Transcript of Listeria monocytogenes - Listeriosis: Morphology, Pathogenesis, Clinical Findings, Treatment

asome everybody today we'll be looking at leria monocytogenes but before getting into the video IID like to tell you guys that these videos are meant for educational purposes things and treatments may change with time if I get wrong or miss anything your input is always welcomed in the comment section so let's jump straight into the video but before talking about leria monocytogenes in detail we should know about the classification of bacteria bacteria are classified into spites acid F micro plasma and on the basis of gr staining into GR negative and gr positive we are not concerned here with gr negative as we are talking about leria monocytogenes and that's gr positive gr positive are further subdivided into coxy and rods we are done with coxi if you want to know more about coxy browse the channel rods are further subdivided into spor forming we're done with them too and nonsporeforming rods which are further subdivided into filaments like gella reginellas nocardia actinomyces and non-filamentous like corny bacterium deia and leria monocytogenes the topic of today's video nonsporeforming rods can also be classified as aerobic and anerobic if they are aerobic they will be motile and immotile the imot are nocardia esteroides and corny bacterium dfia while the motal is the leria monocytogenes leria monocytogenes is the small gr positive Rod it is a robe but it can be a facultative enob it is intracellular it is weekly beta hemolytic which means that it will form a small clear Zone in the blood aggar it is pleomorphic pleo means many and morph is for shapes it means that it has got many shapes not actually many shapes it occurs in rods but it forms V or L shaped formations under microscopes that's why it is called pleomorphic it is catalyzed positive for those of you guys who do not know what is catales it is an enzyme that converts hydrogen peroxide into water and oxygen and oxygen responsible for forming bubbles one really high Y thing that I want to mention here is that leria grows well at cold temperatures leral lives in food we're going to talk about its habitate in a moment but now let's focus on the cold temperature story so storage of contaminated food in refrigerator can increase the risk of gastroenteritis this paradoxical growth in the cold temperature or cold is called cold enhancement leria monocytogenes is nonfilamentous nonpor forming but it is motile because it exhibits an unusual tumbling motility that distinguishes it from corny bacterium Gia which is non-motile leria monocytogenes produces a toxin that is leral lysin to be specific that is leral o l it is responsible for causing listeriosis menitis and sepsis in newborns and pregnant women and in immunosuppressed adults it can also cause fibral gastroenteritis in immunocompetent patients as you can see in this picture this spectum is purple colored which shows that this is scam positive and is Rod shaped Lector outline we are done with the introduction and classification now we'll be looking at morphology habitate and transmission pathogenesis clinical findings lib diagnosis treatment prevention and atheen as usual will review the lecture morphology leria monocytogenes is rot shaped size it varies in length from .5 to 2 micrometers it's purple or blue in color CA of the presence of thick peptid or glycin layer in its cell wood as you can see in this picture this is its thick peptidoglycan layer that stained it purple it is arranged in V or L-shaped formations when seen under a microscope and these formations are similar to corny bacterium D thei structure being gr positive it will have a thick peptidoglycan layer it is not capsulated but this organism exhibits an unusual tumbling movement that distinguishes it from corny bacterium dfia which are know motile it is nonpor forming but it does produce a toxin that is leral LIN o this is how it looks like under the microscope this is It's Rod shaped this is wi shaped formation and also this one is the w-shaped formation the arrangement that is similar to the corny bacterium D theia habitate hosts human beings are the host but it can be found specifically in the genal urinary area and to be more specific in the female genital tract this organism is distributed worldwide in animals plants and soil and from these reservoirs it is transmitted to human via fugo oral route and by primarily ingesting unpasturized dairy products like milk and undercooked or deli meats raw vegetables contaminated food and it can also be transmitted from mother to fetus or baby but the only passage of nutrition between the mother and the fetus is placenta so if the mother is infected the infection will be transmitted from mother to the fetus it can also be transmitted via vaginal transmission during delivery when the baby is being delivered and mother's infected with leria infection baby will get that infection when it passes through the birth canal and also the contact with domestic form animals and their feces leria infection occurs primarily in two conditions number one in the fetus or in a newborn as a result of transmission across placenta or during delivery as we just discussed and number two in pregnant women and immunosuppressed adults especially renal transplant patients why the pregnant women get infected because in their third trimester they have reduced cell mediated immunity pathogenesis the first step in the pathogenesis of any bacteria will be the entry into the human body via ingestion or via skin cut or anything but in case of leria it is ingestion following ingestion the bacteria appear in the colon that can colonize the female genital tract and from there bacteria can infect the fetus if membranes Eruptor or infect the neonate during Passage through the birth canal pathogenesis of leria monocytogenes depends on the organism's ability to invade and survive within cells and the pathogenesis is pyogenic type of pathogenesis let's talk about its pathogenesis in detail don't worry this flowchart is as easy as it seems complex let's T the first thing is that leria will enter the human body and after entry it appears to be in colon and what happens in Colon it is exposed to number one gastric HCL number two proteolytic enzymes and number three B salts and what happens in response to that the stress response genain of leria does what it adheres leria to human cells okay how leria has got internal that adheres it to human cells that has EAD herin let us talk about that in more detail invasion of cells is mediated by internalin that is made by leria and EAD herin on the surface of human cells that is the human cell and that is leria it has got this internalin and human cell has got this EAD herin what happens when they interact they adhere to each other ability of leria to pass