Medical Micro Lecture 2 - Sheet1(2).csv

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Medical Micro Lecture 2 - Sheet1(2).csv
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  1. Pyogenic Cocci
    Gram negative cocci. Contains one family. Neisseriaceae and 15 genera. Common Neisseria Species N. gonorrhoeae. N. meenigitidis. N. sicca. N. mucosa. Pus forming. Diplococci. Coffee bean shaped.
  2. Neisseria gonorrhoeae virulent factors
    Gonococci. Opa (opacity) proteins attachment to host cell. Bind human transferrin (lactoferrin) will bind to host and steal iron. IgA protease enzyme that destroy proteins. Lipooligosaccharide (LOS) Gram negative covering Main factor for damage. Por (porin protein OM) allows intracellular survival. Pili (intial attachment to host cell). Betalactamase
  3. Pathogenesis of Neisseria gonorrhoeae
    "The pilli allow attachment to microvillus and is taken in via endocytosis. Transmission is through sexual transmission. Enter into host cells and can be taken in by macrophages but can survive inside cells. Main attachment is in cervix cells
  4. Clinical Disease of Gonorrhea
    Sexally transmitted. Asymptomatic carriage is major reservoir. Complications in femalse of 10-20 percent. Is under reported. Presents differently between male and females. Can be transmitted to the throat via oral sexual contact. Direct or indirect contact with sexual organs.
  5. Females and gonorrhea
    High right after single exposure. Can be asymptomatic infections frequently not diagnosed. MAJOR RESERVOIR IS ASYMPTOMATIC. Vaginal discharge 7 to 21 days after exposure. Can lead to PID chronic infection can lead to sterility. Can be transmitted to infant at delivery (silver nitrate).
  6. Males and gonorrhea
    Painful burning urination. Yellow and green discharge. Have acute disese with obvious systoms. Rare complications.
  7. Gonococcemia
    Spread or disperse septicemia. skin. and joint infections.
  8. Sensitivity
    Measure of True Positive Rate. No of true positives/No. of actual positives. No of true positives/no of (true postivies + false negatives)
  9. Specificity
    Meaure of true negative rates. No of true negatives/No of actual negatives
  10. Diagnosis of N. gonorrhea
    Gram stain of discharge that shows gram negative diplococcus with a coffee bean shape. Can also use chocolate media to grow N. gonorrhea. It is a media with lysed red blood cells. Can also use a muller hinton agar mixed with chocolate agar along with antibiotics to help isolate N. gonorrhoeae
  11. Treatment of N. gonorrhoeae
    N. gonorrhoeae natural competence changes antigenic composition (naturally transformable). Is diploid has two sets of chromosomes. Most strains now resistant to penicillin. so use ciprofloxacin. CDC recommends ceftriaxone. No effect vaccine. Chemoprophylaxis. Control is mainly public education on safe sex practices and treating infected individuals
  12. Neisseria meningitidis virulence factors
    POLYSIALIC ACID CAPSULE (is an antigenic mimicry. looks similar to host and helps to avoid immune system). Bind human transferrin. lactoferrin. IgA protease. Lipooligosaccharide gives antigenic variation (LOS). Pili.
  13. Clincial diseases of meningitis
    Crosses blood-brain barrier. Effects young children under the age of 5 (primarly). Very hard to diagnosis in very young babies. Is transmitted via close contact in aerosol (very hard to contract). Second most common cause of meningits behind S. pneumoniae.
  14. Pathogeneis of Meningococcal disesae
    Specific receptors (GD1) for bacterial fimbriae on nocilliated columnar epithelial cells in nasopharynx of host. Taken up intracellurally and repilicate to avoid immune system. Produce endotoxin lipid A. This LIPID A cause the inflammation and most damage. Human only natural host.
