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Gram Negative Bacteria and Spirochetes 1 REVIEW 2 5 Types of bacteria Gram positive Gram negative Spirochetes Today’s lecture Today’s lecture Acid-fast (Mycobacteria) Mycoplasma 3 For the Lecture 3 Exam The whole test is matching. Be able to match the following with their description: Virulence factors/enzymes The three hemolysis patterns Disease terms Toxins Match the disease to the organism Know which diseases have which vectors 4 Outer membrane Peptidoglycan 5 GRAM NEGATIVE GRAM POSITIVE ENDOTOXINS (GRAM NEGATIVE ONLY) O Antigen Inner plasma membrane LPS Cell Wall Lipid A (endotoxin) 6 LPS (LOS is LPS with shorter O antigen) Outer plasma membrane Gram Negative Bacterial Cell Walls 7 Figure 3.13b7 Virulence Factors Adhesins (to adhere) • Enzymes Invasins (to get into cells) Endotoxin (LPS, LOS, and Lipid A) Exotoxins Cytotoxins (kills cells) Enterotoxin (GI upset) Neurotoxins (disrupts nerves) H Ag (flagella allows motility) K Ag (capsule) • • • • • • • • • β lactamase (deactivates penicillins) Ribosylase (causes diarrhea) Catalase Coagulase (causes blood clots) Staphylokinase (dissolves blood clots) Streptokinase (dissolves blood clots) IgA or IgG protease (deactivates Ab’s) Hyaluronidase (can move thru tissues) SOD (superoxide dismutase; deactivates WBC lysosomes) Angiotrophic ability (pulls blood vessels close) Facultative intracellular pathogens (can survive with and without O2) MDR plasmids (genetic drug resistance) PG (prostaglandins; promotes inflammation) END OF REVIEW 9 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 10 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis NOTE: All of the organisms on this slide are rods except Neisseria, which are cocci (diplococci). Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Spirochetes Treponema pallidum Borelia burgdorferi 11 Enterobacteriaceae The Enterobacteriaceae is a large family of Gram-negative bacteria that 12 includes, along with many harmless symbionts, many of the more familiar pathogens, such as Salmonella, Escherichia coli,Yersinia pestis, Klebsiella and Shigella. Other disease-causing bacteria in this family include Proteus, Enterobacter, Serratia, and Citrobacter. They are Gram negative rods, most of which are normal flora of the large intestines of humans and animals. Some are found in water or soil, or are parasites on a variety of different animals. When they get into the small intestines (fecal-oral route) or blood, or elsewhere, they cause serious disease. Enterobacteriaceae 13 Infections associated with Enterobacteriaceae 14 Enterobacteriaceae Gram negative rods, oxidase negative Most are motile (peritrichous flagella) Most are encapsulated LPS is a virulence factor, since they are Gram neg Many have “serum resistance” inhibitions of complement proteins (Ab’s can’t attack) Ubiquious (they are everywhere) - soil, water, vegetation, normal intestinal flora ~40 genera, 150 species 15 Cytochrome oxidase Cytochrome c oxidase is the last enzyme in the 16 respiratory electron transport chain. It transfers the last two H+ electrons to one oxygen molecule, converting molecular oxygen to water. The oxidase test is used to determine if a bacterium produces cytochrome c oxidase. Those that have the enzyme (oxidase positive) can use oxygen to break glucose down into ATP (aerobic). Those that are oxidase negative must use another pathway, such as fermentation. All Enterobacteriaceae are oxidase negative. CH2OH GLYCOLYSIS O OH OH Kinase CH2O(P) OH OH Homolactic CH3-C-COOO GLUCOSE-6-P OH O OH Kinase CH2O(P) OH ATP ADP O OH Pyruvate CH3-C-COO- O FRUCTOSE-1,6 DiPhosphate CH2O(P) 2NADH DiOH Acetone Phosphate (3C) P-Glyceraldehyde (3C) OH OH CH3-C-C-CH3 GLYCOLYSIS 1, 3, P-Glyceric acid NAD+ NADH2 ADP + Pi ATP 2 P-Glyceric acid Acetoin 2NAD+ 2, 3, Butanediol H H 1 GLU + 2ATP + 2NAD = 2PYR + 4ATP + 2NADH2 Kinase 2, 3 Butanediolic Fermentation 2PYR + 2NADH Acetoin + NAD + 2 CO2 +2NADH 2, 3 Butanediol + 2NAD NET GAIN = 4 NAD O 2NAD+ OH CH3-C-C-CH3 H O 2NADH OH CO2 C-CH3 CH3-C Adolase NET GAIN = 2 ATP x2 Isomerase x2 O Enol Pyruvate ADP + Pi Kinase ATP Coenzyme A NAD+ NADH2 Pyruvate CH3-C-COOH CO2 Dehydrogenase O Isocitric Acid (6C) NAD+ NADH2 CO2 ά Ketoglutarate Acid (5C) COO- -CH2-CH2-C-COOO NAD+ NADH2 Tricarboxylic Acid Cycle (TCA/ Krebs Cycle) Succinyl CoA Citric Acid Acetyl CoA CH3-C-S-CoA Oxaloacitic Acid (4C) O COO- -CH2-C-COO- PYRUVATE ACTIVATION ETOH CH3-CH2-OH Ethanolic Fermentation PYR + NADH Acetaldehyde + NAD + CO2 +NADH ETOH + NAD NET GAIN = 2 NAD Pyruvate CH3-C-COO- + O CO2 NAD+ NADH O 2, 3 Butanediolic FRUCTOSE-6-P CH2OH CO2 OH Acetaldehyde H CH3-C NAD+ O OH CH2O(P) NADH Pyruvate CH3-C-COO- Ethanolic Homolactic Fermentation PYR + NADH Lactic Acid + NAD NET GAIN = 1 NAD Lactic Acid H CH3-C-COO- NAD+ NADH Pyruvate GLUCOSE OH ATP ADP O OH Isomerase FERMENTATION O TCA Acetyl CoA + 3NAD + 1 FAD + 1GTP = 3 NADH + 1FADH2 + GTP + CO2 MULTIPLY THE ABOVE BY CO2 TOTAL GAIN: TWO 8 H+ 2 GTP GDP+ GTP *First energy-producing step Malate Acid PYRUVATE ACTIVATION Succinate NAD+ NADH2 2 PYR + 2NAD + 2CoA = Acetyl CoA + 2NADH2 + 2CO2 FAD+ Fumorate Acid FADH2 ELECRON TRANSPORT SYSTEM (RESPIRATION / OXIDATIVE PHOSPHORYLATION ETS 16 NADH from glycolysis need to be reduced. H Ox Red +3 H Red Ox Ox Red Ox +2 FMN Fes CoQ Red Ox Red +2 +3 ADP ATP ATPase H2 Cyt b Cyt c Cyt a1 Ox Red Ox ADP ATP ATPase H2O Cyt a3 Red Anaerobic phosphorylation endproducts (instead of H2O) H ADP ATP ATPase O2 H2S SO4 NH3 NO2 Electron Transport Chain Cytochrome oxidase 18 Oxidase Test Put bacteria on paper and add a drop of reagent. Purple means oxidase positive. Enterobacteriaceae are oxidase negative, so they all ferment at least one type of sugar. The sugar is broken down into lactic acid, which will change fermentation media from red to yellow. 19 Lab identification of the enterics http://class.fst.ohio-state.edu www.mc.maricopa.edu Green sheen; black nucleated centers MacConkey agar selective and differential EMB agar selective and differential 20 Yellow = sugar fermentation Black = H2S positive Air bubble = gas production TSI 21 Triple Sugar Iron Agar (TSI) Lactose in the slant Sucrose in the slant Glucose in the butt Phenol red (pH indicator dye) Iron (turns black in the presence of sulfur, which indicates the organism uses sulfur as its electron acceptor instead of oxygen). All Enterobacteriacea ferment glucose, so butt will turn yellow. If it also ferments lactose or sucrose, slant and butt will turn yellow. If it does not ferment lactose or sucrose: slant stays red and butt turns yellow. If the whole tube stays red (e.g. Pseudomonas) it does not ferment glucose, so it is a strict aerobe, not Enterobacteriaceae. 22 Salmonella-Shigella differentiation Salmonella-Shigella agar (SS agar) or Hecktoen agar inhibits most Gram + (sugar fermenters – red/orange; non-fermenters – green) H2S production (black) K. pneumoniae (L); M. luteus (R) S. typhimurium (L); P. vulgaris (R) H2S production (black ppt) www.austincc.edu/microbugz/ 23 Note: Shigella is a non-fermenter, and does not produce H2S, unlike Salmonella Enterobacteriaceae May be primary pathogens (cause disease in healthy people) But they are usually associated with opportunistic infections: Enteric (GI) infections Bacteremia (bacteria in the blood) Septicemia (bacterial toxins in the blood) Pneumonia Meningitis UTIs (urinary tract infections) 24 Enterobacteriaceae and disease http://www.ratsteachmicro.com 25 Hospital-acquired infection A hospital-acquired infection, also known as a HAI or in medical literature as a nosocomial infection, is an infection whose development is favoured by a hospital environment, such as one acquired by a patient during a hospital visit or one developing among hospital staff. Such infections include fungal and bacterial infections and are aggravated by the reduced resistance of individual patients. About 100,000 people die each year in the USA from nosocomial infections. 