Bacterial Respiratory Infections Flashcards
Respiratory Infections
there are a lot so they are divided into upper and lower respiratory systems
upper: head, neck, typically ear, eye, or throat infection
lower: chest and down, can be fatal in some situations
Upper Respiratory Tract
this includes: nose + nasal cavity, pharynx (throat), and epiglottis (closes off lungs when u drink)
they are all lined by mucous membranes (globlet cells make mucous) –> Mucociliary escalator gets rid of mucous + bacteria stuck in it
Tonsils = lymphoid organ, keep!
Eyes = sterile, bathed in lysozyme
Ears = middle and inner should be sterile bc of the wax
often people who get mouth/throat infections are at risk of getting that infection in their ear as well because the eustachian tube connects the ears to the mouth
Lower Respiratory Tract
includes the larynx (voice box), trachea (windpipe), bronchi, and lungs
usually pretty sterile
lungs surrounded by 2 membranes (pleura); inflammation is called pleurisy (pleuritis) and it hurts because your lungs are inflamed which makes it hard to breathe
Pink eye, Earache, and Sinus Infections
they are all really common, and people can often have it at the same time from the same agent because of the Eustachian tube (which connects the mouth to the ears)
infection damages ciliated cells, results in inflammation + swelling, prevents removal of secretions –> fluid, and pus accumulate behind eardrum which causes the pressure for otitis media (earache)
biofilms = chronic
antibiotics (DRS said a story about how you shouldn’t take a generalized antibiotic if you can figure out exactly what’s wrong with you so that bacteria can’t grow resistance)
Conjunctivitis
Pink Eye!
tears, redness, swollen eyelids, sensitivity to bright light, and pus build up
Otitis Media
severe earache, pain often causes vomiting
if kids have it you’ll know because they’ll scream like crazy, and that’s due to the pressure build up by their eardrum –> quick easy fix for the pain is to puncture the eardrum to release the pressure
Sinusitis
facial pain, pressure, headache, malaise, thick green nasal discharge may develop –> Sinus Infection!
commonly caused by Haemophilis influenzae (gram NEG rod) + Streptococcus pneumoniae (gram POS encapsulated diplococcus)
around 1/3 of otitis media is caused by sinusitis viruses
Streptococcal Pharyngitis (Strep Throat)
Signs/Symptoms + Causative Agent
occurs in the lower respiratory tract, and its basically when you have a sore throat, difficulty swallowing, and fever
Causative Agent: Streptococcus Pyogenes
Gram POSitive and grows in chains
Test: B-hemolysis of blood agar (yk it’s S. Pharyngitis if there’s a clearing around the bacteria on the plate)
Fun fact: Group A streptococcus causes necrotizing fasciitis
Streptococcal Pharyngitis
Virulence Factors
Protein F adheres to fibrin of epithelial cells
Protease: an enzyme that cleaves proteins; more specifically they can cleave the protein that holds epithelial cells together
DNase: when a WBC cell dies it spits out a “DNA net” and because DNA is basically made of sugars, bacteria will stick to it and grow (not somewhere productive), so DNase goes through and cleaves the net up so that bacteria are less likely to stick to it
Hyaluronidase: on epithelial cells there’s hyaluronic acid that catches bacteria and stops it from spreading on the cell, hyaluronidase cleaves the hyaluronic acid
More Virulence Factors for Streptococcal Pharyngitis
these virulence factors are trying to avoid the immune system:
some bacteria have a hyaluronic acid capsule and so they disguise themselves as the host, immune system can’t detect them
protein G is an Fc receptor; binds to the Fc portion of IgG, prevents IgG mediated phagocytosis (IgG stands for immune goblin G, and basically it flips the antibody receptors on a WBC so that the WBC can’t detect the bacteria)
C5a peptidase is produced, which destroys C5a which is good for bacteria because it means WBCs can’t find it
Streptolysins O and S make holes in the membranes of erythrocytes and leukocytes, yields B-hemolysis, inhibits immune system
Some make SPEs (streptococcal pyrogenic endotoxin):
1) some are nasty proteases
2) some are super antigens
