Upper Respiratory Tract Infections PDF

Title Upper Respiratory Tract Infections
Course Microbiology
Institution Aston University
Pages 13
File Size 369.1 KB
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Summary

Upper Respiratory Tract Infections ԆUpper Respiratory TractInfectionsCompleted Confidence ⭐μμμ Ex. Reading Module CMC BYԉFCԆ Things to do: Type Lecture Learning Objective: normal flora of the URT primary and secondary bacterial invaders clinical manifestations, associated microorganisms and treatmen...


Description

Upper Respiratory Tract Infections

CMC BY3FC1

Lecture Learning Objective: normal flora of the URT primary and secondary bacterial invaders clinical manifestations, associated microorganisms and treatments options for common URTI Streptococcus pyogens Group A Strep): virulence factors case study: laboratory diagnosis of streptococcal (group A tonsillitis: the diagnostic template Respiratory Tract nose → trachea → alveoli

we have mucous helps prevents infections lower rt - does not have normal flora (sterile environment) upper rt - does have normal flora Normal flora in URT they help keep our urt in healthy conditions but they can become our enemy if not managed  Common Residents 50% of normal people) Viridans streptococci big cluster when you grow them on blood agar, it will form little green colonies e.g. streptococus salivaries Anaerobic Microorgansims large gram negative rods e.g. Bacteriodes sp

Haemophilus influenza tiny gram negative rods Candida Albicans  Occasional Residents 10% they tend to be true pathogens they are transient pathogens - we don't have them all the time Streptococcus Pyognes Streptococcus pneumoniae  Organisms associated with colonisation of URT following antibiotic treatment Coliforms E.coli) Pseudomonas sp. Candida albicans (oral thrush) Professional Invaders True Pathogens) of the URT "successfully infect the healthy respiratory tract: possess mechanisms to attach and spread" without the need for a patient to be depilated rhinovirus - common cause of common cold can affect cells within 15 mis streptococcus pyogenes contains surface proteins - F and M protein (helps bind to fibronectin) True pathogens need to do three things: adhesion to normal mucosa e.g. surface proteins, capsid proteins avoid host defence e.g. capsule

damage local tissue: production of invasins and exotoxins e.g. pneumolysin - produced by streptococcus pneumoniae Secondary invaders of URT "cause disease when host defences are impaired" e.g. normal flora e.g. C. albicans some of our primary invaders can also take advantage of you when you are unwell as well such as S. pneumoniae Times when you are most vulnerable Post viral infections if you have a common cold (rhinovirus), the URT is damaged and if its not taken care of, the normal flora there will take advantage and make it worse Compromised immune response AIDS, cancer chemotherapy, young/elderly, alcoholics Foreign body adding things to the body e.g. endotracheal tube - will cause a little damage and the normal flora will take advantage of that URTIs common cold oral candidiasis sinusitis pharyngitis / tonsillitis acute epiglottitis - directed learning otitis (media externa) - directed learning Common Cold (coryza) the most common URTI - caused most commonly by rhinovirus

clinical manifestation: incubation period: 24 days symptoms usually start after 4 days nasal discharge; sneezing sore throat sometimes temperature 37.5ºc) and headache may descend down to the trachea and the larynx seasonal: common during the winter, more people stay indoors close together making the virus spread quicker common against children 27 symptoms usually go after a week causative organsisms: viruses: rhinovirus - most common RSV coronavirus treatment: no treatment - just giving supportive medicine - paracetamol antibiotics not given Oral Candidias (thrush) clinical manifestations: changes in flora can upset the balance allowing overgrowth of fungi raw inflamed mucous membranes white fungal plaques predisposing factors:

broad spectrum antibiotics - its gets rid of normal flora allowing fungus to grow contraceptive pill - chnages hormonal balances systemic steroids chemotherapy immunosuppression e.g. HIV, extremes of age causative microorganism: candida albicans treatment: dont treat with antibiotics because its a fungus not a bacteria Nystatin / clotrimazole pastilles (antifungal) 1 pastille 4 times a day - gets rid of the thrush Severe oral thrush in HIV patients may need treatment with a systemic antifungal drug e.g. fluconazole 100 mg 1430 days) because the T-cells are really loe Sinusitis clinical manifestations: facial pain and swelling localised tenderness causative organisms: usually viral deinfluenza virus but bacterial infection may occur due to secondary invaders Streptococcus pneumoniae and Haemophilus influenzae treatment:

viral - no treatment - just supportive bacteria - multiple possible treatments  Amoxicillin beta lactin - acts on the cell wall 125250 mg, 35 days  Augmentin amoxicillin + clavulanic acid used for beta lactamase producing bacteria enzyme that are produced by bacteria that break down the beta lactin ring in the penicillin structure 250 mg, 37 days  Doxycycline 100 mg 37 days  Erythromycin 250500mg 37 days to find out if its a viral infection or bacterial - take a clinical sample and put it into culture if nothing id growing on the culture - viral Pharyngitis / Tonsilitis clinical manifestations: common in children, fever, sore throat cervical lymohadenopathy (sollen lymph nodes) purulent discharge causative microorganisms:

viruses - main cause 70% e.g. adenovirus bacteria: streptococcus pyogenes (common) neisseia gonorrhoeae (rare) treatment: viral: - no treatment bacteria: penicillin V 500 mg / 10 days cephalexin: 500 mg / 10 days erythromycin: 500 mg / 10 days Post streptococcal tonsillitis complications really important diagnosis and treat properly if not: Peritonsillar abscess PTA, quinsy) tonsils are hugely swollen - full of bacteria and inflammatory material cant treat with antibiotics either because they wouldn't penetrate all that debris surgically remove the abscess and then treat with antibiotics after Rheumatic fever (autoimmune) affects heart, nerve and the skin Glomerulonephritis (autoimmune) affects kidneys all this happens because S.pyogenes has surface proteins called M proteins that helps the organism bind to us and they share similar structure to our heart, kidneys etc

so when we produce antibodies against the M proteins it will attach our organs as well Scarlet fever (toxin-associated) the organism Group A strep.) produces an erythrogenic toxin and a pyrogenic toxin spreads throughout our bloodstream and causes scarlet fever Streptococcus pyogenes Group A strep) - Mechanisms of pathogenicity ability to colonise the host and invade tissues ability to bypass host defences ability to damage host through production of toxins Adhesion: F-protein and M-protein F protein - most commonly used to adhere recognises host cell fibronectin M proteins - anchored through its carboxyl end in the cytoplasm and protrudes through the cell wall as fimbriae / pili helps the organism to adhere to host organism (exocellular matrix) M proteins are highly antigenic ? - we produce antibodies against them 80 distinct immunological types (re-infection common) Evasion of host defences uses molecular mimicry: hyaluronic acid capsule we have lots of hyaluronic acid in our extracellular matrix - avoiding immune detection also binds to cellular hyaluron receptor CD44 mediating adherence and invasion immunoglobulin binding protein binds to the Fc region of IgG and IgA (wrong way round) preventing opsonisation

C5a peptidase surface protein that cleaves C5a (a potent chemotactic peptide) thus limiting the recruitment of neutrophiles to the site of infection Produces virulence factors (toxins) Streptolysin O and Streptolysin S protein high MW 60000 contributes to heamolysis cardiotoxic - affects our heart antigenic - we produce antibodies against it DNAase produces 4 types A, B, C, D most common is B hydrolyses nucleic acids Streptokinase antigenic protein combines 11 with plasminogen to make functional plasmin plasmin = protease which can hydrolyse fibrin and other host proteins Hyaluronidase dissolves its own cellular hyaluronic acid capsule but also dissolves our own hyaluronic acid and promotes movement of bacteria through tissue Streptococcal pyrogenic exotoxin SPEs) pyrogenic - induces temperature responsible for rash we see in scarlet fever

superantigen - it does not need to be broken down and directly links the T cell receptor with the MHC II receptor non-specific binding - many more T cell being activated 1 in 5 T cells activated (compared to 1 in 10000 look over last years notes Identification of S. pyogenes Basic Identification colonial appearance: 12mm grey colonies entire edge surrounded by a large zone of beta-haemolysis bacitracin sensitive: large zone of inhibition provides presumptive identification of S.pyogenes Full Identification Lancefield Grouping: detection of group specific CHO cell wall antigen how it works: stripping away the surface carbohydrate using nitric acid and then testing the organism against specific antibodies Common Antibiotics Beta - lactams e.g. amoxycilin, pencillin, cephalosporins, augmentin inhibit the penicillin-binding proteins in cell wall synthesis leading to cell lysis (death) side effects: hypersensitivity 1 in 10

anaphylactic shock Diarrhoea and vomiting interactions / patient advice: reduced effectiveness of oral contraceptive complete the course Tetracyclines e.g. doxycycline, oxytetracycline, minocycline inhibits the protein syntheses - prevents the first charged aminoacyl tRNA from binding to the 30S subunit of the ribosome side effects deposited in growing teeth and bone not recommended for children and pregnant women Diarrhoea and vomiting interactions / patient advice: reduced effectiveness of oral contraceptive complete the course Macrolides e.g. erythromycin, azithromycin, clarythromycin, telithromycin inhibits protein synthesis - binds to rRNA in the 50S and blocks translocation (no release of tRNA often used as an alternative to pencillin side effects: nausea, diarrhoea and vomiting interactions / patient advice: reduced effectiveness of oral contraceptive complete the course...


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