26 Contaminated surfaces increase cross-transmission 27 Nosocomial Infections ESKAPE pathogens are a group of the six bacteria with a high rate of antibiotic resistance that are responsible for the a majority of nosocomial infections. Enterococcus faecium Staphylococcus aureus Klebsiella pneumoniae Acinetobacter baumannii Pseudomonas aeruginosa Enterobacter species 28 Bacteria forces closure of Puerto Rico hospital intensive care unit At least 10 patients at the University of Puerto Rico Hospital who have since died were carrying the bacteria Acinetobacter baumannii. The health department's epidemiology director blames the presence of the bacteria on poor hygiene at the hospital's intensive care unit. 29 Diarrhea ~1 billion people worldwide suffer from acute diarrhea at least once/year 5-8 million deaths/year primarily in developing nations ~100 million infections in U.S. 250,000 require hospitalization 3000 die 90% of acute diarrhea caused by infectious agents fecal-oral contamination 30 High risk groups in U.S. Travelers – 40% of tourists to Latin America, Africa, Asia develop “traveler’s diarrhea” ETEC – enterotoxigenic E. coli Shigella Salmonella Campylobacter Giardia (camper’s, swimmers) Consumers of certain foods Chicken, mayonnaise, creams, eggs: picnic, banquet, restaurant (Salmonella, Shigella. Campylobacter) Hamburger: undercooked (EHEC – enterohemorrhagic E. coli) Fried rice (B. cereus) Seafood (Salmonella, Vibrio cholerae, hepatitis A) Fermented tofu (C. botulinum) Immunocompromised 31 High risk groups in U.S. (cont.) Daycare participants and their family Shigella Giardia Cryptosporidium (protozoan) Rotavirus (virus) Institutionalized persons Nosocomial (acquired in a hospital) infections of hospital patients Clostridium difficile (Gram positive) 32 Treatment - gastrointestinal disease Fluid/electrolyte replacement fluid alone for mild cases dehydration most common cause of death due to diarrheal disease Antibiotics not used unless systemic/severe e.g. enteric fever immunosuppressed Antibiotic prophylaxis for those traveling to high-risk countries (esp. immunocompromised) 33 Enteric infections Overview of symptoms non-inflammatory nausea vomiting diarrhea inflammatory Dysentery (severe diarrhea containing mucus and/or blood) Invasive (systemic) Typhoid Fever (enteric fever) 34 “Common” organisms associated with enteric infections I Mechanism: Non-inflammatory II (enterotoxin) (invasive, cytotoxin) Penetrating (invasive, spread) Location: proximal small bowel colon distal small bowel Illness: Diarrhea Dysentery Enteric fever blood, fecal PMNs (polymorphonuclear leukocytes = neutrophils) fecal mononuclear leukocytes (monocytes, lymphocytes) Shigella Invasive E. coli Clostridium difficile Entamoeba histolytica Balentidium coli Salmonella typhi Yersinia enterocolitica Stool exam: no fecal leukocytes Example organisms: Vibrio cholerae E. coli Salmonella Campylobacter Giardia Inflammatory III Cryptosporidium Rotavirus Norwalk-like agents 35 Diarrhea pathobiology, #1 Agent Incubation period Vomiting Abdominal pain Fever Diarrhea Toxin producers B. cereus S. aureus C. perfringens 1-8h 8-24h 3-4+ 1-2+ 0-1+ 3-4+, watery 8-72h 2-4+ 1-2+ 0-1+ 3-4+, watery 1-8d 0-1+ 1-3+ 0-1+ 3-4+, watery Enterotoxin V. cholera ETEC K. pneumoniae Enteroadherent EPEC EAEC Giardia Cryptosporidium Helminthes 36 Harrison’s principles of internal medicine, 2005 Diarrhea pathobiology, #2 Agent Incubation Vomiting Abdominal period pain Fever Cytotoxin producers C. difficile 1-3+, usually watery, occasional bloody 1-3d 0-1+ EHEC 37 12-72h Diarrhea 3-4+ 1-2+ 1-3+, initially watery, quickly bloody Diarrhea pathobiology, #3 Agent Incubation period Vomiting Abdominal pain Fever Diarrhea 1-3d 1-2+ 2-3+ 3-4+ 1-3+, watery moderate inflammation Salmonella Camylobacter V. parahaemolyticus Yersinia 12h-11d 0-3+ 2-4+ 3-4+ 1-4+, watery or bloody severe inflammation Shigella EIEC E. histolytica 12h-8d 0-1+ 3-4+ 3-4+ 1-2+, bloody Invasive minimal inflammation Rotavirus Norwalk agent 38 Pathogenicity of enteric bacteria Host factors personal hygiene fecal-oral contamination gastric acidity enteric flora (your own colon microbes) specific immunity status (how healthy you are) 39 Pathogenicity of enteric bacteria (cont.) Microbial factors Exotoxins: three categories Neurotoxins usually ingested as preformed toxins Staphylococcal toxins (Staph. aureus) Botulinum toxin (Clostridium botulinum) Enterotoxins having a direct effect on intestinal mucosa (elicit fluid secretions) Cholera toxin (Vibrio cholerae) E. coli toxins Cytotoxins mucosal destruction (often see dysentery) Shigella dysenteriae Clostridium perfringens Clostridium difficile S. aureus 40 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis 41 Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida E. coli and the serotypes Lactase positive note: many intestinal pathogens are lactase negative ex. Salmonella, Shigella, Yersinia grouped based on surface antigens (serotypes) O antigen (lipopolysaccharide) H antigen (flagellar) K antigen (capsular) O157:H7 (EHEC – enterohemorrhagic E. coli) O148:H28 (ETEC – enterotoxigenic E. coli) 42 E. coli serotype differentiation 1. immunologic assay 2. Growth on a variant of MacConkey agar called Sorbital-MacConkey agar (sorbitol is an artificial sweetener made from corn sugar) Most E. coli can ferment sorbitol (forms pink colonies) E. coli O157:H7 does not ferment sorbitol (colonies are clear/colorless). www.komed.com 43 E. coli pathology most strains of the pathogenic E. coli are capable of pathology only within the intestinal tract (some exceptions) most pathogenic strains associated with disease in developing countries (except EHEC is common in the USA) dependent upon strain, different disease severity/symptoms (e.g. pathotype) 44 E. coli pathology (cont.) pathogenic strains produce virulence factors found on: Plasmids (a DNA molecule that is separate from, and can replicate independently of, the chromosomal DNA) Bacteriophages (viruses that infect bacteria) virulence factors include: Fimbriae (allow bacteria to stack up on each other to shelter themselves from immune system secretion systems (the process of toxin release) toxins 45 Bacteriophage 46 E. coli strains/serotypes most normal flora E. coli are non-pathogenic in intestinal tract pathogenic strains: EPEC (enteropathic) ETEC (enterotoxic) EHEC (enterohemorrhagic) EIEC (enteroinvasive) EAEC (enteroaggregative) UPEC (uropathogenic) 47 Enteropathogenic E. coli (EPEC) destruction of surface microvilli (small intestines) •fever •diarrhea (infantile) •malabsorption of fluids •vomiting/nausea •hard to replace fluids •non-bloody stools common in developing countries (rare in U.S.) http://www.annauniv.edu/biotech/epec.jpg 48 EPEC pathology - diarrhea since this is primarily a disease of the young (less the 6 months old), fluid replacement is important intense vomiting - i.v. fluids are usually required disease self-limiting (antibiotics usually not required) breast feeding seems to have a strong protective effect IgA and other factors decrease bacterial attachment 49 Enterotoxigenic E. coli (ETEC) “Traveler’s