Medical Micro Final - Sheet1(1).csv

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Medical Micro Final - Sheet1(1).csv
2012-06-11 00:11:14
Final card set

Clostrdium to Coxiella
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  1. Spores (clostridium)
    Clostridium forms endosopres under adverse environmental conditions. Spores are a survival mechanism. Spores are characterized on basis of position. size and shape. (subterminal or central). Most Clostridium spp. havve ovovid subterminal spores. C. tetani have round termial spores.
  2. Important Clostridium species
    C. perfringes. C. tetani C. botulinum. C. difficile
  3. General info on Clostridium species
    anaerboic Gram positive spore forming bacillus. Four braod pathogenisis Histotoxic group (C. perfringes A). Enterotoxigenic (perfringes type C. or C. difficile). Tetanus (C. tetani). (Botulism) C. botulinum
  4. Clostridum perfringens general info
    Commonly in soil. feces contamination. large number. Cause gas gangreen swelling of tissue and gas release due to fermentation products. Wound contamination. Large gram positive rectingular non-motile rapid growth of BA wihit spreading growth. Classified by toxins produced A-E types.
  5. Clostridum perfrringens toxins
    Alpha toxin (produced by all types. Membrane damaging lysis leukocytes). Beta toxin (unknown mechanims possible membrane damage) . Epsilon toxin. Ioda toxin (does not act on cell membrane. works intracellular. disrupts the cytoskeleton). Theta toxin (spore forming toxin. recognizes and binds to cholesterol in cell membrane) . And Enterotoxin (spore forming toxins binds to proteins on cell type A strains).
  6. Clostridum perfringes treatment
    Removal of necrotic or dead tissue (surgical debridement). Amputation. Penicillin G in high doses. Can adminster antitoxins if severe case. Or use hyperbaric oxygen to inhibit growth of bacteria and facilitate healing.
  7. Specific toxins effects on cell
    Alpha toxin damages the cell membrane breaks down lecithine. Beta toxin similarly damages cell membrane (necrotizing activity). Ioda toxin works intracellular and damages cytoskeleton actin binding. All others are toxins produced during sporulation (beta. epsilon enterotoxin etc).
  8. Toxins produced by which type of C. perfringes
    Type A only produces alpha toxins (gas grangrene). Type B Produes Alpha Beta and epsilon. Type C produces Alpha and Beta. Type D produces Alpha and epsilon. Type E produces Alpha and Ioda toxin.
  9. Soft tissue infection caused by C. perfringes (severe)
    Type A produces gas gangrene. Destroy blood vessels and gets deep into tissue anaerobic environment and spread.Caused by intial trama to host tissue. Causes Fever. pain in infected tissue. local tissue necrosis. Gas bubbles. Infected muscle is discolored. Foul smelling exudate. Systemic toxemia. Tissue degrading enzymes. NON PUS FORMING. (dishwater discharge)
  10. Soft tissue infection caused by C. perfringes (minor)
    Cellulitis. faciitis (connect tissue surrounds muscles). Fasciiits a rapidlly progressive destructive process in which the organims spreads through fascial planes. Faciitis causes suppuration and the formation of gas. ABSENCE OF MUSCLE INVOLVMENT. Very rapid
  11. NSTI epidemology
    About 500 to 1500 in US per year. All age groups. Most likely to effect older indivdiuals with immuno complications. IVDA higher riscks. Also surgical procedures. espically those involving the bowel.
  12. Other clincal disease caused by C. pergringens
    Food poisoning (fairly common via enterotoxins by poor food handling). Necrotizing enteritis (rare) mediated by beta toxin (type C).
  13. Lab diagnosis of C. perfringes
    Anaerobic blood agar will grow quickly and show double hemolysis zone (inner beata by theta toxin. outer by alpha toxin). Can be grown in thioglycolate. Can use a Nagler reaction use an antitoxin to double check (alpha toxin on EYA). Look for lecithinase by alpha toxin. Microscoping examination shows large rectangular gram positive bacilli.
  14. Clostridium tetani transmission
    Transmission by contaminated wounds. Surgical wounds. Deep puncture wounds. Crush wounds. Burns. Dental infections. Animal bites. Delivery or abortion. LARGE NUMBER OF SPORES IN ENVIRONMENT.
