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28 Cards in this Set

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Subacute Bacterial Endocarditis
-Gain entry to bloodstream during dental procedures, toothbrushing or other trauma to mouth or skin
-May become trapped in clots formed near deformed heart valves
-May multiply and produce biofilms
-Organisms inaccessible to phagocytic killing
-As organisms multiply more clot is formed
-Bacteria break away from clot and are washed away
-Clots may block significant vessels; leads to tissue death, infarction and aneurysm
-Masses of organism growing in heart can burrow into tissue and cause abscesses
Subacute Bacterial Endocarditis
-Viridians streptococci account for smaller portion of cases
-More cases of disease produced by Staphylococcus epidermidis
-Occur most often in
Injected-drug users
Patients with intravenous catheter
Particularly if used for extended periods
Individuals with artificial heart valves
Subacute Bacterial Endocarditis
-No proven prevention
-Antimicrobial treatment for susceptible population
-Attention to sterile technique helps prevent occurrence in hospital
-Only bacteriocidal medications are effective in treatment
-Usually two or more given together for prolonged period
-Penicillin and gentamicin given over one or more months
Gram-Negative Septicemia Symptoms
-Violent shaking chills and fever
-Accompanied by anxiety and rapid breathing
-In cases of septic shock
*Urine output drops
*Respiration and pulse become more rapid
*Arms and legs become cool and dusky colored
Gram-Negative Septicemia Causative Agent
Causative agent
– Gram (-) bacteria more likely cause of fatal septicemia
– Shock is common despite treatment
– Mortality rate nearly 50%
– Blood cultures from patients usually reveal
• E. coli – Gram (-) facultative anaerobe
• P. aeruginosa – Gram (-) aerobe
» Generally found in natural environment
• Bacteroides sp.
– Gram (-) anaerobe
» Part of normal intestinal and upper respiratory flora
Gram-Negative Septicemia Pathogenesis
– Generally originates outside of bloodstream
• Alterations in normal body defenses may allow organism to infect blood
– Endotoxin is released
• Antibiotics can enhance endotoxin release
– Macrophages respond intensely to endotoxin to try to localize
– Failed localization allows endotoxin into bloodstream
– Lungs particularly susceptible to irreversible damage
Gram-Negative Septicemia Epidemiology
– Mainly a nosocomial disease
• Reflects high incidence of Gram (-) bacteriemia in hospitals
– General trend to increasing disease that relates to increased life span, antibiotic suppression of normal flora, use of immunosuppressive drugs and biofilm formation of medical devices
Gram-Negative Septicemia Prevention and Treatment
– Depends largely on identification and effective
treatment of localized infections – Treatment against causative organisms
• Treatment methods will vary according to infecting organism
Tularemia (Rabbit Fever) Symptoms
– Characterized by development of skin ulcerations and enlargement of regional lymph nodes
– Other symptoms include
• Fever
• Chills
• Achiness
– Symptoms usually abate in 1 to 4 weeks
• Sometimes may become chronic
– High Mortality
Tularemia (Rabbit Fever) Causative agent
– Francisella tularensis
• Non-motile, aerobic, Gram (-) rod
Tularemia (Rabbit Fever) Pathogenesis
– Causes ulcer at entry site
– Lymphatic vessels carry organism to regional lymph nodes
• Become large, tender and filled with pus
– Spread to other body sites via lymphatics and blood
vessels
– Pneumonia occurs in 10% - 15% of lung infections
• Mortality rate as high as 30%
– Multiplies within phagocytes
– Cell mediated immunity responsible for ridding infection
Tularemia (Rabbit Fever) Epidemiology
– Occurs among wild animals in Northern Hemisphere
– In eastern U.S. most infections occur in winter • Result from skinning hunted rabbits
– In western U.S. infections increase in summer
• Due to bites from fleas and ticks
– Other reservoirs for infection include
• Muskrats, beavers, squirrels, and deer
Tularemia (Rabbit Fever) Prevention and Treatment
– Uses of rubber gloves and goggles when working with animal carcasses
– Insect repellents and protective clothing • Inspect routinely for ticks after exposure
– Vaccine available for workers at higher risk of exposure
– Treated with gentamicin
Brucellosis (Undulant Fever) Symptoms
– Onset usually gradual and symptoms vague
– Symptoms include
• Aches and pains • Enlarged lymph nodes • Weight loss
– Without treatment most cases recover within 2 months
• 15% will be symptomatic for 3 months or longer
Brucellosis (Undulant Fever) Causative agent
– Four varieties of genus Brucella cause disease in humans
• All fall into a single species Brucella melitensis – Traditionally each variety given own species name
depending on preferred host
» B. abortus - cattle
