoxins
• Enzymes
  • Streptolysin O
  • Streptolysin S
  • Streptokinase
  • Hyaluronidase
  • DNAse
  • C5a Peptidase

These foundations will be used to look at the disease process, disease types, and the disease management in the next lecture.

In this discussion Dr. Mobeen presents the pathophysiology, clinical aspects, and the current management approach to impetigo, foliculitis, furuncles or boils, carbuncles, cellulitis, and surgical wound infections caused by S. Aureus.

Dr. Mobeen continues the discussion about infective endocarditis. In this short but important session he presents the management approach to acute infective endocarditis. He discusses the treatment approach when the patient is not acutely ill, when the patient is acutely ill, and when the culture and sensitivity is available and you know if the pathogen is methicillin sensitive or methicillin resistant.

Dr. Mobeen discusses the modified duke's criteria and the clinical presentation of acute infective endocarditis. 

Dr. Mobeen starts the discussion of the staphylococcal infections caused by organ invasion. This lecture is the introduction to infective endocarditis in the context of staphylococcus.

Topics discussed are:

• What is infective endocarditis?
• Terms to know when studying or managing infective endocarditis.
  • Infective endocarditis (IE)
  • Native valve endocarditis (NVE)
  • Prosthetic valve endocarditis (PVE)
  • Nosocomial infective endocarditis (NIE)
  • Community acquired infective endocarditis (CIE)
• What tissues are susceptible to infective endocarditis?
• What is the composition of an infective endocarditis vegetation?
• What is the mechanism of tissue damage that leads to IE?
• Which population group is at a higher risk of right sided IE?
• Why are ventricular septal defects at a higher risk of developing IE in contrast to atrial septal defects?

Course: Microbiology
Series: Staphylococcus

Staphylococcal gastroenteritis is an exotoxin mediated pathology with sudden onset of nausea, vomiting, diarrhea, and abdominal pain. 

​​Dr. Mobeen discusses the transmission, growth, toxin production, pathology, clinical presentation, and management of staphylococcal gastroenteritis.

Dr. Mobeen discusses the pathophysiology, presentation, and management of staphylococcal scalded skin syndrome.

Toxic shock syndrome is a rare but deadly disease most common in young women using super-absorbent tampons. Staphylococcal toxin TSST-1 is responsible for this syndrome. Majority of the patient that fall ill with toxic shock syndrome also lack an adequate humoral response to the toxic shock syndrome toxin. In this brief video Dr. Mobeen discusses the syndrome, its presentation, diagnosis, pathophysiology, and the management.

How do staphylococci cause toxic shock syndrome? 
Superantigens are the answer. 
In this important video session, Dr. Syed discusses superantigens in the context of staphylococci.

Following topics are discussed:

• What are superantigens?
• What important pathogens release superantigens?
• What superantigens are released?
• Normal controlled immune response to an antigen.
• How does a superantigen cause massive abnormal activation of the immune system?
• Symptoms of the toxic shock syndrome as a result of superantigen activity.
• Labs

In this lecture, Dr. Mobeen discusses the following topics about Staphylococci:

• Definition
• Description
• Morphology
  • Shape
  • Color
  • Cell wall
  • Cell membrane
  • Penicillin-binding protein
• Species
  • S. Aureus
  • S. Epidermidis
  • S. Saprophyticus
• Diagnostic Tests
  • Gram staining
  • Catalase test
  • Coagulase test
  • Novobiocin test
  • NaCl test
  • Mannitol fermentation
• Diseases
  • Skin infections
  • Infective endocarditis
  • Bacteremia
  • Wound, catheters, and splinter infections
  • Prosthesis infections
  • Splenic abscesses
• The Management Approach to Staphylococci
  • IV vs Oral medications
  • MRSA vs. Penicillin sensitive pathogen management

Dr. Mobeen presents the classification, diagnostic testing, metabolic properties, antigenicity, treatment, and vaccination for streptococcus pneumoniae. This pathogen is also called S. Pneumoniae, Pneumococcus, and Diplococcus.