diarrhea” primarily in developing nations ~650 million cases/year ~80,000 in travelers from the U.S. Two types of toxins heat labile toxins (LT) similar to cholera toxin (although not as severe) lack of absorption of fluids = watery diarrhea heat stabile toxins (ST) no inflammation, self-limiting 50 Enterotoxigenic E. coli (ETEC) many different ETEC strains disease is self-limiting watery diarrhea common symptom exposure provides immunity adults living in endemic areas, often immune children, through exposure to the many strains, eventually develop immunity therapy fluid replacement bismuth subsalicylate tablets (Pepto-Bismol, etc.) provide antibiotics to travelers in the event they get sick while abroad 51 Enterohemorrhagic E. coli (EHEC) usually O157:H7 many different types of E. coli identifying O157:H7…finding a slightly different hay in a large haystack. strain must have virulence/toxin genes. Vero toxin (VTEC) = “shiga-like” toxin (cytotoxin) aka Shiga toxin-producing E. coli (STEC) AB toxin “A” inactivates 28S rRNA = stop protein synthesis death of epithelial cells 52 EHEC ~75,000 cases in U.S./year estimated that only ~100 bacterial cells are enough to cause infection ~60 deaths many EHEC serotypes (~50) in U.S., most diseases due to O157:H7 disease can be mild to severe (hemorrhagic colitis = bloody diarrhea) depends on strain patient status (age, physiological status) 53 EHEC symptoms Hemorrhagic (hemorrhagic coilitis) bloody, copious diarrhea few leukocytes afebrile (no fever) usually self limiting (in ~1 week) Hemolytic Uremic Syndrome (HUS) hemolytic anemia thrombocytopenia (destroys platelets) kidney failure 5-10% of kids infected with EHEC 54 Found in raw or undercooked ground meat, raw milk and fecal contamination of vegetables EHEC cattle seem to be the major reservoir humans become infected by ingesting undercooked meat (beef), unpasteurized milk, fruits and fruit juices (fecal-contaminated fruit), uncooked vegetables detection: O157 strains do not ferment sorbitol (or do so slowly) follow up with serological/biochemical testing to confirm therapy supportive therapy 55 Enteroinvasive E. coli (EIEC ) Dysentery (bloody diarrhea) resembles shigellosis (Shigella dysenteriae) relatively rare in U.S. common strains: O124, O143, O164 need relatively large inoculum: 108-1010 invade and destroy colonic epithelium usually causing watery diarrhea some patients will progress to dysentery organism replicates within cytoplasm of cell 56 Enteroaggregative E. coli (EAEC ) associated with persistent watery diarrhea > 14 days (especially infants) traveler’s diarrhea – maybe as important as ETEC fimbriae allow for bacteria to stack up on each other bacteria stimulate mucous production called biofilm formation (bacterial community) 57 Uropathogenic E. coli (UPEC) most common cause of UTIs females more than males some serotypes have pili that preferentially binds to uroepithelial cells 58 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 59 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Enterobacter aerogenes Normal GI flora that cause opportunistic infection Transmitted by fecal-oral route or aspiration Causes diarrhea, pneumonia, or septicemia 60 Klebsiella pneumoniae Although found in the normal flora of the mouth, skin, and intestines, it can cause destructive changes to human lungs if aspirated. It is an important pathogen in nosocomial infections. This is an ESKAPE organism. Its virulence factors include the O antigen, which is a component of the lipopolysaccharide (LPS), and the K antigen (a capsule). 61 Klebsiella pneumoniae It causes destructive changes to human lungs via inflammation and hemorrhage with cell death (necrosis) that sometimes produces a thick, bloody, mucoid sputum (called currant jelly sputum). These bacteria gain access typically after a person aspirates colonizing oropharyngeal microbes into the lower respiratory tract. Klebsiella infections are seen mostly in people with a weakened immune system. Many of these infections are obtained when a person is in the hospital for some other reason (a nosocomial infection). 62 Klebsiella pneumoniae Klebsiella can also cause infections in the urinary tract, lower biliary tract, and surgical wound sites. For patients with an invasive device in their body, contamination of the device becomes a risk; for example, respiratory support equipment and urinary catheters. Sepsis and septic shock can follow entry of the bacteria into the blood. Klebsiella organisms are often resistant to multiple antibiotics. 63 Proteus vulgaris The term Proteus means “changeability of form”. Proteus vulgaris inhabits the intestinal tracts of humans and animals. It can be found in soil, water and fecal matter. It is grouped with the Enterobacteriaceae and is an opportunistic pathogen of humans. It is known to cause urinary tract infections and wound infections. It is a common agent of nosocomial infections. 64 Proteus vulgaris Virulence Factors Flagella for motility Fimbrae for attachment Interleukon secretion to cause epithelial cells of the urinary tract to desquamate (fall off). Production of urease, an enzyme that breaks urea down into ammonia to make the urine more alkaline so it can survive better. 65 Proteus vulgaris Symptoms Urinary tract infections Bacteremia and sepsis Proteus and Pseudomonas are the most common causes of Gram negative bacteremia. Both exhibit “swarming motility”, in which they rapidly spread across the surface of the agar medium. This allows them to spread quickly in the host. 66 Proteus vulgaris Treatment Antibiotics should be introduced in much higher doses than "normal" when P. vulgaris has infected the sinus or respiratory tissues. For example, Ciprofloxacin should be introduced at a level of at least 2000 mg per day orally in such a situation, rather than the "standard" 1000 mg per day. 67 Serratia marcescens This is a common cause of nosocomial infections, particularly catheter-associated bacteremia, urinary tract infections and wound infections. It is commonly found in the respiratory and urinary tracts of hospitalized adults and in the gastrointestinal system of children. 68 Serratia marcescens Due to its abundant presence in the environment, and its preference for damp conditions, S. marcescens is commonly found growing in bathrooms (especially on tile grout, shower corners, toilet water line, and basin), where it manifests as a pink discoloration and slimy film feeding off phosphoruscontaining materials or fatty substances such as soap and shampoo residue. Once established, complete eradication of the organism is often difficult, but can be accomplished by application of a bleach-based disinfectant. 69 Serratia marcescens S. marcescens may also be found in environments such as dirt, supposedly "sterile" places, and the subgingival biofilm of teeth. Due to this, and the fact that it produces a reddishorange pigment, it may cause staining of the teeth. 