  15. Clostridium tentani general info
    Have round terminal spores. Long thin gram positive organism that stain gram negative. Motile by paratrichous flagella. Grow on blood agar with swarming. Beta hemolysis exhibited by isolated colonies. Spores resist boiling 20 minutes. Produces neruotoxins (block the release of NT)
  16. Toxins produced by C. tetani
    Oxygen labile hemolysisn (TETANOLYSIN unknown pathogenicity). TETANOSPASMIN. Heat liable neurotoxin. Inhibits the release of GABA and GLYCINE from inhibitory neurons. Spasitc paralysis.
  17. Mechanism of Action of Tetanus toxin
    TETANOSPASMIN. inhibit the release of GABA and GLYCINE from the inhibitor neuron. Nothing to inhibit Ach causes irreverisble spastic paralysis.
  18. Law jaw clinical name
    risus sardonicus
  19. Lab Diagnosis and Treatment of C. tetani
    Diagnosis based on clicnal presentation. Treatment debridemnt of wound. Metronidzole. Antitoxin (passive). DTaP vaccintaion (uses toxoid which is ctreaed by formaldehyde)
  20. Epidemology of C. tetani
    1 million causes world wide. High mortality rate 20-50. Developing countries is still one of the ten leading causes of death. In less developed countries very high mortality rate. Increasing rate in IVDA. Fatality rate is 90 with no treatment in newborns.
  21. Clostridium botulinum general info
    Anaerobic gram positive rod shaped sporeformer. PRODUCES A PROTEIN NEUROTOXIN. Prevelant in soil. sediment of lakes. ponds. decaying vegetation. Can be in the intestinal tracts of birds mammals and fish.
  22. Tranmission of C. botulinum
    Spores heat resistant. Usually from improper canning makes indeal anaerobic environment. Aquire botulism from eating uncooked food spores. GI. duodenum. blood strea. neuromusclar synaposes.
  23. Virulence factors of C. botulinum
    alpha and beta toons. Bacterial protease. Is an AB toxin. Light chian A 50kDa heavy chain 100kDa. Disulfide bond. A very potent toxin
  24. Mechanims of C. botulinum toxin
    Binds peripheral nerve receptors due to indgest of toxin in adults. in children is ingestion of spores. Binds to the acetylholine neurotransmitter. Inhibits nerve impulses no release of Ach. Causes flaccid paralysis and death due to respiratory or cardiac failure.
  25. Infant botulism
    Most common in infants because they do not have normal flora to outcompete spores. Due to spores in honey.
  26. Clincal diseases caused by Botulinum toxin
    Foodborne botulism. Infant botulism (most common). Wound botulism (very rare. where spores get into open wound. similar symptoms to food born)
  27. Diagnosis and Treatment of Botulism
    Clincial symptoms (18-36 onset. weakness n/v. neuroglogic features of autonomitc nervous system). Dectect toxin by ELISA or mouse bioassay. Heat specimen (serum or feces) to rnrich spores. Treatment involves ventilatory support. metronidazole. antitoxin.
  28. Prevention of botulism
    Proper food handeling and preparation. Psore survive boiling (100 degrees at 1 atm at 1 hour.) Toxin heat-labile boiling or intense heating inactivate the toxin. DO NOT USE BULGES GAS POILED.
  29. Medical use of botulinum toxin
    Use Botox for blephrospams. strabismus. Under investigation migrane headaches. hperhidrosis. Cosmetic purposes.
  30. Clostridium difficile info
    Normal inhabitant of GI. Kept in low number by other GI bacteria. Can cause pseudomembranous colitis. Fecal oral route of transmission
  31. Pseudomembranous colitis
    Inflamation of the colin by exotoxins (Toxin A and B). Cause inflammation and damage of the colon. Leaves yellow membranous patches. Profuse watery diarrhea (10 times daily). Blood in stool. High fever. Weight loss. Severe abdominal pain and tenderness. Death
  32. Diagnosis and treatment of C. difficile
    Detection toxin. with clinical symptoms. In mild cases of C. difficile infection discontinue antibiotics. Severe cases metronidazole or vancomycin needed.
