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 Variable human microbiome Describe the structure of the skin and mucous membranes, and the ways pathogens can invade the skin. Epidermis, Dermis – secretions and portals for entry*, Subcutaneous layer Dry/salty; lysozyme; fatty acids; defensins  protection Provide examples of normal skin microbiota, and state the general locations and ecological roles of its members Mostly gram positive and some yeasts Aerobic- corynebacterium xerosis Anaerobic- Propionibacterium acnes Yeasts- Malassezia furfur Can grow on oils Staphylococcus Low gc gram + cocci in clusters Coagulase+ in aureus – clots fibrin in blood; other toxinx can cause: Folliculitis, furuncles (boils), carbuncles. Toxemias (occur when toxins enter bloodstream). Scalded skin syndromeand TSS Streptococcus Low gc gram + cocci in chains Categorized by *hemolytic enzymes (A is most important)- why diseases have red color  Virulence factors: M protein- anti compliment/ antiphagocytosis can cause impetico erysipelas , enzymes and toxins Group A Flesh eating* Necrotizing fasciitis many toxins – Streptokinases; Hyaluronidase; Exotoxin A, superantigen; Cellulitis;  Diphtheroids Differentiate Staphylococci from Streptococci, and name several skin infections caused by each. List the causative agent, mode of transmission, and clinical symptoms of Pseudomonas dermatitis, otitis externa, and acne. Gram – rods 5 groups  Pseudomonas dermatitis- self limiting 2 weeks, pools hot tubs,  otitis externa- swimmers ear List the causative agent, mode of transmission, and clinical symptoms of these skin infections: warts, smallpox, chickenpox, shingles, cold sores, measles, rubella. Warts- papilloma virus Smallpox- variola virus (pox)  Chickenpox- herpes virus  Shingles- herpes virus– reactivation of latent VZV- move down peripheral nerve Cold sores- herpes simplex virus – HSV-1 and HSV-2  Measles- paramyxovirus – respiratory transmission; macular rash andkoplik’s spots rubeola Rubella (german measles) – togavirus Macular rash and fever Rubella MMR vaccine Define conjunctivitis. Inflammation of the conjunctiva Aka pink eye or red eye Haemophilus influenzae List the causative agent, mode of transmission, and clinical symptoms of these eye infections:  neonatal gonorrheal ophthalmia,  Neisseria gonorrhoeae gram – cocci transmitted to newborn during birth antibiotics at birth inclusion conjunctivitis Chlamydia trachomatis  Antibiotic ointment Trachoma Chlamydia trachomatis  Leading cause of blindness worldwide Severe conjunctivitis scars lead to blindness herpetic keratitis HSV-1 – leads to infections of cornea and even blindness Trifluride to treatLECTURE 30 Define central nervous system and blood-brain barrier. Brain, spinal chords, meninges (membranes)  Blood brain barrier (capillaries) - prevents passage of materials  Differentiate  Meningitis inflammation of the meninges Encephalitis- inflammation of the brain Discuss meningitis caused by Haemophilus influenzae, Neisseria meningitides, Streptococcus pneumoniae, and Listeria monocytogenes. Bacterial Menengitis (septic meningitis) – headache fever, rash, stiff neck, convulsions, coma, graimt stain or latex agglutination of CSF; treatment with cephalosporins Hemophilus influenza- in young children; gram – aerobic, normal throat microbiota, **prevented by Hib vaccine**, capsule antigen type B Neisseria meningitis- healthy people can be carriers, throat infection/ rash, outbreak in college dorms, gram -  Streptococcus pneumonia- about 70% healthy people are carriers, most common in children gram+ cocci, prevented by vaccination; mortality 30% in kids, 80% in elderly Listeriosis- listeria monocytogenes, gram+ rod, causes still birth, foodborne, reproduce in phagocytes,  Explain how bacterial meningitis is diagnosed and treated. Discuss the epidemiology of tetanus, including mode of transmission, etiology, disease symptoms, and preventive measures. Tetanus-  Clostridium tetani gram + endospore forming obligate anaerobe, grows in deep wounds, tetanospasmin blocks relaxation pathway in muscles Tetanus toxoid (DTP) vaccine  State the causative agent, symptoms, suspect foods, and treatment for botulism. Botulism Clostridium botulinum gram + endospore forming obligate anaerobe, ingestion of botulinal toxin Treat with antitoxin Infant- C. botulinum growing in intestines, wound botulism- growth inwounds Discuss leprosy, including mode of transmission, etiology, disease symptoms,and preventive measures. Leprosy Mycobacterium leprae – acid fast rod, grows in peripheral nerves and skin cells, transmission requires prolonged contact with infected person Tuberculoid (neural) form- loss of sensation in skin areas a positive lepromin test Lepromatous (progressive form) – disfigured nodules all over body, negative lepromin test Discuss poliomyelitis, rabies, and arboviral encephalitis, including mode of transmission, etiology, and disease symptoms. Poliomyelitis Transmitted by ingestion,  Initial symptoms- sore throat and nausea Viremia may occur is persistent, virus can enter the CNS 3 serotypes- salk vaccine- inactivated virus; sabin vaccine- attenuated virus Compare the Salk and Sabin polio vaccines. Look in book  Compare the preexposure and postexposure treatments for rabies. Arboviral encephalitis- anthropod borne , control by controlling mosquitos Rabies-Caused by rabies virus; furious rabies vs paralytic rabiesTreatment and prevention- vaccine immune globin; incubation period may be very long, virus multiplies in skeletal muscles then brain cells causing encephalitis Preexposure prophylaxis: injection of vaccine Postexposure treatment: vaccine plus rabies immune globulin (RIG)Lecture 31 Identify the role of the cardiovascular and lymphatic systems in spreading and eliminating infections. List the signs, symptoms, and causes of sepsis Bacteria growing in the blood Gram-negative sepsis- endotoxins cause decrease in BP Gram-positive sepsis- usually nosocomial  puerperal sepsis- aka childbirth fever Describe the endocarditis. Inflammation of the endocardium, slow progression Subacute- strep staph entero Acute-s. aureus usually fatal and


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FSU MCB 2004 - Notes

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