70 What Diseases Do These Cause? Enterobacteriaceae E. coli Diarrhea, septicemia, UTI Enterobacter aerogenes Diarrhea, pneumonia, septicemia Klebsiella pneumoniae Pneumonia, septicemia Proteus vulgaris UTI, diarrhea, nosocomial wound infections Serratia marcescens UTI, wound infections (catheters), pink grout Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica Yersinia pestis 71 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 72 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Campylobacter jejuni Likely the most common cause of gastroenteritis in the United States 5-7% of cases Many animals serve as reservoirs for the bacteria Humans become infected by consuming contaminated food, milk, or water Poultry is the most common source of infection Infections produce dysentery and frequent diarrhea that is self- limiting Spread of the bacteria can be reduced by proper food handling and preparation 73 Pathophysiology Transmission fecal-oral, person-to-person sexual contact, unpasteurized raw milk and poultry ingestion, and waterborne. Exposure to sick pets, especially puppies infectious dose is 1000-10,000 bacteria incubation period of up to a week 74 Disease – Patients may have a history of ingesting inadequately cooked poultry, unpasteurized milk, or untreated water. • The incubation period is 1-7 days and is probably related to the dose of organisms ingested. – A brief prodrome of fever as high as 40°C (104°F) – headache, and myalgias (muscle pain) lasting up to 24 hours – crampy abdominal pain (abdominal pain and tenderness may be localized) • Pain in the right lower quadrant may mimic acute appendicitis (pseudoappendicitis). – Up to 10 watery, frequently bloody, bowel movements per day – Patients with C jejuni infection who report vomiting, bloody diarrhea, or both tend to have a longer illness and require hospital admission. 75 Salmonella The “L” is silent Gram negative bacilli, lactase negative motile, H2S gas production (some exceptions) ~2500 serotypes! often, the serotypes are considered to be individual species nomenclature is a “mess” 76 Salmonella S. choleraesuis is the “major” species organism that causes typhoid (enteric) fever: Often just called Salmonella Typhimurium Shortened to Salmonella Typhi 77 Salmonella subtyping Serotypes based on: O antigen (LPS outer sugars) Flagella H antigens Various surface antigens most clinical labs divide Salmonella into serogroups (A, B, C1, C2, D, and E) based on O-antigen 78 Salmonella infection Human intestinal disease due to ingestion of bacteria (contaminated food/water) organism gets to small intestines macrophages often ingest bacteria bacteria are then protected from host responses (e.g. complement, antibodies, etc) Salmonella alters host cells: changes host cell to allow for “bacteria-mediated endocytosis (absorbing a substance from outside the cell)” prevents lysosomal enzymes of macrophage from degrading bacteria 79 Salmonella pathology Bacteria is disseminated by macrophages to: liver, spleen, lymph nodes, bone marrow Systemic symptoms likely due to host response against pathogen inflammatory cytokines secreted by activated macrophages. Cytokines are chemicals that call other WBCs to come to the area. 80 Salmonella pathology (cont.) Non-typhoid and typhoid Salmonella infections Typhoid relatively rare in U.S., although 21 million infections worldwide (~200,000 deaths) Non-typhoid Salmonella much more common Human acquire infections from poultry/eggs, dairy, and contaminated work surfaces (cutting boards) In U.S., ~40,000 reported cases (estimated 2 million) 81 Enteric (typhoid) fever systemic disease caused by S. Typhi or S. Paratyphi originally called typhoid fever because of some similarities to typhus (fever, nausea, rash, and other systemic symptoms) different bacteria, different mechanism of spread “better name” is enteric fever disease from ingesting contaminated food humans only known hosts of these strains endemic (commonly occuring) in developing nations not common in U.S. (food/water/sewage care) 82 Enteric (typhoid) fever (cont.) ~70% of U.S. cases obtained from international travel infectious dose is low (~103 versus 106-108 for infections with other species of Salmonella) Clinical manifestations febrile illness disease more severe by S. typhi as compared to S. paratyphi after 10-14 days of initial infection, patients have gradually increasing fever, headache, myalgia (muscle pain), malaise (fatigue). at around 21 days after infection, GI symptoms present (not seen in all patients) – diarrhea 83 Typhoid fever Typhoid fever — also known simply as typhoid — is a common worldwide bacterial disease transmitted by the ingestion of food or water contaminated with the feces of an infected person, which contain the bacterium Salmonella. 84 Went back to work as a cook in 1914 at a NYC hospital. Another 25 got sick and 2 died. 85 Mary Mallon in 1931. Food worker, first diagnosed as carrier in 1907. She infected 50 people, 3 of whom died. Quarantined and then released in 1910. Quarantined permanently to North Brother island in 1915. Typhoid Mary Mary Mallon (September 23, 1869 – November 11, 1938), better known as Typhoid Mary, was the first person in the United States identified as an asymptomatic carrier of the pathogen associated with typhoid fever. She was presumed to have infected some 75 people, 5 of whom died, over the course of her career as a cook. She was forcibly isolated twice by public health authorities and died after a total of nearly three decades in isolation. 86 From 1900 to 1907 she worked as a cook in the New York City 87 area. In 1900, within two weeks of her employment, residents developed typhoid fever. In 1901 she moved to Manhattan, where members of the family for whom she worked developed fevers and diarrhea, and the laundress died. Mallon then went to work for a lawyer, until seven of the eight household members developed typhoid. In 1906, she took a position in Long Island, and within two weeks, ten of eleven family members were hospitalized with typhoid. She changed jobs again, and similar occurrences happened in three more households. In late 1906, one family hired a typhoid researcher named George 88 Soper to investigate. Soper discovered the common element in the outbreaks was an unmarried, heavyset Irish cook, about forty years old. No one knew her whereabouts. After each case she left and gave no forwarding address. Soper traced her to an active outbreak in a Park Avenue penthouse — two servants were hospitalized and the daughter of the family died. When Soper approached Mallon about her possible role in spreading typhoid, she adamantly rejected his request for urine and stool samples. Since Mary refused to give urine and stool samples, he decided to compile a five-year history of Mary's employment. Soper found that of the eight families that hired Mallon as a cook, seven claimed to have gotten typhoid fever. On his next visit, he told her he would write a book and give her all the royalties. She angrily rejected his proposal and locked herself in the bathroom until he left. A few days later, several police officers arrived at Mary's 89 workplace and took her into custody. Mary attracted so much media attention that in a 1908 issue of the Journal of the American Medical Association she was called “Typhoid Mary“. Under questioning, Mallon said she rarely washed her hands when cooking and felt there was no need to do so. Cultures of Mary's urine and stools, taken forcibly with the help of prison matrons, revealed that her gallbladder was teeming with typhoid Salmonella. She refused to have her gallbladder extracted or to give up her occupation as a cook, maintaining stubbornly that she did not carry any disease. Mallon was held in isolation for three years at a clinic located on North Brother Island. Eventually, the New York State Commissioner of Health decided that disease carriers should no longer be kept in isolation. Mallon could be freed if she agreed to stop working as a cook and take reasonable steps to prevent transmitting typhoid to others. On February 19, 1910, Mary agreed that she prepared to change her occupation (that of a cook), and would take such hygienic precautions as would protect those with whom she came in contact from infection. She was released from quarantine and returned to the mainland. 