  33. Other clicnically important species of Clostridium
    C. septicum (gas gangrene). C. sordellii. C. tertium
  34. Peptostreptococcus
    Gram postive cocci. Anaerobe. Causes sinusitis. intraabdominal infections. endrometrisist. pelvic abscesses. cellulitis.
  35. Actinmyces
    Gram positive rod. Anaerobe. Normal mouth flora/vaginal flora. Can cause abcess and sinitusis. Causes Actinomyosis causes neck and face region hard red bumps due to draining sinues. Can also be found on IUD can live on plastic
  36. Propionibacterium acne
    Gram postive rod anaerobic. Common skin flora. Can get infection in the bone. CNS
  37. Mobiluncus curtisii
    Gram positive rod. anaerobe. Prevelant cause of vagniosis. More susepetable to HIV infection. Are often gram variable rod shaped. Marker for bacterial vaginosis.
  38. Lactobacillus
    Gram positive rods. Common contaminant in urine. Isolate from blood. Transient bacteremia from urogential. Can cause endocarditis. and opportunistic septicemia.
  39. Bacteroides fragilis general info
    Gram negative ananerobe rod non otile huge capsule. Part of GI flora. Causes opportunistic infections. Major disease causing strict anaerobic after abdominal surgery. PROMINENT CAPSULE. Anti-phagocytic. abcess formation. ENDOTOXIN. major cause of diarrhea in children. Low toxicity. Structure different that nother lipopolysacharides.
  40. Bacteroides fragilis Pathogensis and Immunity
    Virulence factors from three categories. 1. adherence to tissue. 2. Protection form host immune response. 3. Destruction of tissue. Fimbriae and agglutination function as adhesions. Polysaccharide capsule. Lipopolysaccharide. Oxygen tolerance. Wide array of enzymes.
  41. Clincal disesae caused by B. fragilis
    Liver abcesses and intraabdominal. Also skin/soft tissue. Bacteremia. Gastroenteritis (in adults commonly associated IBS)
  42. Lab diagnosis of B. fragilis
    Resistant to vancomyocin and kanamyocin. Growth on LVK media. Hydrolyses of esculin on BBE plate turns black. Grow fast on media only a few days.
  43. Haemophilus general information
    Small Gram negative non motile bacilli that are aerobic or facultatively anaerobic and have fastidious growth requirements.
  44. General information on Haemophilus influenzae
    Have a growth requirment for X (hemin) and V (NAD or NADP) factors. NO beta hemolysis on horse blood. Does not cause influezna more of a secondary infection. Part of normal flora in nasal passage. Some species have capsules and other do not. Flora ones do not have capsules. Types A-F. Type B causes disease in humans. Pili and cell wall adhesions. Capsule resists phagocyctosis. Can degrade IgA antibodies. Hib (human influenzae B). Primarily problem with infants. Transmission through respiratory droplets.
  45. General infomration on Parahaemophilus influenzae
    Growth factor for ONLY V factor. no Beta hemolysis on horse blood agar. Part of normal flora. Does not typically cause disease but can very rarely cause septicemia. endocarditis.
  46. Treatment and control on H. influenzae
    Antibiotics inlcuding chemoprophylaxis. and Hib vaccine
  47. Haemophilus ducreyi
    Chancroid is an inguinal bubo that devloped from a gential chancroid lesion. Is an STD. Soft open wound that produces pus. PRIMARY HUMAN PATHOGEN. Not common in US due to education. Virulence most related to capsule (polyribose capsule). Normally done diagnosed with microscopy of pus and antibody titer.
  48. Pasteurella General overview
    Small gram negative fermentative pleomorphic coccobacilli. Facultatively anerobic. Infects sutured bites or scratches. Most common human pathogen is Pasturella multocida domestic pets are resivoir
  49. Pasteurella Diseases (3)
    1. Localized cellulitis and lymphadentis following animal bite or scratch. 2. In patietns with underlying lung dysfunction worseing of chronic pulmonary disease from aspiration of organism colonzing patients oropharynx. 3. Systemic infection in immunocompromised. Liver diease patients at highest risk.
