Talk in general about vibrio cholera. | Gram - bacteria
Ingested and transmitted by fecal-oral root
It produces toxins yet it is not an intoxication. |
What kinds of obstacles do vibrio cholera have to overcome? | To invade the GI tract, they have to avoid obstacles of bile, acidity, peristalsis, IgA secretion, skin secretions and iron competition.
It has pili helping in adhering them to cell membrane |
What is the primary site of infection? | After adherence and attachment to sites at the cells, causing the penetration.
After the primary site of infection is done, bacteria starts receiving nutrients from host cells, in order to multiply then when they reach a certain amount they start spreading locally (in case of cholera in intestinal tissue. |
What is the transient spread of bacteria? | When bacteria is spread into distant tissues by the blood or lymph streams, to brain/ intestine/ lungs...
Once infection takes place, the spread stops. |
Talk about persistent spread. | Opposite to transient, germs keep seeding the organ sending more and more on the organ |
What are the virulent factors of vibrio cholera? | Most important one is the cholera toxin, released which is not invasive.
There are also the cilia, flagella... |
How do vibrio cholera infect the body? | We ingest contaminated food/ water, they enter into the epithelium, and then activated by chemotaxis to move towards the endothelia, and then their pili attach to cell receptors and then start producing toxins. |
Talk about cholera toxin. | Not invasive (doesn't destroy cells)
lead to Cl ions leaving into the lumen of the intestine, and water will follow it due to ionic gradient thus causing diarrhea |
What are the properties of cholera infection process? | Multiplication of cells after adhering.
Penetrate into GI tract but not invasive (doesn't enter cells)
Local spread in tissues
Multiply on surface of mucosa to have sufficient amount of cholera toxins. |
Talk about the mode of transmission of vibrio cholera. | Released in stool so its transmitted by stool-contaminated water |
Talk in general about the staph aureus bacteria. | Gram +, One of the most studied bacteria in microbiology, pathogenic bacterium however it is a transient colonizing agent for 20% of population, they are invasive and have capsule which may be involved in making slime to evade the immune system.
It also causes pus and it is immobile. |
What is the mode in infection of the staph aureus bacteria? | They are invasive and have a lot of toxins (hemolysis, lipases, proteases, nucleases, and collagenases.
It has no distant spread, yet it may cause bacteremia. |
What do we mean by bacteremia? | Bacteria found in blood and may spread. |
What do we mean by hematogenous spread? | Spreading via blood of a microorganism. |
Give an example of staph aureus opportunity for infection. | A px with transient colonizing staph aureus in nasopharynx, was subjected to a motorcycle accident, and fractured his nose, then he has hip pain accompanied by fever, after doing a scan it was found that the femur is inflamed (osteomyelitis- myel = core)
So this osteomyelitis was caused by staph aureus infection spreading into the site of fracture after it was a colonizing agent.
So staph aureus took opportunity of the accident. |
Can we consider accidents as part of opportunistic infections? | Usually when we say opportunistic infections, we refer more to immunosupressed patients. |
Why are patients with staph aureus infections put in contact isolation? | Since the infection may be transmitted through direct contact of the blood/skin and thus may cause disease (after spread when we are talking about osteomyelitis)
Staph aureus may also cause endocarditis. |
What is primary bacteremia? | It is when bacteria are not able to leave the bloodstream due to innate immunity and thus they are stuck in blood stream and unable to go towards tissues so they are killed in the stream, without causing any disease
AKA transient bacteremia. |
What is secondary bacteremia? | Its when reticuloendothelial cells (kupfer) are not able to filter blood from bacteria thus causing this bacteria to spread into the heart and bones and causing disease. |
What is the childbed fever? | It is a condition that happened in a period of history where 50% of women who got pregnant died post delivery.
Since there was no antibiotics and doctors didn't wear gloves or use antiseptics they transmitted infections to the vaginal canal.
Ignaz Semmelweis pointed it out but no one accepted his proposal and he was sent into a mental hospital. |
Who proved that our hands are not sterile causing childbed fever? | Joseph Lister , who is the father of anti-septics |
What is septicemia? | When bacteria in blood multiply and produce proteins |
What is pyemia? | When there is production of puss in blood which is then visible in the skin |
What does pyemia indicate regarding bacterial life? | Pyemia means that the infection in vaginal canal started metastasizing like cancer and small group of bacteria reached the skin and ended up in the blood |
How does sepsis occur? | When the excess release of bacterial chemicals and substances starts occuring, the immune system is triggered and sometimes it exaggerates its reaction by releasing a high amount of cytokines, fever and blood pressure decreases, creating sepsis. |
What is disseminated intravascular coagulation? | DIC, its where there are errors in the organization of the coagulation factors so that they are present heavily in a part of the body which clots, and is absent in another leading to blood leakage.