90 Upon her release, Mallon was given a job as a laundress, which paid less than cooking. She soon changed her name to Mary Brown, and returned to her old occupation. For the next five years, she worked in a number of kitchens; wherever she worked, there were outbreaks of typhoid. However, she changed jobs frequently, and Dr. Soper was unable to find her. In 1915, a serious epidemic of typhoid erupted among the staff of New York's Sloane Hospital for Women, with twenty-five cases and two fatalities. Public health authorities located and arrested Typhoid Mary, returning her to quarantine on North Brother Island on March 27, 1915. She was confined there for the remainder of her life. Mallon became a minor celebrity, and was interviewed by journalists, who were forbidden to accept even a glass of water from her. Later, she was allowed to work as a technician in the island's laboratory, washing bottles. 91 Other healthy typhoid carriers identified in the first quarter of the 20th century include Tony Labella, an Italian immigrant, presumed to have caused over 100 cases (with five deaths); an Adirondack guide dubbed Typhoid John, presumed to have infected 36 people (with two deaths); and Alphonse Cotils, a restaurateur and bakery owner. Today, Typhoid Mary is a colloquial term for anyone who, knowingly or not, spreads something undesirable. Individuals can develop typhoid fever after ingesting food or water contaminated during handling by a human carrier. The human carrier may be a healthy person who has survived a previous episode of typhoid fever yet who continues to shed the associated bacteria, Salmonella typhi, in feces and urine. Washing hands with soap before touching or preparing food, washing dishes and utensils with soap and water, and only eating cooked food are all ways to reduce the risk of typhoid infection. 92 ReynoldsUnwrapped.com offers FANTASTIC, inexpensive daily email subscriptions, where you can receive a HILARIOUS new cartoon every day, and it is a MARVELOUS idea for a UNIQUE gift for your family and friends as well. That is how I learned about this...one of my fellow teachers gave me a subscription as a birthday present. He also has FUNNY greeting cards and BEAUTIFUL paintings for sale as well. You can also get reprints suitable for framing, or originals. Here is more info about his work and a YOUTUBE video. https://nccnews.expressions.syr.edu/?p=11515 93 Diagnosis and treatment of typhoid fever positive diagnosis can be accomplished from stool, urine, or bone marrow culture stool culture is often negative in 60-70% early in infection some strains of S. Typhi have been shown to be MDR (multidrug resistant) check for antibiotic susceptibility carrier state requires ~6 week therapy if patient has kidney/gall stones, need surgery as well as antibiotic therapy 94 Gastroenteritis acute gastritis is characterized by vomiting, abdominal pain, fever, and diarrhea (many causes) Gastroenteritis caused by Salmonella: S. Typhimurium (~200 serovariants) many animal reservoirs (hard to control) symptoms often within 8-24hr after ingestion often self limiting diarrhea can be mild to very severe (watery, green, offensive) symptoms usually last 2-3 days (can be up to 1 week) 95 Salmonellosis outbreaks in U.S. attributed to raw chicken, eggs, processed foods, and vegetables and fruits (fruit juices) fecal contaminants exposure to pets (especially reptiles) ~90% of reptiles carry the bacteria 1970s – 14% of human cases of salmonellosis attributed to exposure to turtles birds, rodents, dogs, and cats are also potential reservoirs 96 Salmonella Professional food facilities are not allowed to store eggs or chicken on shelves above other exposed foods in the refrigerator. 97 Salmonellosis diagnosis and treatment stool culture sent to public health departments for phage typing mechanism to identify serotype/serovar disease generally self-limiting replace fluids/electrolytes if needed antibiotics for infants, elderly, immunocompromised, and those with bacteremia many antibiotic resistant strains vaccine for those traveling to endemic areas (especially those going camping) 98 Shigella causes acute infectious inflammatory colitis (colon infection) aka – bacillary dysentery not all infected develop dysentery Gram negative rod (bacillus), non-motile lactase negative (S. sonnei is a weak fermenter) H2S negative genetically similar to Esherichia Shigella are thought to be serotypes of E. coli historically names have not been changed 99 Shigella 4 main species, different serotypes within each species (47 serotypes) S. dysenteriae (Group A) – most pathogenic S. flexneri (Group B) most common cause of shigellosis in developing nations S. boydii (Group C) - India S. sonnei (Group D) – U.S. most common cause of shigellosis in industrial world mildest 100 Shigella ~200 million cases worldwide ~1 million deaths (especially among children) ~15,000 cases reported/year in U.S. (real number is higher - ~500,000/year?) pathogen of humans and higher primates infection from fecal-oral transmission from infected humans highly communicable (need only ~200 cells to produce disease) high rate of secondary household transmission 101 Shigella pathology Clinical manifestation abdominal cramps, diarrhea, fever, bloody stools large numbers of WBC in stool inflammatory damage to intestinal epithelium Diagnosis standard microbiological testing (selective/differential media: MacConkey followed by SS or Hektoen-enteric, etc) Therapy most cases self-limiting antibiotic therapy for those with severe symptoms because of high rate of spread, all patients should be treated 102 Shigella pathology virulence proteins cause “ruffling” of epithelial cells allows for endocytosis of the bacteria actin rearrangement allows for cell-to-cell spread S. dysenteriae produces shiga toxin (similar to EHEC) 103 Yersinia Enteric pathogens: Y. enterocolitica, Y. pseudotuberculosis Y. pestis – Black Plague (carried by fleas on rats) Gram negative, pleomorphic rods primarily found in animals (rodents, swine, cattle, etc) – all are zoonotic diseases Y. enterocolitica 104 www.emedicine.com Y. pestis Bubonic and Pneumonic plague formation of bubos: live pathogens in lymph nodes bacteria resists phagocytosis painful inflammatory lesions Pneumonic plague – high mortality (90% of untreated) highly infectious 105 Bubonic plague still kills thousands Bubonic plague, the deadly scourge that wiped out half of Europe during the Middle Ages, still lurks in pockets of the globe. Although plague is now rare in Europe, it recently sickened more than 10,000 people in Congo over a decade, and cases still occasionally emerge in the Western United States. 106 Yersinia pestis The plague bacteria, Yersinia pestis, had lain dormant in China's Gobi Desert for centuries. But in the 1300s, it emerged with a vengeance, fanning out via trade routes from Asia to Europe and killing millions of people along the way. The plague was transmitted by fleas harbored by rats, which flourished in the overcrowded, filthy cities of the Middle Ages. By the end of the 1500s, between a third and half of Europe's population had died from the Black Death. Even during the 1900s, the plague still killed millions of people, but since then, the advent of better hygiene in cities and swift treatment with antibiotics has reduced this erstwhile killer into a rare disease. 