  50. Pasteurella multocida
    Transmitted by aniaml bites. infections. chronic pulmonary diease. bacteremia. meningits.
  51. Cutlure of Pasterurella
    Will grow on BA or CA and will show large buttery type colonies. WILL NOT GROW ON MAC.
  52. Bordetella general overview
    extremely small. Aerobic nonfermenters. Gram negative coccobacilli. True pathogens isolation alwasy associated with diseases always clicnally significant. TRUE PATHOGEN
  53. Bordetella pertussis
    Man is only natural host. Causes whooping cough. Mild in adults. high mortality in children. Person to person spread via inhalation of infectious aerosols. Decrease incidence after DPT vaccine. Fimbriae not primarily involved in adherence. Exotoxins and hemagglutin mediate attachement to ciliated epithelium of bronichial tree. Cells multiple among cilia of epithelial cells
  54. Virulence factors of Bordettela pertussion
    Adhesion pertactin filamentous hemagglutin (FHA). TOXINS PERTUSSIS TOXIN. adenylate cyclase toxin. dermonecrotic toxin. and tracheal cytotoxin
  55. Pertussis toxin
    AB toxin (6 protein subunits). Subunit 2 and 3 attach to the cell. 2 binds to human tracheal cells (cilia). Filamentous hemagglutin help to attach the toxin to cell. This has an systemic effect. T cell lymphocytosis (destrosy lymphocytes). Insulin and histamine production. Increased IgE production. Impaired phagocyte functions
  56. Adenylate cyclase toxin
    (B. pertussis). Both adenylate cyclase and hemolysisn. Secrete an invasive toxin. found on surface of bacteria cell penetrates the phagocytes and binds to calmodulin and disrupts normal cellular function by increased cAMP. (leads to inhibition of chemotaxin. inhibition of phagocytosis. and apoptosis of the cell)
  57. Other toxins produced by B. pertussis
    1. Dermnectrotic toxin which is a strong vasoconstrictor. 2 Tracheal cytotoxin. prevents cillated eptithelial cells from beating. 3. Lippolysaccharide which is an endotoxin.
  58. Laboratory Culture prevention and Treatment of Bordetella
    Nonmotile. Fastidous and slow growing. Taken by a nasopharyngeal swab that it placed deep into the nasal pathogen. Requires nicotinamide and charcoal starch blood or albumin to absorb toxic substances. Requires prolonged growth. Isolated on modifed Brodet Gengou agar. Inactivated whole bacterial cells and toxid are prepared in formalin and inclusion in DPT vaccine. Treatment with erythromycin suction oxyten. Treatment does not elimninate symptoms.
  59. Treatment and Prevention of Bordetella pertussis
    Supportive treatment macrolide antibiotics. Vaccine which is part of DTaP.
  60. Stages of B. pertussis
    First stage is colonization. (fever sneezing regular cough) where is most infective but not diagnosed. Second stage more intensive coughing with whooping sound. Last stage is convelesnce. antibiotics dont have any effect on the disease.
  61. General overview of Bordetella. Francisella. and Brucella
    Extremely small. Aerobic non fermeneters. Gram negative coccobacilli. TRUE PATHOGENS. isolation alwasy associated with disease.
  62. Brucella General info
    Has 2 chromosomes. No plasmids. Decreased milk produciton. Serious disease of live stock. Causes spontaneous abortion. Highly infectious. Zoonotic. In humans is called undaulant fever. Causes brocellosis. B abortus is causative agent of abortion in cattle and brucellosis (undulant fever) in humans. WORLS MOST COMMON BACTERIAL ZOONOSIS.
  63. Brucella spp associated with humans disease
    B. abortus (cattle. bison). B melitensis (goats. sheep). B. suis (pigs). B. canis (dogs. foxes. coyotes).
  64. Pathogensis of Brucella
    Low infection dose. Facultative anaerboe intracellular pathogen. Able to survive and replicate within macrophages. Disseminated to spleen liver. bone marrow. Can cause granulomas. Starts off with generalized flu like symptoms. Can cause long term infection. Outer member (LPS) is the major virulence factor of Brucella. (LPS is different that classical LPS. low toxicity). HAS THE ABILITY TO INFECT ALL SYSTEMS. epithelial cells lines. phagocytic cells. respiratory tissue. neurvons. male and female reproductive tissues. Enters the animals and is transmitted.
