LS-MCRB 121 1st Edition Lecture 25Chapter 23: Diseases of the Cardiovascular and Lymphatic SystemsI. Sepsis and Septic Shocka. Blood is normally sterileb. Nosocomial invasion commonly due to interventions involving medical devices i. Catheters, IVs, breathing tubesc. Blood bore cellular (phagocytes) and soluble defensesi. Defensins, complement, and iron restriction (transferrin) check growth of microbesii. If defenses fail, microbes can proliferated. Septicemia: acute illness associated with pathogens in blood streami. Generale. Sepsis: Systemic inflammatory response syndrome (SIRS)i. Result of infection-associated inflammatory mediators being released in the blood, although the source of the etiology is not necessarily bloodii. Response the body is undergoing in response to the infectioniii. Symptoms: fever, rapid heart or respiratory rates, elevated white blood cell count1. release of iron from RBCs by microbial action can stimulate microbial growthf. Lymphangitis: red streaks up appendages indicative of inflamed lymph vessels i. Often associated with sepsis or septicemiag. Results if the infection is not quickly controlled and results is SIRSi. Progresses to shock and death from the release of proinflammatory cytokines in response to infectionii. Symptoms: fever, chills, accelerated breathing and heart rate, drop in blood pressure, organ failureiii. Severe sepsis: drop in blood pressure and organ failureiv. Septic Shock: final stage when low blood pressure can no longer be controlledThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.v. These symptoms can progress to further stages in a matter of hoursII. Gram-Negative Sepsisa. Septic shock is most often caused by gram-negative bacteriumb. The outer envelope of gram-negative bacteria contain lipopolysaccharide (endotoxin) which itself can induce ALL of the symptoms of septic shocki. An intravenous injection of endotoxin can be fatal depending on the dose givenii. 1 nanogram of the purified endotoxin is sufficient to cause symptoms like feveriii. 750,000 cases in U.S. annually and 225,000 deathsc. Antibiotic therapy is crucial as a treatment to reduce effects of an endotoxind. Xigris: reduces clotting associated with septic-mediated organ failureIII. Brucellosis (Undulant Fever)a. World’s most common bacterial zoonosisi. 500,000 new human cases/yearii. Middle east is endemic region1. Mediterranean and SE European region, Latin America, and Caribbean also prevalentb. Brucella: small, aerobic, gram-negative coccoid rod shaped bacteriumc. Three common species: i. Abortus (cattle)ii. Suis (swine)iii. Melitensis (goats and sheep)1. Most common and dangerous human pathogend. Economically important animal disease in developing world because of ethical choice of vaccinating animals or killing them offe. Highly infectious, dangerous to handle, easily aerosolized, and highly transmissiblef. Infection by inhalation, ingestion, or break in sking. How it occurs and symptoms:i. Most often occurs by handling carcasses of infected animal, or consumingunpasteurized food products 1. Mexico and Central America in this hemisphereii. Disease in cattle causes abortion of fetus1. Vaccination of cattle has reduced the incidence of disease by B. abortusiii. Incubation period is 1-3 weeksiv. Duration of illness can be weeks to monthsv. Bioterrorism threat: incapacitation and easy transmissionvi. Symptoms: 1. fever (rising and falling (undulant))2. Malaise: overwhelming sick/ill feeling, cannot get out of bed3. Night sweats4. Muscle achesvii. Treatment: combination antibiotic therapy for several weeksIV. Plaguea. Known in the middle ages as the “black death”i. Plague devastated Europe during the 14th centuryii. Nearly 50% of population of some western European countries succumbed to plagueiii. Several successive pandemics reoccurred until the 19th centuryiv. In Middle Ages, there was no accounting for cause other than the wrath of an angry godb. Bubonic Plague: a disease of rodents, transmitted by flea bitei. When rodents die, fleas feed on closest available mammalii. Man is an accidental host of bubonic plaguec. Pneumonic Plague: respiratory transmissioni. Once human is in final stages of plagueii. Follows a septicemic stage that itself is often fataliii. Lung involvement leads to highly transmissible and virulent form1. Pneumonic plague has mortality rate of about 100%iv. Process1. Flea feeds on infected rodent, flea gut becomes occluded2. Upon next feeding, flea regurgitates stomach contents including Y. pestis into bite of new host3. Organism travels through lymphatic system, capsule prevents phagocytosis, enters blood stream, lungs, etc4. Only ~10 bacteria required to initiate a fatal diseased. Etiologic agent: Yersinia pestis gram-negative facultative bacterium, member of Enterobacteriaceaee. Buboes: swollen lymph nodes, usually in groin or under arms, extremely painfulf. Skin becomes darkened and black due to hemorrhaging (black death name)g. Streptomycin and tetracycline effectiveh. Control of rodent population will also help eliminate diseaseV. Lyme Disease Backgrounda. First appeared in 1975 as a cluster of disease cases in young adults first diagnosed with rheumatoid arthritis near Lyme, Connecticutb. Disease progression and lack and rash preceding symptoms suggested tick-borne diseasec. 1983: a spirochete later named Borreliaburgdorferi was identified as the etiologicagentd. Most common tickborne diseasee. In U.S.i. East: Ixodesscapularisii. Westcoast: Ixodespacificusf. Hostsi. Most important reservoir for disease: field miceii. Maintains disease: deer1. Less likely to harbor the ticks most likely to carry the diseaseiii. Ticks feeding on infected mice are deposited in woodlands, grasslands, etc1. Humans usually pick up nymphs (immature ticks), which largely gounnoticed due to small sizeVI. Lyme Diseasea. First symptom is usually a rash at bite sitei. Red area that clears at center as it expands to final diameter of about 15 cmii. Rash in 75% casesiii. Flu-like symptoms in 2-3 weeks as rash fades1. Antibiotics taken at this stage are very effectiveb. If symptoms are not treated earlyi. Enters second phase: heart involvement, irregular heartbeat, chronic neurological symptoms, incapacitation, facial paralysis, meningitis, encephalitisii. Third phase: months or years after infection, arthritis in some