  15. Diagnosis of Neisseria meningitis.
    GRAM STAIN of sterile CSF. Few host cells. Note bacteria and host cells. About 10 percent of people are healthy naso-pharyngeal carriers. Culture from CSF. blood. and sputum
  16. Epidemiology of Meningococcal disease
    Humans only host. Person to person transmission by aerosolization and respiratory tract secretion in crowded contidtions. Highest rate in children younger than 5 years.
  17. Vaccines for bacterial meningitis
    There are conjugate vaccines made by attaching antigen to carrier protein. Is a polyvalent vaccine against the N. meningitidis.
  18. Meningococcal rash
    About half the children or adutls with meningoccal meningitis have rash that does not fade. The pressure test shows the rash does not fade under pressure.
  19. Meningococcemia
    disseminated septicemia. characterized by petechial skin leisons. Waterhouse-Friderichsen syndrome
  20. Meningococcal pneumonia.
    Usually a complication of a prior respiratory tract infection. Prognosis is good.
  21. Laboratory Diagnosis of Neisseria meningitidis
    Large number of encapsulated small gram-negative diplococci can be seen microscopically in cerebrospinal fluid. Transparent non pigmented nonhemolytic colonies on chococlate agar with enhanced growth in moist atmosphere with 5 percent CO2. OXIDASE POSITIVE. Acide production from glucose and maltsose but not from other sugars.
  22. Treatment of N. meningitidis
    Susceptible to penicillin and cephalosporin. Vaccine available. Polyvalent vaccine.
  23. General characteristics of Neisseria spp.
    Aerobic. Gram negative cocci often arranged in paris with adacent sides flattedned like coffee beans. Oxidase positive. Nonmotile. Acid from oxidation of carbohydrates. not from fermentation.
  24. Actinobacteria
    Suborder Corynebacterineae. Has seven families with many know gernera such as Corynebacterium. Mycobacterium. nocardia. CMN Group
  25. CMN cell walls
    contain waxes with 60 to 90 CARBON MYCOLIC ACID. Acid-fast basic fuchsin dye cannot be removed from cell by acid-alcohol treatment.
  26. Genus norcardia
    Along with Rhodococcus make up the family Nocardiaceae. Develope a stubstrate of mycelium that readily breaks into rods and coccoids elemtns. Look very similar to fungi. Some also form a aerial mycelium. Slow groing (3-5days). AERIAL MYCELIM help to identify it.
  27. Impact of Nocardia
    Most are free-living saprophytes. Can degrade many molecules. Some are opportunistic pathogens causing nocardiosis. USUALLY INFECT LUNGS. can infect central nervous system.
  28. Virulence factors of Nocardia
    CORD FACTOR. Protects them from phagocytosis. CATALASE AND SUPEROXIDE DISMUTASE (allows them to survive harmful oxygen products)
  29. Clinical Disease caused by Nocardia
    Supperative infections. Pus forming infection. Normally causes chronic infections. Main disease is Bronchopulmonary disease (can spread to CNS). Can cause brain abcesses. Or Cutaneous infections (mycetoma slow growing fungal infection that is localized)
  30. Lab Diagnosis and Treatment of Nocardia
    Microscopy of sputum samples. Culture on BCYE (buffered charcoal yeast extract). and elevated CO2. ID via rRNA and housekeeping genes. TREATMENT. treat localized infection with sulfa drugs. if disseminated use cephalosporin (broadspectrum).
  31. Housekeeping genes
    Genes that code for essential functions. Are constutive genes which are always expressed at a constant level
  32. Rhodococcus equi
    Primarily infects horses. Can be found in the environment (soil). Very rarely infects humans. Are intracellular bacterium with rod to coccus are pleomorphic.
  33. Clincial disese caused by Rhodococcus equi
    1. Abscessses. inflammation (granulomas collection of walled off bacteria by macrophages). 2. Can be invasive and cause pulmonary disese. dissemination to lymph nodes. meninges. skin. COMMON CAUSE OF PHEUMONIA IN ANIMALS. RARE IN HUMANS PRIMARILY IMMUNOCOMPROMISED (AIDS). Does respond to antibiotic treatment VANCOMYOSIN.