Super Antigens
a virulence factor for Streptococcal Pharyngitis sometimes, and it is one of two options SPEs (Streptococcal Pyrogenic Endotoxin) can be
it makes T-Cells bind to MCH-II even if there is no bacteria (antigen) for the B-Cell to present for it, which makes the T-Cell make tons of cytokines and the “cytokine storm” ensues
staph makes TSST-1 (Toxic Shock Syndrome Type 1), NOT strep
Streptococcal Pharyngitis (Strep Throat)
Epidemiology and Treatment/prevention
Epidemiology: naturally only infects humans, but people can be asymptomatic for it; usually it’s spread through respiratory droplets or contaminated food
Treatment/Prevention:
-you can confirm you have strep through diagnostic tests and throat culture
-treat with penicillin or erythromycin which is 90% effective (make sure to treat or else sequelae will pull up)
Sequelae: occurs if there’s left over strep, or if you’ve had strep before (it’s like a door to other infections
Post-Streptococcal Sequelae
Rheumatic Fever: you make antibodies for strep and it crosses w/heart valves, which causes compliment and inflammation of the heart
Endocarditis: bacteria that grow on the heart valve
Glomerulonephritis: nephrons refer to kidney, so it’s the inflammation of the kidneys (what happens is multiple antibodies stick to one bacteria, causing a huge chunky thing floating around in the blood)
Diphtheria
Signs/Symptoms + Causative Agent
Diphtheria is a deadly A-B toxin mediated disease and it’s pretty rare in the US bc we get DBT vaccines
Signs/Symptoms: mild sore throat, malaise, swelling of neck (bull neck) and formation of a pseudomembrane on tonsils and throat, or in the nasal cavity (pseudomembrane is the dead epithelial cells killed by the toxin in the back of your throat that could break off and suffocate you –> cause embolism)
Causative Agent: Corynebacterium diphtheriae
Pleomorphic (morphology changes as it develops), it’s a non-motile, non-spore forming Gram POSitive rode (stains irregularly)
Club shaped, often occur side by side in “palisades”
They are lysogenized which means at some point a phage (virus for bacteria) infected the bacteria, resulting in the bacteria from getting a piece or weird DNA from the bacteria
Diphtheria Toxin Info
it’s an A-B toxin mediated disease; B is the binding part, and A is the active part of the toxin that causes the issue
during something like phagocytosis the A-B unit binds to a receptor and it separates instead of getting eaten up, and the A sub unit ends up become a functional enzyme that inactivates ribosomes, resulting in a halt to protein synthesis and ultimately cell death
Diphtheria
Epidemiology/Treatment + Prevention
Epidemiology: humans are the primary reservoir (where you find it in nature), and usually it’s spread through air, acquired via inhalation
Treatment/Prevention: injection of an antiserum (antibody against the toxin) or just antibiotics for C. diphtheriae, but that only kills the bacteria, not get rid of the toxin
even w/treatment there is a 10% mortality rate!
immunization is v effective
Pneumococcal Pneumonia
Signs/Symptoms + Causative Agent
this is what most adults have, not kids
Signs/Symptoms: cough, fever, chest pain, and sputum production (wet cough, pus, shit from the lungs)
Sputum becomes pinkish or rust colored from blood (redish brown color), and it’s known for causing severe chest pain because you cough so much that you have shallow breathing and the patient develops a dusky color from poor oxygenation
Causative Agent: Steptpcoccus Pneumoniae
it’s a Gram POSitive Diplococcus known as Pneumococcus; has a super thick capsule (virulence factor)
Pneumococcal Pneumonia
Pathogenesis
Pathogenesis: encapsulated pneumococci inhaled into alveoli multiply rapidly, cause inflammatory response
can effect nerve endings, leading to pleurisy
in the capsule there is pneumococcal surface protein (PspA) that interferes with C3b of complement system, blocks phagocytosis
Pnemolysin protein that pokes holes, damages epithelium
Pneumococci may enter blood stream, leading to sepsis of blood, endocarditis (heart valve infection), or meningitis (infection of brain), spinal cord meninges –> all of these are sequela!