107 Yersinia pestis In the United States during that time period, 56 people contracted the plague and seven died. The cases occurred mainly because plague has become endemic in squirrels and wild rodents in the American West. 108 Man who contracted bubonic plague from cat bite An Oregon man who escaped death after contracting the bubonic plague from his cat has opened up about the terrifying experience and how lucky he is to be alive. Paul Gaylord was in a coma for 27 days in 2012, on life support as his internal organs began to fail, his extremities rotting. “I had collapsed lungs, my heart stopped and my hands and feet turned black. Technically, I shouldn’t be here.” Gaylord’s condition was so bad that the day before he woke up, doctors considered pulling the plug. 109 Man who contracted bubonic plague from cat bite “My recovery shocked everybody,. I’d been told I’d be on dialysis for the rest of my life, but I had one treatment and I recovered. Everything in my body did, except my hands and feet.” The retired welder lost all of his fingers except for parts of both thumbs, all of his toes and a part of his right foot. Gaylord recalled that his cat Charlie showed up on the porch, swollen and choking on a mouse. He tried to pull it out, but the cat bit his finger and ran away. The next day Charlie returned, “clearly suffering.” 110 “It was as if the mouse had died in his mouth and was rotting, and I was worried about bacteria,” Gaylord wrote. “I called a friend over to put him down, then we buried him.” Gaylord’s own symptoms kicked in at work the next day. He had a fever and felt sick before his skin turned grey and his wife rushed him to the hospital. Man who contracted bubonic plague from cat bite After being given antibiotics for cat scratch fever, a doctor told Gaylord he thought bubonic plague was the correct diagnosis. “I had glands under my arms the size of lemons and that’s one of the symptoms,” he said. Gaylord spent a month in the hospital — most of it unconscious — before returning home. Health officials dug up Charlie’s body and determined he was infected with the plague. Author: RHEANA MURRAY http://m.nydailynews.com/1.1600598 111 Gaylord has since retired, and spends his time making hunting knives in his workshop. “It’s hard to believe it happened to me, but rather than feel depressed, I’ve always felt positive and happy to be alive,” he wrote, calling his experience “a fluke.” Y. enterocolitica (and Y. pseudotuberculosis) Y. enterocolitica more common than other enteric Yersinia sp. acute enterocolitis mesenteric lymphadenitis (can mimic appendicitis) over 60 different serotypes serotypes 3, 8 and 9 account for most human infections ingestion of contaminated food/milk (can grow at lower temperatures, 4°C or 39°F. associated with a blood transfusion septicemia 112 Y. enterocolitica transmission bold lines = common spread 113 Yersinia Diagnosis for Yersinia isolation of organism from stool or blood sample may need to do “cold enrichment” growth at 4-7°C for 28 days with weekly subculture on SS agar Therapy Plague antibiotics (control rodent population) Enteric infections: often self-limiting (except if progress to septicemia) 114 What Diseases Do These Cause? Enterobacteriaceae E. coli Diarrhea, septicemia, UTI Enterobacter aerogenes Diarrhea, pneumonia, septicemia Klebsiella pneumoniae Pneumonia, septicemia Proteus vulgaris UTI, diarrhea, nosocomial wound infections Serratia marcescens UTI, wound infections (catheters), pink grout Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia Salmonella typhi Diarrhea and typhoid fever; feces on food, raw chicken, reptiles Shigella dysenteriae Bloody diarrhea from human feces Yersinia enterocolitica Diarrhea; lymph node inflammation Yersinia pestis Bubonic (black) plaque 115 Exotoxins and their classification Cytotoxins Toxic Shock Syndrome toxin (Staph aureus) Exfolatin (Scalded Skin Syndrome; Staph aureus) Necrotizing Fasciitis Toxin (group A Strep) Anthrax Diphtheria Verotoxin (Shigella-like toxin; E. coli EHEC) AB toxin (Kills colon epithelium; E. coli EHEC) Pertussis and tracheal cytotoxin Enterotoxins Neurotoxins Botulism Tetanus 116 These all have endotoxins, but what EXOTOXINS do they produce? E. coli (EHEC) Verotoxin, AB toxin E. coli (ETEC) Enterotoxin, heat labile and heat stable toxins Klebsiella pneumoniae Enterotoxin Campylobacter jejuni Enterotoxin Salmonella typhi Enterotoxin Shigella dysenteriae Shigatoxin Vibrio cholerae Cholera toxin Bordatella pertussis Pertussis toxin 117 Gram positive exotoxins (no endotoxins) Staphylococcus aureus Cytotoxins (TSS, NF, exfolatin), Neurotoxin, Enterotoxin Clostridium difficile Cytotoxin, Enterotoxin Clostridium perfringens Cytotoxin, Enterotoxin Clostridium botulinum Neurotoxin (botulism toxin) Clostridium tetani Neurotoxin (Tetanus toxin) Bacillus cereus Enterotoxin Bacillus anthracis Cytotoxin (Anthrax toxin) Corynebacterium diphtheriae Cytotoxin (Diphtheria toxin) 118 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis 119 Neisseria gonorrhea and meningitis The only Gram neg cocci Vibrio cholerae Helicobacter pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Neisseria gonorrhoeae with pili 120 Neisseria two major pathogenic species N. gonorrheae associated with STDs N. meningitidis associated with respiratory and CNS infections 121 Microbiology/Pathology Gram-negative intracellular diplococcus Contains LOS in outer membrane. infects mucus-secreting epithelial cells evades host response through alteration of surface structures Oxidase positive 122 In vitro growth Obligate aerobes Sensitive to drying (“delicate”) and some products in blood (that is why one uses “Chocolate agar” for culture) called fastidious Chocolate agar is blood agar that has been slowly heated so the red blood cells lyse, to release the hemoglobin. Also needs 5% CO2 123 Endotoxin LPS - lipopolysaccharide Lipid A, core sugars, outer sugars LOS - lipooligosaccharide present in Neisseria as well as several other Gram negative bacteria 124 NG: Incidence and Prevalence Significant public health problem in U.S. Number of reported cases underestimates incidence incidence remains high in some groups defined by geography, age, race/ethnicity, or sexual risk behavior Increasing proportion of gonococcal infections caused by resistant organisms 125 Gonorrhea — Rates by state: United States and outlying areas, 2006 67.3 20.7 VT 11.6 NH 13.7 MA 38.0 RI 47.2 CT 74.4 NJ 63.0 DE 176.0 MD 130.8 DC 342.8 10.4 24.0 40.1 64.4 14.4 125.1 47.3 23.6 81.5 115.6 66.3 79.2 92.2 158.2 139.2 36.0 93.4 80.5 89.9 139.5 167.4 52.5 85.6 175.9 78.5 Guam 58.1 100.2 90.7 154.9 199.4 162.6 154.9 242.5 Rate per 100,000 population 216.8 257.1 234.0 133.2 240.6 94.9 69.4 134.8 <=19.0 (n= 5) 19.1-100.0 (n= 27) >100 (n= 22) Puerto Rico 7.7 Virgin Is. 31.3 Note: The total rate of gonorrhea for the United States and outlying areas (Guam, Puerto Rico and Virgin Islands) was 119.4 per 100,000 population. The Healthy People 2010 target is 19.0 cases per 100,000 population. 