  34. General information on Genus Mycobacterium
    In family mycobacteriaceae. Are straight or slightly curved rods that sometimes branch or form filaments. Aerobic and catalase positive. Acid fast (long mycolic acid chains). High G +C in their DNA content. Very slow growers. Can be pigmented or not.
  35. Cell wall of Mycobacterium
    Lipid rich cell wall. Are poly peptides in the cell wall (PPD). Have mycolic acid.
  36. M. bovis
    Causes tuberculosis in cattle and other ruminants.
  37. Photochromogenic
    Are species of Mycobacterium that when exposed to light will enhance their pigmentation. Are NTM (non-tuberculosis mycobacterium). MYCOBACTERIUM KANSASII will change color on middlebrook agar
  38. Runyon Groups
    Mycobacteria pathogenic for humans are differentated by these groups. Are done by speed of growth and production of chromogenic pigment.
  39. Global infection rate of tuberculosis
    1.7 billion people infection. About 8.4 million cases and 1.9 million deaths per year. Most cases are from foriegn born ethnic groups. Is spread in close proximities by airborn droplets.
  40. Clinical disease tuberculosis
    Primary TB. Secondary TB. or reactivation of TB. Pulmonary TB. Lumph node. CNS menigits. skeletal joints. Miliary TB (micro lesions on lungs seen on Xray)
  41. Diagnosis of Active TB
    Microscopy of sputum with an acid fast stain. Chest Xray of the lungs. The tubercuol skin test (PPD). Myocbacterium tuberculosis has mycolic acid which makes it difficult to treat. Must be done with long regiments of antibiotics.
  42. Mycobacterium leprae information
    Cant culture in lab. Humans and armidillos are only known species to host the bacteria. Can use mice feet for culturing. Is very slow growing and makes it very difficult to diagnosis.
  43. Lepromatous Leprosy
    More server form of the disease. Causes skin condition of macules. Macule is a skin pale lession that is raised or malformed. Not well defined. different sizes. Less than 5 to 10 mm in size. Causes teh decrease of activation of T-helper 1 cells to help clear the disease. REDUCED T-HELPER 1 CELLS. Has increased number of bacteria in this infection
  44. Tuberculoid Leposry
    Less severe form of leposry. Characterized by single lesions. Have a white pigmentation.
  45. Mycobacterium tuberculosis and culture
    Is grown on lowenstein jensen media and middlebrook 7H10. Is a slow grower. Is found in sputum. BACTEC broth made specifically for rapid growth. (up to 10-12 days).
  46. Mycobacterium avium
    Intracellular pathogen. Found in immunocompromised peole (AIDS). Located in lungs. Called MAC mycobacterium avium complex
  47. Treatment of Mycobacterium tubuculosis
    First line drugs. ISONIAZID (IHN). Rifampin. pyrazinamide (PZA). ethanmbutol. Is a vaccine for TB but is not normally given in US.
  48. Two different populations of TB test
    1. Active TB. 2. Positive PPD test.
  49. Antibiotic Resistance in M. tuburculosis
    Supsecpted resistance treat with 4 or more 1st line drugs. Resistance developes use 2 new drugs (kanamycin and quinolones). Long term treatment over 2 years. Very expensive and toxic. Drug resistance is increasing as a world wide phenomenon.
  50. Enterobacteriaceae General illness
    Gram Negative. Facultative anerobes. Rods. Oxidase Negative. Ferment glucose. Motile via peritrichous flagella.
  51. LPS of Enterobacteriaceae
    The cell wall is the major antigen. The main types to serotype them is by the Flagella (H antigen). Capsule (K or VI antigen). Contain the lipopolysacchardie endotoxin.
  52. Illnesses associated with Enterobacteriaceae
    Major causes is gastrointestinal illness. Can also cause infections in CNS. Lower respiratory tract. Blood (septicema). GI tract. and Urinary tract
  53. Most common bacteria of Enterobacteriaceae associated with bacteremia
    Escherichia coli about 45 percent.