through the placenta enter the men Andes the three protective layers of the brain and spinal cord and in Wade the gastrointestinal tract depends on the interaction of these two the internalin and EAD herin and the EAD herin present on these tissues and what happens when they interact leria enters into the human cells in the human cells there is fome in some places or books you'll find fome but in the other you'll find fome what's the difference fome is just the fome and the fome is the fusion of fome with the liome and that's the mature fome that has a full capacity to kill any microb and leria will be engulfed by that fome the intracellular fluid of human cells is acidic so that acidity will cause leria to release what to release its toxin the bacterial l leral Len o and what will that toxin do it will form pores in the cells that will help the leria to escape from fagone and enter into cytoplasm of the cell and thereby distracting the fagone and also it will release phospholes C this is an enzyme it will does what it will break down the phospholipid of phagosome and its cell membrane now this Sac having the leria is destroyed so leria is free now and it will enter the cytool means the cytoplasm of the cell as now leria is present in the cell let me tell you something really amazing leria will enter the cell leria produces leral lien and it escaped foma and it's now in the cell what's the amazing thing that I wanted to tell you it is that leria monocytogenes can move from one cell to the other by means of actin Rockets what are these actin Rockets I'm glad you asked these are the filaments of actin they polymerize and Propel the bacteria through the membrane of one human cell into another and like that bacteria is moving from one cell to the other and is spreading the infection as leria preferentially grows intracellularly cell mediated immunity is more important toost defense than humoral immunity suppression of cell mediated immunity predisposes to leria infections we almost done with the pathogenesis but let's talk about the verance factor the first verance factor that played a major role in the pathogenes of leria monocytogenes is internalin that does what it helps the leria to attach to the host cells the second wearless factor is a toxin released by leria monocytogenes and that is leral len o the lllo that does what it helps the bacteria to escape from the phagosome destruction and get into the cytoplasm of the cell to actually cause infection the third virulence factor is the fosol lipas its action is similar to leral lysin that is to help the bacteria escape the phagosome and get into the cytoplasm the fourth virence factor is the actin Rockets or the actin polymerization the ACT a they does what they allows bacterial movement between the cell the rocket tail that asymmetrically connects to host cytoskeleton propelling the pathogen between the cells and the fifth your lens factor is survival at low temperatures low temperatures induce RNA helay that stimulate the replication of bacteria bacteria will also form biofilm at low temperatures the fella propulsions occurs at low temperatures following are the diseases caused by leria the first one is listeriosis the second one is man itis the third one is sepsis and we've got fibral gastroenteritis bacteremia and the last one is granular mosis infanti septica as its name shows that infants will get that disease clinical findings infection during pregnancy can cause abortion premature delivery or sepsis during peripartum period newborns infected at the time of delivery can have acute menitis 1 to 4 Weeks Later bacteria reach the men GES via bloodstream so there will be bacteria infected mother is either asymptomatic or has an influenza like illness leria monocytogenes infections in imuno compromised adults can be either sepsis or menitis and menitis will have its own symptoms like fever neck stiffness headache altered mental status in immunocompetent patients gastroenteritis can occur and that will be characterized by water diarrhea Fe fever headache myalgia abdominal cramps but little vomiting La diagnosis of leria monocytogenes is primarily dependent on CR staining and culture for lib diagnosis we will need the samples of blood a spinal fluid cause Jus menitis placenta CU mother and baby both are involved and some samples from some of the body tissues and we'll go for ground staining and this bacterium is Grand positive because of purple or blue color under microscopy this bacterium is shaped and has v or L-shaped formations and these formations resemble the dorids of the corny bacterium D theia and the bacterium varies in size from .5 to 2 micrometers and it's purple or blue in color cuz it's SC positive as in this picture you can see this is the rod shaped bacterium this one and it has got V shaped formations or L-shaped formations and these resemble the dorids of coron bacterium D theia culture colonies of the leria monocytogenes are small gray colored and they have a narrow zone of beta hemoid on blood egar plate if the organism found in colonies is leria monocytogenes then it will be morti and that distinguishes it from corny bacterium D theia this is how it look on culture the small colonies and there is some sort of beta hemolysis just like that the narrow zone of beta hemolysis on blood agar plate identification of leria monocytogenes is also made by sugar fermentation tests and Camp test treatment of invasive diseases such as menitis and sepsis consists of ampicilin with or without gentamycin if this one is not useful then trimethoprim sulfamethoxazol can be used and the resistance strains of lisam monocytogenes are rare prevention is difficult cuz there's no immunization we can go for proper hand wash in and the only important thing we can do is by limiting the exposure of pregnant women and immunosuppressed patients to potential sources such as farm animals and pasteurize rary products like milk and raw vegetables all right guys let's review everything in this short table the organism we discuss today is leria monocytogenes it is responsible for causing listeriosis menitis sepsis gastroenteritis spontaneous abortion and bacteria it is trans transplant during delivery by consuming certain foods and also F orally its hosts are humans and the main reservoirs are animals plants and soil and from these reservoirs the bacteria is transmitted to humans diagnosis is primarily based on grum staining microscopy and culture treatment is done with ellin if not then trith sulfam oxisol is useful But be sure that ellin is given with or without chomy and that's it for today's video I hope you enjoyed it if you've got any suggestions feel free to leave them Below in the comment section and if you want to connect with me on my socials I've got my Instagram Twitter and I'll catch you in the next video till then assalamu alaykum