  65. Brucellosis in animals
    Infects organs rich in erythritol (sugar metabolized in preference to glucose) like breast uterus placenta and epididymis. Asymptomatic carriage sterility or abortions. Transmitted between animals in aborted tissues.
  66. Brucellosis in Humans
    Very rarely fatal. Bangs disease. Facultative intracellular pathogens of mononuclearphagocyte system. Survive intracellulary by inhibiting apoptosis. Form granulomas (mass of granulation tissue produced in response to choronic infections inflammation. or foreign bodies) and cause destructive tissue damage. Small tissue inflammation walled off macrophages. Pus forming bacteria. B. meliteusis main severe disease in devloping countries.
  67. Clinical Presentation of Human Brucellosis
    Acute disease often developes with intial nonspecific symptoms of malaise chills fatigue weekness myalagies. MILD disease with rate suppurative complications. CHRONIC disease and recurrence are common because it can survive in phagocytic cells and multiply to high concentrations. May also take teh form of destructive lesions.
  68. Lab diagnosis of Brucella
    Serum agglutination test. Oxidase postive. Urease postive. Slow growers hard to culture.
  69. Treatment and Control of Brucella
    Combinatino doxycycline(6 weeks) and streptomycin or rifampin (2 to 3 weeks). For infants tetracyline is toxic so children are treated with trimepthorpim sulfamethoxazole. NO vaccine availbe for humans Main control is prevention. USDA established teh National Brucellosis Eradication Effector managed by animal lant and health inspection service (APHIS). Is located yellow stone park with Bison Elk and Deer.
  70. Epidemology of Brucellosis
    Animals are natural resirvoir. Cattle pigs goats sheep bison. TRANSMISSION 1. Ingestion of contaminated products 2. direct contact with infected animals or animal products. 3. Inhalation (higly aerosoliztion in lab)
  71. Brucella and Bioterrosim
    Catageory B. Most likely route of intentional exposure would be Respiratory. Could also happen via contamination of food and drink. Should identify intentional exposure as any BT agent.
  72. Key points on prevention of Brucellosis in Humans
    Occupational hygiene and food hygiene. All products should be prepared from heat treated milk. Consumption of raw milk or products of raw milk should be avoided. Meat should be adequately cooled. Special precautions for labworkers. Public health education should emphasize food hygiene and occupational hygiene.
  73. Franceisella tularensis general info
    Highly infectious intraceullular pathogen. Low infectious dose. Aerosolized very easy. Cause the disease Tularaemia. Similar to brucella. Fram negative strict aerobe
  74. Pathogenesis of Francisella tularenis
    Is transfered via vector or aerosol. Lives intracellulary and resides in macrophages (or amoeba). Primarty target is the macrophage where it repilcates 1000 folds does not trigger respirative burst (super oxide enzymes). Reside no within phagosome but in the pm of the macrophage. Causes APOPTOSIS of macrophage and bacteria is released.
  75. Epidemology of F. tularensis infection
    Rabbits. ticks. and muskrats are main reservior in US. Two biochemical varieties. F tularensis biovar tularensis . F. tularensis biovar palaearctica. Jellison type A are major biovar associated with servere disease in North america.
  76. Transmission routes of Francisella tularensis
    1. Tick and deer and fly bites (most common). 2. Skin contact with infected animals. 3. Ingestion of contaminated 4. Lab exposure. 5. Inhalation of contaminated dust or aerosols.
  77. Virulence Factors of Fransicella
    Antiphagocytic capsule. Have LPS. Found several genes that code for protiens that are used for intracellular survival within macrophages. IglC. MgIAB and MinD (intracellular survival). IgLC Inhibit production of tumor supressor alpha and disrupt toll like receptors. MgIAB. involved in transcription regulation production of phosphatases. MinD not exactly sure of mechanism could be a possible pump for radicals produced by macrophages.