Following identifying characteristics are presented:

• Gram positive staining
• Catalase negative
• Bile sensitive
• Optochin sensitive
• Latex agglutination test positive for pneumococcal antigens
• Teichoic acid
• Diseases caused:
  • Conjunctivitis
  • Meningitis
  • Otitis Media
  • Pneumonia
  • Sinusitis
• Quellung positive testing
• Alpha hemolysis
• Antigenecity
  • IgA protease
  • Pneumolysin
• Vaccination
  • 23 valent polysacchride vaccine
  • 13 valent conjugated polysacchride vaccine
• Penicillin G and V
• 3rd Generation cephalosporins
  • Ceftriaxone
  • Cefotaxime
• Vancomycin

Dr. Mobeen will discuss the following properties and traits of S. Viridans:

• S. Viridans is not a single species of bacteria, instead it is a big group of pathogens.
• S. Viridians are catalase negative.
• S. Viridans are gram positive.
• S. Viridans are bile insoluble.
• S. Viridans are optochin resistant.
• S. Viridans do not have a capsule.
• S. Viridans cause the following infections:
  • Dental carries.
  • Subacute bacterial endocarditis (SBE.)
  • Brain and liver abscesses.
• Pathologies of the above mentioned infections.
• Signs and symptoms of SBE
• Treatment of SBE

Dr. Syed starts the series about the antibiotics' usage. The first lecture in the series presents the following topics about penicillins: 1. Discovery. 2. Types. 3. Mechanism of action. 4. Coverage of gram positive and negative pathogens by various types. 5. Pathogen resistance to penicillins. 6. Penicillin combinations with lavulanic acid etc. to overcome the resistance. 7. Usage in various infections.

This lecture presents visual memory aid for Pneumococcus identification virulance factors diseases and treatment.

This video is first in the series of videos presenting bacterial lab algorithm. Recalling the pathogens will become a breeze! Video presents characteristics of alpha hemolytic streptococci. Their bile and optochin solubility main metabolic properties tissues infected and pathologies caused. Video covers S. Viridans and S. Pneumoniae (Pneumococci)

A discussion of structural components of a bacteria. Covers: Plasma membrane Cell Wall N-acetylglucosamine N-acetylmuramic acid for peptidoglycans wall Outer membrane of the gm-ive bacteria Flagellum Fimbriae/Pilli Sex pili F+ and F- bacteria DNA Plasmid Ribosomes and nutritional granules

Review:  Remember the structure of bacteria is slightly different between the gram +ive and gram -ive, and pleomorphic bacteria which don’t have a cell wall.

• *Think of a bacterium as a tiny bean shaped globule floating about like a balloon filled with cytoplasm.  The wall of the capsule has many layers. The inside layer is a cytoplasmic membrane, made up of a lipid bilayer and penicillin binding proteins.

• *Outside the plasma membrane, is a cell wall made up of multiple layers of peptidoglycans(PG),  the sugars  N-Acetylmuramic acid (NAM) and N-Acetylgalactosamine.

• *In gram +ive bacteria there are up to 60 PG layers. In gram -ive, up to 3 layers of PG. In gram -ive, the space between the layers is called periplasmic space.

• *Outside the PG layer is another lipid bilayer membrane which contains lipopolysaccharides (LPS) made up of two sugar molecules and a phosphate, and above that is a five sugar core, and above that is a chain of sugars of up to 25 units.  That is the outer membrane. (TC 5:32 You gotta see the pictures to understand it. Trust me. ed.)  

• *Gram +ive have protein molecules or peptides coming out of the cell wall called teichoic acid (TA). Some are connected all the way through to the plasma membrane.  If they are connected to the lipids of the plasma membrane they are called  lipoteichoic acid (LTA). 

• *In the case of gram -ive, it is LPS which induces the TNF and IL-1.

Additional Structures

• *Bacterial motility is generated by  flagella connected through the cell walls to the inner membrane which use ATP for energy to move the bacteria.  Three types of movement depending on how the flagellum moves.  If clockwise, then the bacterium moves like a jet; counterclockwise causes tumbling motility; if flagellum is wrapped around the cell, then a rotary movement.

• *Fimbria or Pili are small proteinaceous materials mostly on gram +ive (gram -ive have less), of two types: 1) sticking out like hair functioning to stick bacteria to surfaces and creating films; 2) sex pili which connects to another bacteria. Through the pilus there is an exchange of plasmids (circular DNA molecules present inside the bacteria) from one bacteria to another.  The gene that creates the sex pilus is on the surface of the plasmid.