» B. canis - dogs
» B. melitensis - goats
» B. suis - pigs
– Organism is Gram (-) rod
Brucellosis (Undulant Fever) Pathogenesis
– Organism penetrates mucous membranes or break in skin
– Disseminated via lymphatic or blood vessels • Generally to heart and kidneys
– Spleen enlarges in response to infection
• Organisms resistant to phagocytic killing – Can grow within phagocytes
» These organisms inaccessible to antibodies and some antibiotics
– Mortality generally due to endocarditis • Rate is approximately 2%
– Osteomyelitis is often serious side effect
Brucellosis (Undulant Fever) Epidemiology
– Chronic infection of domestic animals
• Generally involving the mammary gland and uterus – Causes contaminated milk and abortions
» Abortion not a feature of human disease – Occurs in workers in meat packing industry
– Major problem in animals used for food
Brucellosis (Undulant Fever)Prevention and Treatment
– Pasteurization most important control measure
– Inspection of domestic animals
– Protective eyewear and gloves when working with animals or animal carcass
– Attenuated vaccine controls disease in domestic animals
– Tetracycline combined with rifampin used for treatment
• Treatment usually given for 6 weeks
Plague (Black Death) Symptoms
– Develop abruptly 1 – 6 days post infection • Transmission via bite from infected flea
– Disease characterized by large tender lymph nodes called buboes
– Other symptoms include • High fever
• Shock • Delirium • Patchy bleeding under the skin
• May also have cough and bloody sputum – Only in lungs infected
» Pneumonic plague
Plague (Black Death) Causative agent
– Yersinia pestis
• Facultative intracellular bacteria
• Resemble safety pin in stained preparation
• Has three kinds of plasmids – Smallest is Pla
» Causes protective clots to dissolve via activation of plasminogen activator
– Middle plasmid codes Yops proteins and regulators of Yops proteins
» Yops interferes with phagocytosis – Last is F1
» Becomes antiphagocytic capsule » Used in plague vaccine
Plague (Black Death) Pathogenesis
– Masses of organism obstruct digestive tract of rat fleas – Flea regurgitates infected material into bite wound – Pla is essential to spread from site of entry
– Organisms multiply within macrophages • Produce F1 capsule while in macrophages
– Macrophages die and release organism • Organism encapsulated and produces Yops proteins and other
mechanisms that enhance survival – Inflammation in nodes results in characteristic swelling
• Nodes become necrotic and spill organisms – Septicemic plague
– Mortality rate of untreated reaches between 50% and 80%
Plague (Black Death) Epidemiology
– Endemic on rodent populations in all continents except Australia
– Prairie dogs, rock squirrels and their fleas are main reservoir
• Hundreds of fleas can transmit plague and can remain infectious for a year
– Can spread person to person by household fleas
– Organism can remain viable for weeks in dried sputum and flea feces
Plague (Black Death) Prevention and Treatment
– Prevention directed by rat control • Proper garbage disposal
• Rat-proof buildings • Guards on mooring ropes • Extermination programs
– Killed vaccine gives short-term partial protection – Treatment via tetracycline for some exposed
individuals to control epidemics
– Gentamicin, ciprofloxacin and doxycycline effective on disease if given early
Infectious Mononucleosis Symptoms
– Appear after long incubation • Usually 30 to 60 days post infection
– Symptoms include fever, sore throat covered with pus, fatigue, enlarged lymph nodes and spleen
– Most cases fever and sore throat disappear within 2 weeks, lymph node enlargement within 3
Infectious Mononucleosis Causative agent
– Caused by Epstein-Barr virus • Double-stranded DNA virus • Belongs to herpesvirus family
Infectious Mononucleosis Pathogenesis
– Infection begins in cells of throat and mouth and
become latent in another cell type
– Virus carried to lymph nodes after replication in epithelial cells of mouth, saliva producing glands and throat
– Infects B lymphocytes
• Infection can be productive or nonproductive – Productive – kills cells – Nonproductive – virus is latent
– Virus activates B cells to produce multiple clones • Clones produce immunoglobulin
Infectious Mononucleosis Epidemiology
– Distributed worldwide
– Infects individuals in crowded, economically disadvantaged areas
• Infects at early age without producing symptoms producing immunity
• More affluent populations missed exposure and lack immunity
– Occurs almost exclusively in adolescents and adults who lack antibody
– Virus present in saliva for up to 18 months • Mouth-to-mouth kissing important mode of transmission
– No animal reservoir
Infectious Mononucleosis Prevention and Treatment
– Avoiding saliva of another person
– No vaccine
– Acyclovir inhibits productive infection
• Has no activity on latent viruses