Some DICs are Sepsis induced (caused by bacteria that cause sepsis or septicemia) some are not |
Talk about the shigella bacteria. | It is a bacterium like vibrio cholera, ingested through fecoral route.
They arrive to the mucosa in intestine, and target a cell called M cells, and then they try to leave to M cell so macrophages find them and attack.
Its a very invasive bacterium since it acts intracellularly lead to diarrhea. |
What is the virulence factor of shigella? | The fact that they may be able to escape macrophages and hide inside enterocytes make them virulent. |
What is the difference between diarrhea caused by cholera and shigella? | Shigella releases shiga toxins, which destroy cells leading to presence of blood and mucus in the stool, while cholera releases cholera toxins, to release Cl, but no blood is released with stool, since it is not invasive |
What are the modes of transmission of brucella? | Intestinal tract, mucus membrane, skin (animals), ingestion of cheese (most common one) when its not pasteurized after milking the cow |
What are the effects caused by brucella infection? | They will go to lymphatic tissues macrophages, and then to thoracic duct (largest lymph duct) and do bacteremia and transmit to all parenchymatic organs (spleen, liver...) and do abscesses. |
What is the most important/difficult to deal with virulent factor? | Being facultative intracellular bacteria. |
What is sepsis? | Immune reaction towards infection on a spectrum (occurs for many syndromes, sepsis syndrome, SIRS) occuring by activating polymorph nuclear cells (neutrophils, monocytes and macrophages) |
What is the septic shock? | End stage of sepsis, were peripheral vascular dilation occurs so no venous return is able to go to the heart to be able to nourish other organs
Not responding to antibiotics in the ICU-> he will die |
What does endothelium injury induce? | Release of cytokines, proteases, kinins, reactive oxygen species (ROS), NO, leading to capillary leak of proteins in vessels leading to no blood to pump. |
What are the symptoms of sepsis? | S = shiver
E = extreme pain
P = Pale skin
S = Sleepy, Slow Cognition
I = I might feel like i am dying (close to death)
S = SoB |
Can cholera infection cause sepsis? | No, since it is not a bacteria that causes a disease in an invasive way, since only those are what trigger the immune system to release cytokines and thus causing sepsis or septic shocks |
What are endotoxins? | Toxins similar for all Gram- bacteria, Trigger sepsis through cytokines, and has 2 active domains, A for action and B for binding |
What are exotoxins? | Any toxin released outside the bacteria can be enterotoxin or neurotoxin |
Give examples on cytotoxins. | Hemolysins (alpha beta or gamma) and phospholipases, nucleases |
What are superantigens? | They are antigens that cause a toxic shock which looks like a septic shock because it stimulates immune system to bind the MHC molecules |
What are the differences between endotoxins and exotoxins? | Endotoxins are structural (LPS) while exo are released after transcription/ translation pathway.
Endo are highly antigenic attach to non-specific proteins, while exo need to be attached to specific receptors.
Endo stimulate immunity by presence of cells, while exo by antigen binding
Endo have no antibodies while exo are targeted by ones
Endo is only in gram- while exo for gram + and -
Endo is LPS while exo is polypeptide
Endo is heat stable (stay toxic with heat) while endo is heat labile
Endo are potent (all same strength) while exo are non-potent. |
List the procedures to get rid of bacteria. | Preservation, Pasteurization, Sanitization, Disinfection, Sterilization |
Talk about the process of preservation. | Use of salt to preserve (like pickles) not scientific |
Talk about the process of pasteurization. | One way of preservation, heat milk not too much to avoid killing the beneficial proteins.
We denature proteins but not destroy them (not boil) |
Talk about the process of sanitization. | Keeps environment safe (using detergents) but doesn't c;ear them from microorganisms |
Talk about the process of disinfection. | Usage of liquids like alcohols, subtype of sanitization, more specific way to kill bacteria but not viruses, important in epidemiology |
Talk about the process of sterilization. | Making a medium empty of any microorganisms or life at all through heat |