• *Bacteria with the ability to encode the sex pilus are called the F+(male) bacteria, and those that do not are called F- (female).  When a plasmid makes a sex pilus and the F+ genes are exchanged, the receiving bacteria become F+.

• *The bacterial DNA is a double stranded chromosome the ends of which are tied, making a continuous loop

More..

• *Endotoxins are encoded by the primary DNA, however in gram+ive, secreted exotoxins are encoded by plasmids.

• *The outside capsule of a bacteria is made up of negatively charged polysaccharide molecules. The function of the capsule is to: 

          1. prevent phagocytosis by repelling neutrophils which are also negatively charged, like two negative poles of a magnet; 

           2. Thus cause virulence by evading phagocytosis;

           3. For lab diagnosis the presence of the capsule can help with the Quellung test.

• *Some bacteria can secrete a glycocalyx that makes biofilm.

• *Spores are formed by some gram +ive bacteria. When spore-forming bacteria are dehydrated, the peptidoglycan layer compresses into a tight ball, squeezing out its cytoplasm along with ribosomes and protein granules, but retaining its plasmids and DNA. As the spore forms, an additional outer peptidoglycan layer forms.  The inner layer has good sugar crosslinks and the outer layer does not.  A final outside layer of keratin insulates the spore capsule. Spores are strong and can withstand heat, dehydration, chemicals and lots of abuse.  Once the nutritional status is restored however, the spore will regerminate into bacteria.

• *The following are spore forming pathogens relevant to human disease:

               Bacillus (Aerobic) :  B. anthracis, B.cereus, B. subtilis

              Clostridium  (Anaerobic):  C. tetani, C. botulinum, C. perfringens, C. difficile

  More about those sugar crosslinks in the discussion of penicillins.  On to the next lesson!

Mechanism of Gram staining - Dr. Mobeen Syed

Put bacteria on plate (if from another plate then dilute agar first);

1. Warm the plate to fix bacteria;

2. Add gram stain; 20-30 seconds; wash it;

3. Add iodine (mordant)

4. Add drops of  alcohol, to wash out the gram negative bacteria’s color - 20 - 40 seconds;

5. Put safranin (counter stain) 20-40 seconds

• What Happens?

  • * Gram positive (+ive) bacteria turns purple
  • * Gram negative(-ive) bacteria turns red

Go to TC 2:57 in the video for illustration of how it happens:

• * Covering the Gram +ive plasma membrane (phospholipid bi-layer), there are up to 60 peptidoglycan (PG) layers.
• * The gram -ive plasma layer is covered by up to three PG layers and an outer membrane containing lipopolysaccharides.
• * Beta-Lactamase is the most important factor in the periplasmic space, enzymes that can break down penicillins. 

What happens to the gram stain?

• *The small molecules of dye get trapped in the PG layer of gram +ive bacteria and in both the outer membrane and the PG layers of the gram -ive bacteria.
• * At this stage both gram +ive and gram -ive look purple under the microscope.
• * When iodine (+) is added, it attaches to the molecules of dye (-) and creates a bigger molecule, which gets trapped in the PG layers.  Color does not change.
• *When alcohol is added it dissolves the lipid portion and dehydrates the cells.
• * In the gram +ive cells the water is pulled out by the alcohol and the 60 layers are compressed, trapping the molecules of dye, keeping the purple color
• * In the gram -ive cells, the alcohol dissolves the more abundant lipids, and the three PG layers are too weak to trap the dye molecules so they escape, making the cells colorless.
  NB: Using too much alcohol on the gram +ive cells will eventually break down the PG layers allowing the dye to escape so you have to be careful. 
• *The final step is to add safranin, a counterstain, that will turn the colorless gram -ive cells red, but will not be absorbed by the compressed gram +ive cells which stay purple.

And that is how gram staining works!

Dr. Luis A. Verduzco Intensivist, Anaesthesiologist Dr. Verduzco presents the diagnosis, labs, pathophysiology, and management of sepsis and septic shock.

Objectives:

Objectives of this lecture are:

• Pediatric vaccines and the diseases they help prevent.

