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28 Cards in this Set
- Front
- Back
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Subacute Bacterial Endocarditis
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-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 |
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Subacute Bacterial Endocarditis
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-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 |
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Subacute Bacterial Endocarditis
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-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 |
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Gram-Negative Septicemia Symptoms
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-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 |
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Gram-Negative Septicemia Causative Agent
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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 |
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Gram-Negative Septicemia Pathogenesis
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– 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 |
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Gram-Negative Septicemia Epidemiology
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– 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 |
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Gram-Negative Septicemia Prevention and Treatment
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– Depends largely on identification and effective
treatment of localized infections – Treatment against causative organisms • Treatment methods will vary according to infecting organism |
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Tularemia (Rabbit Fever) Symptoms
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– 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 |
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Tularemia (Rabbit Fever) Causative agent
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– Francisella tularensis
• Non-motile, aerobic, Gram (-) rod |
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Tularemia (Rabbit Fever) Pathogenesis
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– 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 |
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Tularemia (Rabbit Fever) Epidemiology
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– 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 |
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Tularemia (Rabbit Fever) Prevention and Treatment
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– 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 |
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Brucellosis (Undulant Fever) Symptoms
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– 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 |
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Brucellosis (Undulant Fever) Causative agent
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– 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 |
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Brucellosis (Undulant Fever) Pathogenesis
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– 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 |
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Brucellosis (Undulant Fever) Epidemiology
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– 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 |
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Brucellosis (Undulant Fever)Prevention and Treatment
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– 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 |
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Plague (Black Death) Symptoms
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– 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 |
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Plague (Black Death) Causative agent
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– 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 |
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Plague (Black Death) Pathogenesis
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– 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% |
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Plague (Black Death) Epidemiology
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– 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 |
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Plague (Black Death) Prevention and Treatment
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– 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 |
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Infectious Mononucleosis Symptoms
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– 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 |
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Infectious Mononucleosis Causative agent
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– Caused by Epstein-Barr virus • Double-stranded DNA virus • Belongs to herpesvirus family
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Infectious Mononucleosis Pathogenesis
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– 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 |
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Infectious Mononucleosis Epidemiology
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– 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 |
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Infectious Mononucleosis Prevention and Treatment
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– Avoiding saliva of another person
– No vaccine – Acyclovir inhibits productive infection • Has no activity on latent viruses |
