Transcript chapter28
Blood and Lymphatic Infections Chapter 28 Tularemia (Rabbit Fever) Symptoms Characterized by development of skin ulcerations and enlargement of regional lymph nodes Other symptoms include Fever Chills Achiness Tularemia (Rabbit Fever) Causative agent - Francisella tularensis (aerobic, Gram- rod) Pathogenesis Causes ulcer at entry sight Lymphatic vessels carry organism to regional lymph nodes, which may rupture 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 90% of infected individuals survive in the absence of treatment 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 Animals generally free of illness 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 (Gram- rod) 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 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 plasmids Smallest is Pla Causes protective clots to dissolve via activation of plasminogen activator Middle plasmid codes Yops (Yersinia outer-membrane proteins) and regulators of Yops proteins Yops permits entry of organism into macrophages where they replicate and interfere with innate immunity Last is F1 Becomes anitphagocytic capsule Used in plague vaccine Not very good and notorious for adverse reactions Pathogenesis Plague (Black Death) 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 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 Gentimicin, 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 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 Pathogenesis of Epstein-Barr Virus 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 Yellow Fever Symptoms Disease can range from mild to severe Most common form may be only fever and slight headache lasting a day or two Severe disease characterized by high fever, nausea, nose bleeds and bleeding into the skin, black vomit from GI bleeding and jaundice Mortality rate of severe disease can reach 50% Reason for the variation in symptoms is unknown Yellow Fever Causative agent Enveloped, single stranded RNA arbovirus Belongs to flavivirus family Virus multiplies in mosquitoes Mosquitoes transmit virus to humans Pathogenesis Introduce via bite of Aedes mosquitoes Multiplies and enters blood stream Carried to liver Jaundice results in liver damage Injury to small blood vessels produces petechiae Kidney failure is a common consequence of disease Yellow Fever Epidemiology Reservoir mainly infected mosquitoes and primates in tropical regions of Central and South America and Africa Periodically spread to urban areas via mosquito bite Prevention and Treatment Control achieved by spraying and elimination of breeding sites Control almost impossible in jungle regions Attenuated vaccine available for high risk groups No antiviral treatment Malaria Symptoms “flu-like” Includes fever, headache and pain in the joints and muscles Generally begin 2 weeks post infection Transmission via bite of infected mosquito Symptom pattern changes after 2 to 3 weeks Fall into three categories Cold phase – abruptly feels cold and develops shaking Hot phase – follows cold phase Temperature rises steeply reaching 104°F Wet phase – follows hot phase Temperature falls and drenching sweat occurs Malaria Malaria Causative agent Human malaria caused by four species of genus Plasmodium • P. vivax, P. falciparum, P. malatiae, P. ovale Infectious form of parasite injected via mosquito Carried by bloodstream to liver Infects cells of liver Thousands of offspring released to produce infection in erythrocytes Pathogenesis Malaria Characteristic feature Recurrent bouts of fever followed by times of wellness Caused by erythrocytic cycle of growth and release of offspring Each species has different incubation periods, degrees of severity and preferred host age and range Spleen enlarges to cope with large amount of foreign material and abnormal RBC Common cause of splenic rupture Parasites cause anemia by destroying red RBC and converting iron from hemoglobin to an unusable form Stimulates immune system Overworked immune system fails and immunodeficiency develops Malaria Epidemiology Once common in both temperate and tropical areas Now dominantly disease of warm climate Eliminated from continental U.S. in late 1940s Mosquitoes of genus Anopheles are biological vectors Infected mosquitoes and humans constitute reservoir Transmission via mosquitoes, blood transfusion and sharing of syringes Malaria Prevention and Treatment Treatment is complicated Due to different stages of mosquito life cycle Chloroquine Effective against erythrocyte stage Will not cure liver infection Primaquine and tafenoquine Generally effective against exoerythrocyte stage and certain species gametocytes