  54. Definition of Diarrhea
    Stool of decreased consistency and increased volume due to imbalance of secretion and absortption of water and salts in the intestine. Large amounts of stool
  55. Gastroenteritis caused by Enterobacteriaceae
    1. Secretory (noninflammatory. non invasive). Toxin produced by bacteria stimulate secretion of the salts and electrolytes and decrease absorption of water. 2. Invasive (inflammatory). Actually enters cells and causes damage. (Samonella). 3. Systemic. emcompases all systems
  56. Fecal oral route transmission
    5 F's. Fields (soil). fingers. flies. fluids (water). food. Typical transmission route of Enterobacteriaceae. Bacteria is shed in feces.
  57. Preventative Interventions for Diarrhea mortality
    Improving food safety. water. sanitation. and hygiene. Breatfeeding (fluids and immunity). Future and current vaccines. Vit. A. Zinc (reduces lenght and severity of diarrhae).
  58. Escherichia coli virulence factors
    Most are common residence that are pathogenic. Flagella H antigen. Have genes on plasmids that code for enterotoxins. Colinization factors (adherence). Capsular K antigen helps prevent phagocytosis.
  59. ETEC
    Enterotoxigenic Escherichia coli. Result in cholera diarrhea (is milder). Binds to microvilli and increase cyclic amp production which leads to loss of water and electrolytes. Is a self limiting mild and brief diarrhea. Sudden onset of diarrhea. Rarely accompanied by high fever and vomitting.
  60. EPEC
    Enteropathogenic Escherichia coli. E. coli will adhere to microvilli and block usage of them and cause lesions on the cell. First step is the formation of a bundle forming pilus (intial adherence). For a pedetal then will bind to cell and disrupt the cytoskeleton (intimate) with actin.
  61. EAEC
    Enteroaggregate Escherichia coli. Bind to large and small intestine in a a biofilm formation. In addtion to the decreased surface area many cytotoxins and enterotoxins are released. Make it hard to serotype due to biofilm formation.
  62. EHEC/STEC
    Enterohemorrhagic E. coli. Causes hemorrhagic colitis. Stomach cramps. diarrhea (often bloody). and vomiting.(HUS) Complications Hemolytic uremic syndrome. Decreased frequency of urination. feeing very tired. and losing pink color of skin and membrane due to anemia. Can lead to kidney failure
  63. Shiga toxin escherichia coli
    About 265k STEC infections each year in the US. O157 CAUSES ABOUT 36 percent of these infections. STEC typically disappear from teh feces by the time the illness is resolved but may be shed for several weaks after symptoms resolve.
  64. Other disease caused by E. coli
    Urinary tract infections (ascending. most common casuse). Neonatal meningitis. Septicemia.
  65. Salmonella enterica general info pluse diseases
    Has a very low infectious dose. 1. Gastroenteritis (self limiting). 2. Septicemia 3. Typhoid fever (caused by Typhi. Paratyphi A these are only found in humans) high fever. lethargy. GI symptoms. possible rash
  66. Salmonella enterica Typhimurim mechanism for invasion
    Will cross the epithelial barrier at the M cells and destroy them. They will enter macrophages and cause apoptosis.
  67. Shigella basic info
    Common species. dysenteriae. flexneri. boydii. sonnei. Typically causes bloody diarrhea with fever (dysneteriae). Low infectious dose. Highly transmitable. Humans only host. Very resistant to low pH. can survive in gut. Causes Shigelosis which is fever and bloody diarrhea. Some produce a toxin very similar to shiga toxin. Normally infects children around 7 years old.
  68. Shigella mechanism of intection.
    Similar to Salmonella and enter in through the M cell and enter into the macrophage and destroy it. Can move from one cell to another intracellularly.