126 Men 750 Rate (per 100,000 population) 600 450 300 150 0 6.3 279.1 Age 10-14 0 Women 150 300 605.7 25-29 185.7 294.9 30-34 130.8 40-44 53.0 117.1 125.5 35-39 93.5 45-54 65.7 33.9 12.9 18.4 55-64 2.9 4.2 65+ 0.7 Total 750 647.9 20-24 320.9 600 35.1 15-19 454.1 450 124.6 127 Transmission Efficiently transmitted by: Male to female via semen Female to male urethra Rectal intercourse Fellatio (pharyngeal infection) Perinatal transmission (mother to infant) Gonorrhea associated with increased transmission of and susceptibility to HIV infection 128 Virulence Factors of Gonococcus Pilus Phase variation and Antigenic variation (of pilus) phase variation – differences in colony appearance antigenic variation – varying pili antigenic type development of a vaccine will be difficult Endotoxin (LOS) Serum resistance IgA protease – cleaves at hinge region 129 Gonorrhea: Gram Stain of Urethral Discharge 130 Source: CDC/NCHSTP/Division of STD Prevention, STD Clinical Slides Neutrophils Containing Neisseria 131 biology.clc.uc.edu/Fankhauser/Labs/Microbiolo... Genital Infection in Men Urethritis – inflammation of urethra typically purulent or mucopurulent urethral discharge asymptomatic in 10% of cases Epididymitis – inflammation of the epididymis unilateral testicular pain and swelling Infrequent NOTE: Gonorrhea: men have symptoms, women do not Chlamydia: women have symptoms, men do not 132 Genital Infection in Women most infections are asymptomatic Cervicitis – inflammation of the cervix non-specific symptoms: abnormal vaginal discharge, intermenstrual bleeding, dysuria, lower abdominal pain, or dyspareunia (difficult or painful sexual intercourse) clinical findings: mucopurulent or purulent cervical discharge, easily induced cervical bleeding 50% of women with clinical cervicitis have no symptoms Urethritis – inflammation of the urethra 133 Complications in Women Pelvic Inflammatory Disease (PID) Pelvic inflammatory disease (PID) is a term for inflammation of the uterus, fallopian tubes, and/or ovaries as it progresses to scar formation with adhesions to nearby tissues and organs. This can lead to infertility. may be asymptomatic may present with lower abdominal pain, discharge, dyspareunia, irregular menstrual bleeding and fever. 134 Pelvic inflammatory disease (PID) PID is a vague term and can refer to viral, fungal, parasitic, though most often bacterial infections. In the United States, more than 750,000 women are affected by PID each year, and the rate is highest with teenagers and young women. PID causes over 100,000 women to become infertile in the US each year. N. gonorrhea causes 40–60% of cases of PID. There is NO CURE for PID. Women will have severe pain for the rest of their lives. Although the PID infection itself may be cured, effects of the infection may be permanent, due to the scar tissue that develops. 135 Syndromes in Men and Women Conjunctivitis usually autoinoculation in adults symptoms/signs: eye irritation with purulent conjunctival exudate Disseminated gonococcal infection (DGI) systemic gonococcal infection occurs infrequently. More common in women than in men associated with gonococcal strain that produce bacteremia without associated urogenital symptoms clinical manifestations: skin lesions, arthralgias, arthritis, hepatitis, myocarditis, endocarditis, meningitis 136 Gonococcal Ophthalmia 137 Source: CDC/NCHSTP/Division of STD Prevention, STD Clinical Slides Disseminated Gonorrhea— Skin Lesion 138 Source: CDC/NCHSTP/Division of STD Prevention, STD Clinical Slides Septic Arthritis 139 www.learningradiology.com/images/boneimages1/... Gonorrhea Infection in Children Perinatal: infections of the conjunctiva, pharynx, respiratory tract ophthalmia neonatorum silver nitrate, antibiotics Older children (>1 year): considered possible evidence of sexual abuse 140 Diagnostic Methods • Culture tests – Thayer-Martin agar – This is 5% chocolate sheep blood plus antibiotics. – It is used for culturing and primarily isolating pathogenic Neisseria bacteria, including Neisseria gonorrhea and Neisseria meningitides, because this medium inhibits the growth of most other microorganisms. – Neisseria is fastidious, so it needs chocolate agar, and it also needs the below three antibiotics mixed into the medium because other organisms will out-compete it and it will not grow. The antibiotics that are used will not kill Neisseria. 1) Vancomycin to kill Gram positives 2) Colistin to kill all other Gram negatives 3) Nystatin to kill most fungi 141 Reporting Laws and regulations in all states require that persons diagnosed with gonorrhea are reported to public health authorities by clinicians, labs, or both. 142 Meningococcus Capsule 143 meningitisuk.org Diseases caused by N. meningitidis Meningococcal meningitis Meningococcemia, sepsis 144 Virulence Factors of Meningococcus Endotoxin (LOS) Polysaccharide capsule Serum resistance IgA protease 145 Control of Meningococcus Vaccine does not display same types of phase/antigenic variation as seen in other Neisseria, so it may not work against the strains that have mutated. Antimicrobials somewhat susceptible to penicillins (although some degree of resistance reported) 146 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis 147 Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Vibrio Vibrio are small Gram negative rods, shaped like a comma. Members of this genus share many characteristics with enteric bacteria such as Escherichia and Salmonella Found in water environments worldwide Vibrio cholerae is the most common species to infect humans Causes cholera Humans become infected with V. cholerae by ingesting contaminated food and water Found most often in communities with poor sewage and water treatment 148 Haiti cholera outbreak after earthquake, 2010 The ongoing Haiti cholera outbreak is the worst epidemic of cholera in recent history, according to the U.S. Centers for Disease Control and Prevention. After the 2010 earthquake, in little over two years, as of August 2013, it has killed at least 8,231 Haitians. Since the outbreak began in October 2010, more than 6% of Haitians have had the disease. Then, hurricane Sandy struck in 2012, and the subsequent cases of cholera caused more deaths than the cyclone took in all countries combined. 149 Cholera Outbreaks After Storms Hurricane Sandy (Oct 2012) Cholera outbreak 150 Cholera Outbreaks Outbreaks occur seasonally and are associated with poverty and poor sanitation. Serious disasters, such as hurricanes, typhoons, or earthquakes, cause a disruption in water systems resulting in the mixing of drinking and waste waters. Compared to diseases like smallpox and tuberculosis, which have been around for thousands of years, cholera is a relatively new disease. Its origins can be traced to India in 1826, but by 1830, 40,000 people a year were dying from cholera. In 1831, nearly 200,000 Russians died. The same year, cholera spread to Poland, Hungary, and Germany, killing hundreds of thousands. As it spread throughout Europe, the death toll rose dramatically. In 1848, Russia alone suffered 3 million deaths! 151 Cholera Outbreaks Cholera spread throughout the world in seven large pandemics. The seventh pandemic began in 1961 in Indonesia and subsequently affected approximately 100 more countries. In some areas, more than 20 percent of the people got sick and often half of them died because medical treatment was not available. The pandemic reached Africa in 1970 and moved rapidly throughout the region. By the end of 1971, 25 African countries were reporting cholera outbreaks. Between 3,000 and 43,000 cholera cases were reported in Africa every year until 1990. The following year, a large epidemic affected 14 countries and resulted in more than 100,000 cases and 10,000 deaths. 152 Cholera Vaccine There are two oral vaccines with few side effects that are given outside the United States. These vaccines provide 60 to 100 percent protection against major outbreak strains, but the vaccine only lasts for six months. 