  78. Clincal presentation of Tularemia
    Uleroglandular (75 to 85 percent). Ulcers at the site of exposure and adenopathy of the draining lymph nodes. Grandular adenopathy. Adenoppathy but no uclers. Typhoidal systemic sings but no aenopathy or uclers. Oculoglandular.
  79. Ulceroglandular
    Incubation periods 3 to 5 days. After this onset disease often rather abrupt with flue like symptoms. Most common form. Ulcers at the site of exposure and adenopathy of the draining lymph nodes. Direct contact wtih flesh vector born. Infection through skin or mucous membrane. Can be treated with antibiotics. will progess to lungs if it is not treated. Usually caused by F. tularensis holartica
  80. Oculoglandular Tularemia
    Very uncommon. Cause conjuctivitis. photophobia. swelling puss from eye. Due to direct contamination of the eye.
  81. Oropharyngeal tularemia
    Via ingestion of contatiminated water or food.
  82. Pneumonic ularaemia
    Infection by inhalation. Two types of presentation F tularensis holarctica give mild respiratory infection. F tularensis tularensis causes acute serious infection. Flu like symptoms. 30 percent mortalitity . Very low wiht antibiotics. Can be used as a bioterosim agent.
  83. Lab Diagnosis of Franceilla tularensis
    Non motile. Fastidous and slow growing. Requires cysteine supplemented specialized media. Requires prolonged growth. Cysteine enriched CA. Aslo grows on BCYE agar.
  84. Prevention of Francisella tularensis
    Avoidance of reservoirs and vectors. Protective clothing and gloves. Laboratory personnel should be made aware of potential for Francisella in clinical specimens.
  85. Treatmetn of Franceisella tularensis
    Antibiotics (gentamycin treatment). Live attenuated vaccine availaibe for at risk popultion. Could possible revert to virulent strain. Stay away from sick rabbits.
  86. Legionella pneumophila
    Tanmission via aerosols. Facultative intracellular pathogen. Gram negative that stains poor. No person to person tranmission. Difficult to gorw.
  87. Pathogensis of Legionella
    Phyagocytosis into the monocytes binding to complement receptors. Inhibition of phagolysomes fusion NO FUSION. Replication within the phagosomes. Lysis of the phagosome lead to apoptosis and release of the organism. TH1 cells and IFN (interferon) destorying. Humoral response very little effect.
  88. Legionnaires disease
    Legionellosis (severe) incubation period of 2 to 10 dyas. Systemic acute illness. Primary manifestation causes pneumoniae. is 75 mortality treatment with erythromycin.
  89. Pontiac fever
    1 to 2 incubation. Flu like symptoms milder absence of pneumonia. No mortality. Self limiting
  90. Epidemoiology of L. pneumophila
    Disease worldside. Exposure water based aerosols. Air conditioning cooling towers. Whirlpools Sauna or mister. Survival environment amoebae. and biofilms.
  91. Lab diagnosis Legionella pneumophila
    Microscopy is unreliable poor gram stain. Antigen test done from uninary antigen test. Difficutl to grow must us BCYE agar (difficult to make).
  92. Treatment and control of Legnionella pneumophila
    No antibiotic sensitivity testing. Macrolides fluoroquinolnes used. Control of reservoirs.
  93. Alpha proteobacteria
    Obligate intracellular parasites. Rickettsia anthropod borne. spotted fever (R. prowazekil. R. typhi. R. rickettsii) Orentia scrub typhus. Ehrilcia. Tickborne
  94. Rocky mountain spotted fever
    Caused by Rickettsia rickettsii. A small gram negative bacterium that is an OBLIGATE INTRACELLULAR PARASITE. Detected by serological testing. Transmission by Vectors (tickborne) . Takes a few days to incubation. Causes macropaplular (flat red rash) rash begins on palms and soles then spreads to other parts of the body. High fever and other flu like symptoms. Can be treated with antibiotics. (seasonal)
  95. Epidemic Typhus
    Caused by Rickettsia prowasekii. Transmission is by human louse. Epidemeic often in areas with reduced sanitation. High fever and high fatality rate. Rash begins on trunk of body and spreads to the extermities (STARTS ON TRUNK) vs rickettsii
  96. Endemic Typhus
    Casued by Rickettsia typhi. Transmission via feas espically rodent flea. Endemic in many areas. Often with mild or no symptoms.
