Pathogenic Midterm Exam II

What are the virulence factors of Staphylococcus aureus, and what is the difference between generalized and localized Staphylococcal scalded skin syndrome (SSSS)?

staph aureus sticks using MSCRAMMs, spreads with hyaluronidase, hides with its capsule and protein A, and makes toxins that can kill cells, cause food poisoning, toxic shock, or scalded skin. it resists antibiotics with B-lactamase and MRSA. generalized means toxins all over the body but no bacteria in the blisters. Localized means the infection is only in one area with both bacteria and toxins in the blisters.

What are the virulence factors of Streptococcus pyogenes, and identify the pathogen most known to cause “Necrotizing Fasciitis” emphasizing the mechanisms by which this bacterial pathogen evades their host immune system?

Streptococcus pyogenes sticks to tissues using lipoteichoic acid, M protein, and Protein F. It spreads with hyaluronidase, streptokinase, and invading cells. It evades the immune system with its hyaluronic acid capsule, M protein, C5a peptidase, and streptolysins that kill immune cells. It also makes toxins like SPEs that can cause toxic shock.

Strep pyogenes is the main cause. Its capsule, M protein, C5a peptidase, and streptolysins hide from the immune system, survive in deep tissues, spread fast, and destroy tissue, making it life threatening.

What are the virulence factors of Streptococcus pneumoniae, and what are the factors by which this pathogen prevents its killing by phagocytes?

Strep pneumoniae sticks to epithelial cells and invades tissues. It evades phagocytes with its capsule, PspA (blocks complement), and pneumolysin, which kills immune cells and damages tissue. Pneumolysin also harms cilia, making it harder to clear the bacteria. Even though inflammation brings immune cells, the bacteria can resist killing and use tissue damage to spread.

What are the virulence factors of Bacillus anthracis, and what are the roles of plasmid px-01 and plasmid px-02 in the pathogenecity of this pathogen?

Bacillus anthracis sticks to host cells using Protective Antigen (PA), which lets Edema Factor (EF) and Lethal Factor (LF) enter. EF causes swelling, LF kills cells, and together they help the bacteria invade and damage tissues. The capsule (from pXO2) prevents phagocytosis, and EF/LF also weakens immune cells.

pXO1 makes toxins

pXO2 makes the protective capsule.

What are the virulence factors of Bacillus cereus, and what are the differences between the two clinical diseases this pathogen causes?

Bacillus cereus sticks to food or tissues with spores and surface structures. It does not invade and has no capsule its toxins do the damage. Emetic toxin is heat and acid stable, causes fast vomiting from preformed toxin in food. Enterotoxin is heat and acid labile, made in the small intestine, and causes diarrhea after a longer incubation.

emetic disease is fast and caused by preformed toxin

diarrheal disease develops more slowly and is caused by toxin made in the gut.

What are the virulence factors of Listeria monocytogenes? what is the special characteristic of this bacterium when it comes to growth temperature? And what the unique way of movement this bacterium uses to move in and in between cells? 

Listeria monocytogenes uses Internalins to invade cells, Listeriolysin O and Phospholipase C to escape the phagosome, and ActA to move inside and between cells by using the host’s actin. These help it cross the intestinal mucosa, blood-brain barrier, and placenta. 

Special characteristic (temperature): 
Listeria monocytogenes can grow at refrigeration temperatures (4°C). 

Unique movement: 
It moves by actin-based motility, forming actin tails that let it move inside and from one cell to another. 

What are the virulence factors of Corynbacterium diphtheriae? What disease it causes? And what is the structure and function of its exotoxin. What is the nature of the vaccine used to prevent the disease? 

The main virulence factor is the diphtheria toxin, an A-B exotoxin that stops protein synthesis. 
The tox gene comes from a bacteriophage (Beta-phage). 
The bacteria stay on the throat or skin and don’t need to enter the blood to cause disease. 

Disease caused: 
Corynebacterium diphtheriae causes diphtheria, which forms a gray pseudomembrane in the throat and can damage the heart and nerves if the toxin spreads. 

Toxin structure and function: 

• B subunit = binds and helps the toxin enter the cell. 

• A subunit = active part that blocks protein synthesis by inactivating EF-2, killing the cell. 

Vaccine: 
The vaccine is a toxoid (inactivated toxin treated with formalin). 
It’s safe, builds antibodies, and is given as part of the DTaP/Tdap vaccine. 

What are the virulence factors of Mycobacterium tuberculosis? Describe in details “Granuloma” formation and breakage in the development of tuberculosis. What stage of the disease that the microbe can be transmitted to other hosts? 

The virulence of Mycobacterium tuberculosis is mainly due to its complex, lipid-rich cell wall containing mycolic acids, arabinogalactan, and lipoarabinomannan. This structure makes the organism resistant to acids, alkalis, and many antibiotics, and allows it to survive within macrophages by preventing phagolysosome fusion. The bacterium grows slowly and can persist for long periods inside host cells. 