  69. Yersinia general info
    Common species pestis. enterocolitica. pseudotuberculosis. Enterocolitis is a sacrophylic (lives in cold environment). Causes bacteremia and has a high infectious dose. Last a few days to a week. Non specific self limiting diarrhea. Y. pestis Causes the plague not food born like the other is zoonotic. caused by rats (urban) or sylvanic (wild)
  70. Klebsiella spp.
    Commonly found in nature is all around us. Can cause Pneumoniae. liver abcess. and septicemia. Klebsiella granulomatis is a sexual transmitted disease with low transmission causes ulcerations (granuloma inguinale)
  71. Proteus mirabilis
    Common cause of UTI and can cause menigitis in neonates. Not really GI causing. Common cause of noscomial infections
  72. Other important enterobacteriaceae
    Enterobacter (found in nature commonly occuring). Can cause enterocolitis. Citrobacter (opportunistic bacteria normal GI resident can produce a shiga toxin and HUS). Serratia not found in gut another common cause of noscomial infections.
  73. Lab Diagnosis of Enterobacteriaceae
    Use selective media if sample is taken from stool. Sterile sites use a general media. Chemical tests are used to identify bacteria. Uses of API strip.
  74. General Characteristics of Vibrio. Aeromonas. Plesiomonas
    Gram negative. Facultative anaerobes. Fermentative bacilli. POLAR FLAGELLA. OXDIASE POSTIVE. Primary found in water sources. Causes gastrointestinal diseases.
  75. Morphology and Physiology of Vibrio
    Comma shaped bacilli. V. cholerae. V. parahaemolyticus. V. vulnificus are most significant human pathogens. Can grow in broad temperature and pH for growth on media. Common in environment like warm brackish water. V. cholera CAN GROW WITHOUT SALT.
  76. Ecology of V. cholerae
    Have a symbiotic relationship with zooplankton and phytoplankton. Live in warm brackis water. Can live in various salt contents. Found in environment. More common in brackish water.
  77. Vibrio cholerae Pathogensis
    After gaining entry into the body will attach to small intestine they multiply and causes secretory diarrhea. The mechanism is similar to ETEC. The Cholera toxin will bind to receptors on the gut and cause increased cAMP activity. Causing the loss of water and salts. Leads to Profuse diarrhea. RICE WATER DIARRHEA.
  78. V. cholera associated disease adn source of infection
    Water and food. Causes Gastroenteritis
  79. V. parahaemolyticus
    Comes from raw shellfish. seawater. Causes gastroenteritis. wound infections. and bacteremia. Has a different type of hemolysis. Kanagawa hemolysin associated with pathogenic strains. Is a very alkaline high salt content blood agar is used for culture.
  80. Virbrio vulnificus
    Capsule and pili are essential for virulence. Also has cytolysins and collagenase which will cause tissue destruction. Infections come from saltwater and shellfish. Cause bacteremia. wound infections. cellulitis. ONLY SKIN no GI
  81. Treatment and Prevention of Vibrio cholera
    Use cholera cot to measure amount of fluid loss. REPLACE LOST FLUIDS AND SALTS. REHYDRATION. Then comes maintances of fluid loss. Assess for dehydration. rehydrate. monitor. unitil diarrhea stops. Give antibiotics.
  82. TCBS medium
    Used for culturing Vibrio pathogens. Is a enriched media. contains alkaline peptone. Thiosulfate-citrate-bile salts-sucrose agar is used to differentiate Vibrio species
  83. Ameromonas general info
    Gram negative. rods. motile by single polar flagellum. facultative anaerobe. Ubiquitis which cause huge diversity. Cause diarrhea. wound infections and systemic diseases.
  84. V. cholera outbreaks
    Increase number in incidents due to poor sanitation and water treatment. A third world disease primarily.
  85. Ameromonas virulence factors
    Hemolysins. Enterotoxins. Cytotoxins. Easily adhere to cells.