• The typical primary pediatric vaccine schedule.

• Some myths about vaccination.

In this lecture, Dr. Zaafran continues to explore the world of anti-histamines. In this presentation, he discusses:

-What are decongestants?
-What are the two main types used?
-Are there different administration modalities?
-What are the types of symptoms most often seen in patients requiring - 
 nasal decongestants?
-Discussion of cough physiology
-Different types of cough
- Mechanisms of anti-tussive (cough) medications
-What are the different types of anti-tussives?
-Review of the anti-tussive side effects

This video presents following topics about the typical pneumonia: Definition Onset and Risk Factors Presentation Clinical Findings Pathogenesis Stages X-Ray findings Histopathology Complications

This video presents following topics about tuberculosis: Epidemiology Etiology Pathogenesis Primary Tuberculosis Morphology Clinical

This video presents following topics about tuberculosis: Epidemiology Etiology Pathogenesis Secondary Tuberculosis Morphology Clinical

Dr. Alikhan discusses the diagnosis and management of: 1. Bronchitis 2. Pneumonia

This video presents following topics about the Atypical pneumonia: Definition Onset and Risk Factors Presentation Clinical Findings Pathogenesis X-Ray findings Following pathogens are disucssed: Mycoplasma Coxiella Burnetti Chlamoydophila Pneumoniae Influence A,B,C Rhinovirus Coronavirus Rubella Adenovirus Vericella

This video presents following topics: Nosocomial Pneumniae Aspiration Pneumonia Chronic Pneumonae

Mir Alikhan MD, Pulmonologist discusses upper respiratory tract infections.

This video presents following topic COPD Definition CB Definition CB vs Bronchiolitis CB vs Emphysema Pathogenesis of Ch. Bronchitis Clinical Findings of Ch. Bronchitis Treatment of Ch. Bronchitis

This video presents following topics: Causes Complications Clinical approach

We will present pneumonia classification based on: Clinical types i.e. acute, fulminent, and chronic Histological patterns and tissue involved Anatomical types based on the lugn lobes invovled And clinical settings for example community acquired or nosocomial pneumonia

This video presents following topics about the typical pneumonia: Definition Onset and Risk Factors Presentation Clinical Findings Pathogenesis Stages X-Ray findings Histopathology Complications

Dr. Steven Phillips Discusses Dementia and Chronic Diseases

Today we have Dr. Steven Phillips with us to discuss the higher incidence of dementia in individuals with comorbidities in their early part of life. 

Dr. Steven Phillips' bio:
Steven Phillips, MD is a well published, Yale-trained physician, researcher, and bestselling author, whose focus of medical practice and research is that chronic and autoimmune illness can be caused by underlying infections.

Disclaimer:
This video is not intended to provide assessment, diagnosis, treatment, or medical advice; it also does not constitute provision of healthcare services. The content provided in this video is for informational and educational purposes only.
Please consult with a physician or healthcare professional regarding any medical or mental health related diagnosis or treatment. No information in this video should ever be considered as a substitute for advice from a healthcare professional.

URL list from Thursday, Feb. 3 2022

Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases? A Response to a Critical Review of the BMAA Hypothesis - PMC
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7904546/

Number of adults with dementia to exceed 150m by 2050, study finds | Dementia | The Guardian
https://www.theguardian.com/society/2022/jan/06/number-adults-with-dementia-exceed-150-million-2050-study

Two or more chronic health problems in middle age ‘doubles dementia risk’ | Dementia | The Guardian
https://www.theguardian.com/society/2022/feb/02/two-chronic-health-problems-middle-age-double-dementia-risk-multimorbidity-study?CMP=oth_b-aplnews_d-1

Association between age at onset of multimorbidity and incidence of dementia: 30 year follow-up in Whitehall II prospective cohort study | The BMJ
https://www.bmj.com/content/376/bmj-2021-068005#:~:text=Compared%20with%20people%20with%20no,multimorbidity%20was%20at%20age%2070

Chemically induced models of Parkinson's disease - PubMed
https://pubmed.ncbi.nlm.nih.gov/34673252/