After inhalation of infectious droplets, M. tuberculosis reaches the alveoli and is engulfed by macrophages, where it survives and replicates. The immune system responds by activating T-cells, which release cytokines that stimulate macrophages. When the infection cannot be cleared, the body walls it off, forming a granuloma with a caseous (cheesy) necrotic center containing dormant bacilli. This latent stage can persist for years without symptoms. If immunity declines, the granuloma breaks down, the caseous material liquefies, and bacteria begin to multiply actively, forming cavities in the lungs. 

Transmission occurs only during this stage of active pulmonary tuberculosis, when bacteria from these lung cavities are released into the air through coughing or sneezing. Latent and extrapulmonary forms are not infectious. 

What are the virulence factors that Neisseria gonorrhoeae? How they attach, invade and evade? 

The main virulence factors of Neisseria gonorrhoeae are its pili, Opa proteins, Por proteins, lipooligosaccharide (LOS), and Rmp protein. The pili enable initial attachment to non-ciliated epithelial cells and allow antigenic and phase variation, helping the bacterium evade antibodies. Opa proteins promote intimate adhesion to host cells, while Por proteins assist in invasion by facilitating entry into the host cell and also block phagolysosome fusion in neutrophils, allowing survival inside them. The LOS acts as an endotoxin, triggering inflammation and attracting neutrophils, and the Rmp protein further aids in immune evasion by binding antibodies and preventing them from targeting Por and LOS. Together, these factors allow N. gonorrhoeae to attach, invade, and survive within host tissues while resisting immune clearance. 

What are the general virulence factors of Enterobacteriaceae? What are the various types of pathogenic E. coli both intestinal and extra-intestinal? What are the detailed steps by which Enteropathogenic E. coli (EPEC) forms attaching and effacing lesions in the host?

Enterobacteriaceae virulence factors include endotoxin, capsule, phase variation, TTSS, siderophores, serum resistance, and antimicrobial resistance.
Pathogenic E. coli types:

Intestinal:

Enteropathogenic (EPEC)

Enterohemorrhagic (EHEC)

Enterotoxigenic (ETEC)

Enteroinvasive (EIEC)

Enteroaggregative (EAEC)

Extra-intestinal:

Neonatal Meningitis (NMEC)

Uropathogenic E. coli (UPEC)

steps by which Enteropathogenic E. coli (EPEC) forms attaching and effacing lesions in the host:

1.       Bundle-forming pili (BFP) mediate the first attachment to intestinal epithelial cells.

2.       EPEC injects its own receptor, translocated intimin receptor (Tir), into the host cell.

3.       Bacterial surface protein intimin binds to Tir, creating a strong, intimate attachment.

4.       The normal microvilli on the epithelial surface are destroyed, reducing absorption of the surface area.

5.       Host actin rearranges beneath the site of attachment, forming a pedestal-like structure under the bacteria.

What are the virulence factors of Yersinia pestis? What are the virulence factors of
Shigella? What are the differences between Typhoidal and non-typhoidal Salmonella?

Yersinia pestis is attached by following a flea bite, invades phagocytized by macrophages, replicate in macrophages and are eventually released, released cells are resistant to phagocytosis which is mediated by TTSS and an antiphagocytic protein capsule.

Shigella attaches to intestinal epithelial cells, invades phagocytosis using TTSS, Evades the phagosome and replicates in the cytoplasm, S. dysenteriae produces an exotoxin called shiga toxin.

Typhoidal: causes typhoid and enteric fever, only found in humans, low infectious dose, can shed for up to a year.

Non-typhoidal: Causes salmonellosis, infect animals and humans, high infectious dose, can shed for weeks.

What are the virulence factor of Vibrio cholerae? What is the epidemiology of Cholera?
What is the disease caused by V. parahaemolyticus? And how one can get such an
infection?

Vibrio cholerae virulence factors are the toxin-coregulated pilus and cholera toxin. Cholera spreads through contaminated food and water, mainly in areas with poor sanitation.

Vibrio parahaemolyticus causes gastroenteritis, usually from eating raw or undercooked seafood or exposure to contaminated seawater.

Identify “Capnophilic” and “Microaerophilic”. Name two bacterial pathogens that are
both capnophilic and microaerophilic. Which one of the two pathogens can survive well in the stomach? and why?

Capnophilic: require carbon dioxide at a higher level than found in the atmosphere

Microaerophilic: require oxygen at a level lower than found in
the atmosphere

o   Campylobacter jejuni

o   Helicobacter pylori: can survive well in the stomach because it produces the enzyme urease which neutralizes the stomach acid around it allowing it to live in the acidic gastric environment.

Both need low oxygen and increased carbon dioxide for optimal growth.