  86. Aeromonas hydrophila
    Main opportunistic bacteria of the aeromonas. Is ubiquitus found in many water systems. Can live for month longer in freshwater due to adaptation of environment.
  87. Campylobacter Species Morphology and Physiology
    Small. thin. helical (spiral or curved). with typical gram negative cell walls. Tendency to form coccoid and elongated form. Distrinctive rapid darting motility. One polar or 2 (bipolar) flagella. Microaerophilic and capnophilic. Thermophilic (except C. fetus). Maybe nonculturable in nature.
  88. Campylobacter jejuni species associated with human disease
    Campylobacter jejuni infect poultry. pigs. bulls. dogs. cats. bird. mink. rabbit. insects. Causes Gastroenteritis. septicemia. meningitis. spontaneous abortion. Guillain Barre syndrome. Very common
  89. Campylobacter coli
    Infects pigs. poultry. bulls. sheep. birds. Cause gastroenteristis. septicemia. gastroenteritis. spontaneous abortion. meningitis.
  90. Campylobacter fetus
    Infects cattle adn sheep. Septicemia. gastroenteritis. spontaneous abortion. Meningitis.
  91. Epidemiology of Campylobacteriosis
    Contaminated poultry account for more than half of the camylobacteriosis causes in developed countries but diffretn epidemiological picture in developing countries. Peak incidence in children belowone year of age and young adults (15 to 24 years old) BLOODY DIARRHEA. In developing counties where campylobacter are hyperendemic. symptomatic disease occurs in young child WATER DIARRHEA DUE TO FECAL ORAL ROUTE.
  92. Pathogenesis of campylobacter jejuni
    In poultry the bacteria primary lives in the mucus membranes and then spreads to water source and associate with ameobas. After entering body the bacteria crosses the mucus layer and into the intestinal epithelium. PRODUCTION OF ENTOLUCANS AND CHEMOCYANS ill infect neutrophils. DC. an marcophages. Infectious does is about 10.000. Is self limiting and will clear after a few days typically. C. jejuni displays extensive genetic variation. NATURALLY COMPETENT. HORIZONTAL GENE TRANSFER. Occurs in vitro and during chick colonization. CAPSULE!
  93. Guillain Barre Syndrome
    Post infection autoimmune disease associated with C. jejuni. Cross reactiity with peripheral nervous system. joints (reactive arthritis). Destruction of myelin sheath.
  94. Infections of Campylobacter fetus
    Can spread to blood and central nervous system. Resivoir is in cattle sheep. Can cause GI illness but can cause MENINGITIS OR SEPTICEMIA.
  95. Diagnosis of Campylobacter
    Microaerohilic. Increased CO2. Use immunoassay. Culture on charcoal based medium. Since the samples are stoool.
  96. Helicobacter pylori
    Major causes of gastritis. peptic ulcers (duodenal and gastric). gastric adenocarcinoma. MALT B-cell lymphoma.
  97. Epidemiology of Helicobacter Infections
    Family clutsers. Possible transmission person to person. 20 percent of people below 40 are infected. 50 above 60 years are infected. H. pylori is uncommon in young children.
  98. Virulence factors of Helicobacter
    UREASE. Flagella. Acid-ihibitory protiens. Adhesions. Heat shock protein
  99. Pathnogenesis of Helicobacter pylori
    Enters stomach acid and penetrates mucus layer then produces Urease taht will produce NH3 and will neutralize the gastric acid. Creates a microenvironment in the stomach. Then they begin to causes inflammation and leads to mucosal cell death.
  100. H. pyloir worldwide phenomenom (WHO/CCL)
    H. pylori is on the list of items that should and possibly could be rated in drinking water supplies from the CCL (contaminant Candidate List). Is WHO classifed as a class I carcinogen because of the associated with gastric malignancies. 50 percent of US pop. are symtomatic or asymptomatic. SOURCE OF HUMAN INFECTION NOT WELL KNOWN.