Klebsiella Pneumonia
Signs/Symptoms + Causative Agents
Signs/Symptoms: just like pneumococcal pneumonia but also repeated chills because it’s a Gram NEGative rod (LPS causes fever + chills), and production of bloody gelatinous sputum (it’s gelatinous becuase of the sugar capsules mixing w/the blood)
Causative Agent: Klebsiella pneumoniae, Gram NEGative rod
Klebsiella Pneumonia
Pathogenesis + Epidemiology + Treatment/Prevention
Pathogenesis: contracted via inhalation, contact, or medical equipment (ventilators), has potent iron chelator (siderophore: grabs available iron and brings it into bacterium, virulence factor), tissue death and lung abscessed (mega pimple, WBC pus on tissue) may permanently damage tissue, it also often enters the blood, which can cause endotoxic shock
Epidemiology: usually in super old/young people and it circulates hospitals making it increasingly antibiotic resistant
Treatment/Prevention: antibiotics effective if susceptible (some make beta-lactamases which cleave up penicillin); increasingly resistant though so mortality rate goes up to 50% making carbapenemases the last line
Pertussis (Whooping Cough)
Signs/Symptoms + Causative Agent
Signs/Symptoms: you’ve got two stages:
1) Catarrhal Stage: inflammation of mucous membranes, and it’ll looks like a normal upper respiratory infection (runny nose, sneezing, mild cough) and u are v CONTAGIOUS
2) Paroxysmal Stage: repeated sudden attacks, you have violent uncontrollable dry coughs, causes eye blood vessels to rupture, neck veins stand out, and forceful inhalation makes a “whoop” wound
convalescent stage means you’re almost cured and the coughs decrease
Causative Agent: Bordetella Pertussis, Gram NEGative rod
Pertussis (Whooping Cough)
Toxins + Ptx Causes
Toxins: it’s also an A-B mediated toxin disease; it targets a regulatory protein G that runs enzymes on/off. It basically modifies the protein so that it’s stuck on “on” mode, which causes the cell to make TOO much mucous, and it builds around the cilia so it can’t move anymore
Ptx Causes: ciliary action decreased due to an increase in mucous production, lungs can collapse, spasms (partial mucus plugging let air enter but not escape)
Tuberculosis TB
Signs/Symptoms + Causative Agent
Signs/Symptoms: it’s an infection by mycobacterium, and at first it’s an asymptomatic lung infection and so people can have it for months are not know it; once it’s active though you get a slight ever, weight loss, night sweating (v indicative), persistent cough for months, and you get blood streaked sputum; it can be dormant and not active for a bit and that’s when people have LTBI (latent tuberculosis infection)
Causative Agent: Mycobacterium tuberculosis and it’s a slender, ACID-fast, rod-shaped bacterium; it’s a strict aerobe w/a long generation time of 16 hours (an issue because antibiotics work better if it divides fast), and it’s cell wall contains mycolic acids (WAXY wall), doesn’t make endospores
TB mainly infects lungs, bit can cause disease in other tissue including bones, kidneys, joints, and CNS
How Tuberculosis works at a bacterial level? DRS drawing explanation –> basically Pathogenesis
when a WBC gets infected with the mycobacterium it sends out a signal (MHC-I) to tell other WBCs to come kill it, so they surround it and try to kill it but they are unable to; this creates a protective barrier for the bacteria live happily, and that structurer of WBCs is called a tubercle (that’s how we get the name tuberculosis), when they are in the tubercle then they aren’t considered, but when they break out that’s when you have active tuberculosis
the macrophages that surrounded the infected WBC becomes foamy and oily like, and when the tubercle bursts it can get into the airway and blood stream to spread —> activated macrophages release into infected tissue and it causes death of tissue resulting in the a “cheesy” material, Caseous Necrosis! (sign of active tuberculosis)