  97. More information of RMSF
    Rickettsia rickettsii. Is a zoonosis. Reservior is mammals. Vectors ticks. Characteristic hemorrhagic rash. maculopopular starts on palms and soles. Can damage vital organs. Spread via Rocky Mountain Wood Tick. and the American dog Tick. and Brown dog tick.
  98. Arthropods and Rickettsia
    Arthorpods can be both the vector and the host. When a tick bites infected aniamal will lay eggs and produce infected eggs. These new host can infect other animals when they feed.
  99. Ricettsia
    Obligate intracellular parasite. Have a slime layer. Only grwo within a host cell. Infect endothelial cells blood vessels. This is why you get red spots from the leaking of the capillaries.
  100. Life cycle of Rickettsia within Eukaryotic Host cell
    First attachement and then are phygocytosed by host cell. (Induce phagocytosis by cells that do not normally do this). Adhesions are part of the outer membrane. Enter cell and begin to multiple after escaping from the phagosome. Then they DO NOT LYSE CELL when they leave. (caused by rash leaking blood vessel)
  101. Lab Diagnosis of Rickettsiae
    Indriect immunofluorescence assay (IFA). Some bacteria can not be cultured in bitro. Chamydia and rickettsia. Culture like viruese. Serological assay.
  102. Treament of Rickettsial Disease
    Antibiotics doxycycline. No vaccine available for most clincal diseases. (EXCEPT ENPIDEMIC TYPHUS_
  103. Rickettsia akari
    Causes Rickettsial pox. intracellular. Aquire a eschar (dead tissue coming off skin where bite by vector). Reservior Mites and wold rodents.
  104. Rickettsia prowazekii
    Causes eidemic typhus. Spread by the human body louse (vectors). All rodents are resivor
  105. Rickettsia typhi
    Causes endemic typhus. The vector is the flea and the reservior is the wild rodent.
  106. Orientia tsutsugamushi
    Causes scrub typjus. Vector is chiggers (mite larva).
  107. Ehrlichiosis
    Caused by Ehrlichia species and tranmitted by Ixodes ticks. disease of animals and humans. OBILGATELY INTRACEULLAR. Nonspecific symptoms (similar to other diseases). Mostly in southern central states in US. Infect leukocytes primary and inhibit ifussion with lysome and released by lyings.
  108. Morulae
    Where the replication within the cell where Ehrilichosis will grow. In leukocytes.
  109. Ehrlichiosis chaffeensis
    Human monocytic ehrilchiossi. Ressembles RMSF but no rash. Casuse decreased leukocytes. leukopena. Low mortality rate
  110. hrlichiosis ewinggi
    infects dogs. Wide varity of clinical signs (fever. lethargy. enlarged speen. enlarged lymphnodes. bleed disorders. blindness). Dogs are resivior.
  111. Lab diagnosis and treatment of Ehrlichiosis
    Culture not performed. Giemsa stain blood. SEROLOGY PCT. Treatment doxycycline and avoidance of ticks bug repelents.
  112. Gammaproteobacteria
    Legionellales and Coxiella fall into this group
  113. Coxiella burnetii
    Onfects macrophages and lysis for release. Infection form express phase I antigen. LCV multiplies in macrophages. Expresses phase II antigen. Very stable in the environment (spore like) infects a large variety of animals. Found in the placenta and feces of infected animals can be passed in milk. Humans can inhale infectious material and ingestion of unpasterized milk.
  114. Q fever
    Clincal disease of Coxiella burnetii. Ranges from very mild to severe. Acute you have fever. pneuonia. hepatitis. chills. mild respiratory symptoms. Chronic months to years post exposure subacute endocarditis. Chronic has poor diagnosis.
  115. Lab diagnosis of Coxiella burnetii
    Serology is the gold standard. Antibiotics to phase I antigens vs antibodies to both phase I and phase II antigens
  116. Treament and control of Coxiella burnetii
    Prolonged treatment with doxycycline (acute). Vaccine available outside US. Chronic infection is combination thearpy.