  101. Non-germentative Gram Negative Rods General info
    Opportunistic pathogens. Aerobic nonfermenters 10 to 15 percent. Oxidative gram negative bacilli including Pseudomonas. produce acid from glucose or carbohydrates ONLY IN THE PRESSENCE OF O2. Pseudomonas oxidizes but does not ferment glucose.
  102. Laboratory Diagnosis of H. pylori
    Gastric biopsy. Silver stain of gastric biopsy. Barry Marshall ingested H. pylori and used self to study bacteria.
  103. General Info Pseudomonas aeruginosa
    Motile (single or polar flagella) gram-negative rods. Obligate (strict) aerobes. Oxidase and Catalase Positive. Nonfermenters. chemoheterotrophic respiratory metabolism. Minimal nutritional requirements. Has a grape like odor and blue green pus and colonies. BROAD ANTIBIOTIC RESISTANCE.
  104. Virulence factors of Psedomonas aeruginosa
    Capsule (adhesins and antibiotic resistance). BIOFILM FORMING. Pili. LPS (endotoxin). PYOCYANIN. (impairs cilary functions. stimulates inflammatory response). Toxins. Exotoxin A and S. Cytotoxins (leukocidins). ANTIBIOTIC RESISNTANCE. Phospholipase C (ALGINATE). aids in formation of biofilm.
  105. Epidemology Pseudomonas aeruginosa
    Ubiquitous normally found in moist environmental sites in hospital (NOSOCOMIAL). Can transiently colonize the repiratory and gastroinestinal tracts of hospitalized patients. Specifcally pt. on broad spectrum antibiotics. Oil eating can survive on many different environments. High Numbers in older patients with chronic lung disease. DAMAGED TISSUE.
  106. Pseudomonas aeruginosa Infections
    Pulmonary Infections. BURN WOUNDS. UTI (catheter). ALMOST NEVER INFECT UNCOMPRIMSED TISSUE. Eye infections.. Characteristic grape like odor. Bluish green color clinically. Folliculitis. Endocarditis (rare on heart valves). Bacteremia. NORMALLY UNDERLYING CONDITION OR MEDICAL DEVICE.
  107. Treatment of Pseudomonas aeruginosa
    Combination use of effective antibiotics (due to increasing resistance). Hospital infections control efforts shold concentrate on preventing contamination of sterile medical equipment.
  108. Diagnosis of Pseudomonas aeruginosa
    Readily grows on laboratory media. Identified by colonial characteristics (pigment (blue). grapelike odor. hemolysis beta). and simple biochemical tests. (positive oxidase reaction)
  109. Alginate
    Is a polysaccharide (sugar sticky) made by Pseudomonas aeruginose. Helps to create biofilm which helps to resist phagocyctosis and allows breaking of the biofilm of large amount of bacteria to break off.
  110. Water soluble pigment of P. aeruginosa
    Floresenct pigment Pyovirdin. The other is Pyocyanin is a water soluble pigment that is a blue color which is primarily formed when there is a low iron concentration involved in iron metabolism.
  111. Burkholderia pseudomallei and Burkholderia cepacia complex BURKHOLDERIA SPECIES
    Can cause melioidosis. Infections are primarly in tropical climates. Infects many different animals and humans. Can cause pulmonary infection. Can also caused skin (cutaneous infections). Two methods of exposure INHALATION AND CUTANEOUS.
  112. Moraxella catarrhalis
    Sapprophyte can cause pulmonary infection. Most common of middle ear infection. Usually infects immuno compromised
  113. Acinetobacter species
    Gram negative bacilli. Common in freshwater and soil. Part of the normal skin flora. Can infect the oral cavity. respiratory tract. GI. UTI. bacteremia. skin infections
  114. Stenotrophomonas maltophilia
    Found in many aquatic environments. Not very virulent. Can infect water sources. Can cause wound infections.