Pesticide use in agriculture and Parkinson’s disease in the AGRICAN cohort study | International Journal of Epidemiology | Oxford Academic
https://academic.oup.com/ije/article/47/1/299/4609336?login=false

Amazon.com: Chronic: The Hidden Cause of the Autoimmune Pandemic and How to Get Healthy Again (Audible Audio Edition): Steven Phillips MD, Dana Parish, Teri Schnaubelt, Thomas Allen, Brilliance Audio: Books
https://www.amazon.com/Chronic-Hidden-Autoimmune-Pandemic-Healthy/dp/B0851RT3C6/ref=sr_1_1?crid=Q2RRSHAQ0S90&keywords=chronic&qid=1643936441&sprefix=chronic%2Caps%2C129&sr=8-1

In this lecture, we will discuss the properties, pathogenesis, and diseases caused by Clostridium Perfringens. We will discuss the extensive set of exotoxins that cause cellulitis, fasciitis, gas gangrene, and food poisoning. We will discuss the management and prevention as well.

Pork tapeworms or Taenia Solium can cause taeniasis or cysticercosis. Let's review the lifecycle and pathogenesis of these diseases.

CDC - DPDx - Diagnostic Procedures
https://www.cdc.gov/dpdx/diagnosticprocedures/index.html

CDC - Cysticercosis - Resources for Health Professionals
https://www.cdc.gov/parasites/cysticercosis/health_professionals/index.html#:~:text=Diagnosis%20usually%20involves%20both%20serological,treatment%20of%20increased%20intracranial%20pressure.

Cysticercosis: Overview, Symptoms & Treatment
https://my.clevelandclinic.org/health/diseases/23534-cysticercosis

Taeniasis/cysticercosis
https://www.who.int/news-room/fact-sheets/detail/taeniasis-cysticercosis#:~:text=Taeniasis%20can%20be%20treated%20with,days%20has%20also%20been%20used%20.

Taenia solium - Wikipedia
https://en.wikipedia.org/wiki/Taenia_solium

Oncosphere - Wikipedia
https://en.wikipedia.org/wiki/Oncosphere

SEM image of the Taenia Solium Scolex.  | Download Scientific Diagram
https://www.researchgate.net/figure/SEM-image-of-the-Taenia-Solium-Scolex_fig1_228743272

Oncosphere - an overview | ScienceDirect Topics
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/oncosphere

Cysticercus - Wikipedia
https://en.wikipedia.org/wiki/Cysticercus

Taenia Saginata is a type of tapeworm that causes taeniasis in humans and cysticercosis in cattle. Unlike Taenia Solium this worm does not cause cysticercosis in human beings, hence, is relatively benign. Let's review its properties, lifecycle, pathogenesis, clinical symptoms, diagnosis, and management.

CDC - Taeniasis - Disease
https://www.cdc.gov/parasites/taeniasis/disease.html#:~:text=Taenia%20saginata%20does%20not%20cause,cysticercosis%20in%20humans%20or%20not.&text=For%20Healthcare%20Providers%2C%20Emergency%20Consultations%2C%20and%20General%20Public.

Taenia Saginata - an overview | ScienceDirect Topics
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/taenia-saginata#:~:text=Taenia%20solium%2C%20Taenia%20saginata&text=Cattle%20are%20frequently%20the%20intermediate,tissues%20and%20develop%20into%20cysticerci.

CDC - Taeniasis - Resources for Health Professionals
https://www.cdc.gov/parasites/taeniasis/health_professionals/index.html#:~:text=saginata%20taeniasis%20is%20more%20frequently,%2C%20diarrhea%2C%20or%20hunger%20pains.

Taenia Saginata (Beef Tapeworm) Infection - Infectious Diseases - Merck Manual Professional Edition
https://www.merckmanuals.com/professional/infectious-diseases/cestodes-tapeworms/taenia-saginata-beef-tapeworm-infection

label
https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/018714s018lbl.pdf

Efficacy of ivermectin and oxfendazole against Taenia solium cysticercosis and other parasitoses in naturally infected pigs - ScienceDirect
https://www.sciencedirect.com/science/article/abs/pii/S0001706X13001575#:~:text=Ivermectin%20was%20not%20efficacious%20against,solium%20cysts%20and%20gastrointestinal%20nematodes.