Yellow causative agent Green symptoms unique to disease Light Blue toxins virulence factors Purple vaccine Violet specific medicine Blood and lymph infections Endocarditis infection of heart valves and surfaces o Acute bacterial endocarditis starts suddenly with fever Usually Staph aureus or strep pneumonia Quickly destroys heart valves form abscesses in muscle that lead to heart failure o Subacute bacterial endocarditis likely to be fatal SBE proceeds more slowly less Caused by organisms with little virulence Causative agent Viridians streptococci and staph epidermidis Shed from heart valve into blood Identified by cultivating samples from arm vein PCR nucleic acid probes used to identify Symptoms Noticeable fatigue slight fever Typically become gradually ill and slowly lose energy over weeks or months May suddenly develop stroke Pathogenesis Bacteria enter blood during dental procedures tooth brushing or trauma Can get trapped in thin blood clots that form around deformed heart valves Biofilm Bacteria continually wash off into circulation Can cause aneurism High antibody levels found glomulonephritis Epidemiology Viridians streptococci less common but increasingly more resistant may be from prophylactic treatment Also occurs in injected drug abusers patients with intravenous catheters artificial heart valves Prevention and treatment Long term antibacterial meds Artificial implants often must be replaces No methods to prevent Sepsis and septic shock Causative agent Symptoms Pathogenesis Can be caused by any microorganism Most fatal cases involve Gram due to endotoxin Normal members of microbiota E coli enterobacteria Bacteroides Or environmental such as Psurdomonas aeruginosa Violent shaking chills fever Often rapid breathing anxiety If septic shock developes urine output drops respiration and pulse increase arms and legs cool and dusty Almost always from infections site other than bloodstream Normal body defenses compromised Toll like receptors on macrophages neutrophils detect pathogen Progresses in stages associated molecular patterns PAMPs release cytokines Systemic release yields cytokine storm This response yields bad outcomes o Inhibiton of systems that normally control inflammation o Suppress adaptive o Activate coagulation cascade o Widespread clotting disseminated intravascular coagulation DIC may lead to multiorgan failure o Phagocytes release tissue damaging lysosomal enzymes Epidemiology damage lungs Mainly healthcare associated disease Rates increasing due to longer life spans antibiotic suppression of normal microbiota immunosuppressive meds Use of medical equipment where biofilms readily form Prevention and treatment Prevented by quick identification Antimicrobial meds to clear initial infection Treatment for shock tissue hypoxia New treatments being evaluated Fluid replacement and support for organ dysfunction Tularemia rabbit fever Causative agent Francisella tularensis Gram Non motile aerobic requires medium enriched with cysteine Symptoms If injury ulceration typically develops at site after 2 5 days o Regional lymph nodes enlarge o Fever chills aches o Usually clears in 1 4 weeks sometimes last months If organism inhaled or infects lungs from bloodstream pneumonia can occur o Dry cough pain beneath sternum due to enlarges lymph nodes o Rare mortality rate 30 if untreated Pathogenesis Epidemiology Enters breaks in skin mucous membranes Carried to regional lymph nodes become large and tender may fill with pus and drain spontaneously Spreads via lymphatics and blood vessels Grows within phagocytic cells Found in wild animals Widespread in northern hemishpers including US except Hawaii Tick bites Inhalation occurs from mowing lawns rodent infested buildings Category A highest risk bioterrism agent Prevention and Treatment Streptomycin or ciprofloxacin or gentamicin Rubber gloves and goggles when handling wild animals Thorough cooking of meat of wild animals Insect repellants Plague black death Causative agent Yersinia pestis Gram Facultative anaerobe non motile Forms biofilms in digestive tract of infected fleas Symptoms Bubonic most common o Following flea bite symptoms appear 2 6 days o Rapid onset of fever Enlarged and tender lymph nodes buboes usually inguinal axillary or cervical o Shock delirium patchy bleeding under skin Pneumonic animal o Inhalation of respiratory droplets from infected patient or o Cough bloody sputum arise 1 3 days o High fever overwhelming pneumonia cough bloody sputum chills Septicemic o Spread by bloodstream o Endotoxin released causes shock o DIC causes bleeding into skin and organs red or black patchy rash o Fever prostration hemorrhagic or thrombotic pneumonia Pathogenesis multiple virulence factors progression to acral gangrene clears lymphatics and capillaries of clots inactivates Protease certain complement system components Infected macrophages die release bacteria YOP s proteins and capsule to avoid phagocytosis Epidemiology Killed 25 of Europe Listed as category A bioterrorism disease In US occurs in about 15 states in the west Prevention and Treatment No current vaccine Tetracycline given preventatively to exposed individuals Antimicrobial medications given within 24 hours of onset of symptoms Rat control measures Viral diseases Infectious Mononucleosis Causative agent Epstein Barr virus EBV dsDNA of herpesvirus family Symptoms Appear after long incubation period usually 30 60 days Fever sore throat covered with pus marked fatigue enlargement of spleen and lymphnodes Fever and sore throat gone in 2 weeks others in 3 weeks Pathogenesis Infects mouth and throat Replicates and is carried to lymph nodes Infects B lymphocytes o Productive o Non productive virus replicates kills B cell plasmid or provirus causes proliferation of B cells production of immunoglobulins most common latent infections as B cell proliferation causes lymph node and spleen enlargement spleen can rupture fatal T cells actively respond and destroy infected B cells EBV genome detectable in nearly all cases of Burkitt s lymphoma and nasopharyngeal carcinoma Epidemiology Prevention and Treatment Worldwide distribution In more affluent populations fewer are infected lack immunity and get exposed later in life entering college EBV present in saliva for up to 18 months after infection occurs intermittently for life Mouth to mouth kissing is important mode of transmission By middle age most have antibody indicating infection Avoid saliva of others No vaccine