  115. General Characteristics of Bacillus
    About 60 species. Gram positive. Large. Most are saprophytic contaminants or normal flora. PRODUCE ENDOSPORES. Catalase postive. Aerobic or facultative anaerobic. On blood agar are large spreading gray white colonies with irregular margins. SSPORES ARE PRODUCED AFTER SOME KIND OF STRESS.
  116. Epidemology of Bacillus anthracis
    Very rare in US (17cases). Enzootic in certain foreign countries. ANTRAX SPORES INFECTIOUS FOR DECADES. Biologic warefare experiments (annual tests for 20 years at Gruinard). Primary a desease of herbivorous animals (hoofed animals). Commonly transmitted to humans with direct contatct with animal products (wool and hair). Also acquried via inhalation and ingestion (increased mortality with this entry).
  117. Cycles of Bacillus anthracis
    Survival of spores in the soil. Animal infection. Infection in humans
  118. Method of infection of Bacillus anthracis and mortality
    1. Inoculation (cutaneous) contact with skin animal products (hide. wool. hair) 20 percent. Ingestion of contaminated food products 95 percent. Inhalation of contaminated dust woolsorters disease (95 percent).
  119. Bacillus antrhacis toxins
  120. Spore information of bacilllus anthracis
    Sporulation requires poor nutrients condition and presence of oxygen. Spores are very resistant. Survive for decades. Taken up by host and germinate. Leathal does from 2500 to 55000 spores.
  121. Clincal Presentation of Anthrax Cutaneous
    95 percent human cases are cutaneous infections. 1 to 5 days after contact. Small pruritc non painful papule at inoculation site. Slow healing painless ucler covered with black eschar surrounded by edema. 20 percent mortality in untreated
  122. Clincal Presentation of Anthrax Gastrointestinal (ingestion)
    Virtually 100 percent fatal. Abdominal pain. Hemorrhagic ascites. Paracentesis fluid may reveal gram positive rods.
  123. Clincal presentation of Anthrax Inhalation
    Virtually 100 percent fatal (pneumonic). Meningitis may complicate cutaneous and inhalation forms and disease. Pharyngeal antrhrax will produce fever. pharyngits. Neck swelling.
  124. Laboratory Characteristics of B. anthracis
    Gamma hemolytic. Large spreading gray white coloneis with irregular margins on Blood Agar. Motility negative. Geltatin hydrolysis. Sailcin fermentation negative. Growth on PEA blood agar negative.
  125. Treatment and Prophylaxis of Bacillus anthracis.
    Penicillin is drug of choice. Erythromycin chloramphenicol acceptable. Doxyclcline now commonly recognized as prophylactic. Usually long treatment regimen of antibiotics. Vaccine is availbile for laboratory workers. employees of mills handling goat hair. Active military.
  126. Emetic food poisoning
    Emetic food poisoning. Example of a foodborne INTOXICATION. Involves heat stable enterotoxin. Come from rice. Incubation less than 6 hours. Symptoms vomting. nausea. abdominal crapms. During about 8 to 10 hours. Enterotoxin heat stablizied
  127. Diarheal food poisoning
    Example of a foodborne INFECTION. Involves a heat liable (non resistant) enterotoxin. Meat and vegetables. Incubation greater than 6 hours. Diarrhea. nausea. abdominal cramps. Duration 20 to 36 hours. Enterotoxin heat labile
  128. B. cereus disease caused
    EMETIC FOOD POISONING. DIARHEAL FOOD POISONING. Eye infections. Servere pneumonia (rare)
  129. General consideration for culturing and identifiy anaerboes
    Anaerobic infections usally polymicrobial. Usually endogenous. Associated with intraabdomianl. pulmonary. wound. genitourinary tract infectinos.
  130. Basic Principles of Handling and Transport of anaerobes
    Be prompt. Urine is a good culture media. Keep sampels moist. do not refridgerate. Use tight fitting caps. anaerobic transport medium. PRAS pre-reduced anaerobically sterillized. Fluid thioglycollate medium.

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