153 Vibrio A large inoculum is required to cause disease because the bacteria are susceptible to the acidic stomach environment. Cholera toxin is the most important virulence factor of V. cholerae. 154 Cholera Pathology Some infections are asymptomatic or cause mild diarrhea Can cause severe disease resulting in abrupt watery diarrhea and vomiting “Rice-water stool” is characteristic Results in severe fluid and electrolyte loss Can progress to coma and death 155 Rice water stools 156 Cholera Beds 157 Diagnosis, Treatment, and Prevention Diagnosis Usually based on the characteristic diarrhea Treatment Fluid and electrolyte replacement Antimicrobial drugs are not as important because they are lost in the watery stool Prevention Adequate sewage and water treatment can limit the spread of V. cholerae 158 Florida officials warn of deadly seawater bacteria after man's death Sept, 2013, authorities in Florida are advising residents to avoid eating raw shellfish and exposing open wounds in seawater. 59-year-old Henry "Butch" Konietzky died after he was exposed to bacteria called Vibrio vulnificus. He had been fishing for crabs in the Halifax River. Statewide, 29 cases and nine deaths have been linked to the bacteria this year. 159 Florida officials warn of deadly seawater bacteria after man's death Vibrio vulnificus is a bacterium that normally lives in warm seawater and is in the same family as cholera. Symptoms include diarrhea, vomiting and abdominal pain. Health officials say people should wear gloves and wash their hands after handling raw shellfish. He noticed lesions on his legs several hours after fishing and went to the emergency room with his wife. But the bacteria had already spread through his body, causing his kidneys to shut down. 160 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 161 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Helicobacter pylori Slightly helical, highly motile bacterium that colonizes the stomach of its hosts Causes most (if not all) peptic ulcers H.pylori produces numerous virulence factors that enable it to colonize the stomach Many people have this organism in their stomach, but don't get an ulcer or gastritis. Coffee drinking, smoking, and drinking alcohol increase your risk for an ulcer 162 Symptoms If you are a carrier of H. pylori, you may have no symptoms. Symptoms of an ulcer or gastritis include: Abdominal pain Bloating and fullness Dyspepsia or indigestion Feeling very hungry 1 to 3 hours after eating Mild nausea (may be relieved by vomiting) 163 Diagnosis Simple blood, breath, and stool tests can determine if you are infected with H. pylori. The most accurate way to diagnose is through upper endoscopy of the esophagus, stomach, and duodenum. Because this procedure is invasive, it is generally only done on people suspected to have an ulcer, or who are at high risk for ulcers or other complications from H. pylori, such as stomach cancer. Risk factors include being over 45 or having symptoms such as: Anemia Difficulty swallowing Gastrointestinal bleeding Unexplained weight loss 164 Treatment Patients who have H. pylori and also have an ulcer are most likely to benefit from being treated. Patients who only have heartburn or acid reflux and H. pylori are less likely to benefit from treatment. The treatment does not work in all patients. Treatment must be taken for 10 to 14 days. Medications may include: Two different antibiotics Proton-pump inhibitor (inhibits acid secretion) Bismuth subsalicylate (Pepto-Bismol) 165 Haemophilus Small, pleomorphic (various shaped) bacilli Obligate parasites due to their requirement of heme and NAD+ for growth Colonize the mucous membranes of humans and some animals Contains LOS in outer membrane. 166 Lipooligosaccharides (LOS) LOS is like LPS, except it lacks the O-antigen and possesses only the lipid A. LOS are glycolipids found in the outer membrane of some types of Gram negative bacteria, such as Neisseria, Haemophilus, and Bordetella. LOS allows for bacteria to display antigenic diversity, aiding in the evasion of host immune defenses and thus contributing to the virulence of these bacterial strains. 167 Haemophilus influenzae Most strains have a polysaccharide capsule that resists phagocytosis and is used in classification of the bacteria H.influenzae type b is the most significant Was the most common form of meningitis in infants prior to the use of an effective vaccine Can cause a number of other diseases in young children Use of the Hib vaccine has eliminated much of the disease caused by H.influenzae b Other strains still cause a variety of diseases 168 169 Other Species of Haemophilus H. aegypticus Causes conjunctivitis with pus H.ducreyi Causes a sexually transmitted disease Results in the formation of a genital ulcer called a chancroid Often asymptomatic in women but in men the chancroid is often painful H.aphrophilus causes a rare type of endocarditis Other species primarily cause opportunistic infections 170 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis 171 NOTE: All of the organisms on this slide are rods except Neisseria, which are cocci (diplococci). Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Bordetella Small, aerobic, nonmotile coccobacillus (partly round and partly rod-shaped) B. pertussis is the most important Causes pertussis, also called whopping cough Most cases of disease are in children Produce various adhesins and toxins, including pertussis toxin, that mediate (causes) the disease Bacteria are first inhaled in aerosols and multiply in epithelial cells Then progress through three stages of disease 172 Stages Catarrhal (coughing) Paroxymal (comes and goes) Convalescence 173 Bordetella Clinical significance B. pertussis – causes whooping cough Acquired by inhalation of droplets containing the organism The organism attaches to the ciliated cells of the respiratory tract. During an incubation period of 1-2 weeks, the organism multiplies and starts to liberate its toxins. 174 Catarrhal Stage (Coughing) Pertussis toxin Has one A subunit (toxic part), plus five different kinds of B subunits (involved in binding). 175 Catarrhal The pertussis toxin (cytotoxic) inhibits host cell phagocytic cell responses and the inhibition of natural killer cell activity. The toxin also causes strong vasoconstriction effects. 176 Catarrhal Tracheal cytotoxin – is related to the B. pertussis peptidoglycan. might contribute to the killing and sloughing off of ciliated cells in the respiratory tract. Lipooligosaccharide (LOS) has potent endotoxin activity. 177 Paroxymal Stage (comes and goes) Lasts 4-6 weeks. The patient has rapid, consecutive coughs with a rapid intake of air between the coughs (has a whooping sound). mucous has accumulated, and the patient is trying to cough up the mucous accumulations. The coughs are strong enough to break ribs! Other symptoms due to the activity of the released toxins include: oIncreased peripheral lymphocytes oMetabolic alteration such as increased insulin release and the resulting hypoglycemia oIncreased capillary permeability and increased susceptibility to histamine, serotonin, and endotoxin shock 178 Convalescence Stage Symptoms gradually subside. This can last for months. B. pertussis rarely spreads to other sites, but a lot of damage may occur, such as CNS dysfunction which occurs in ~10 % of the cases and is due to an unknown cause. Secondary infections such as pneumonia and otitis media are common. 179 Bordetella B. parapertussis – causes a mild form of whooping cough B. bronchoseptica Widespread in animals where it causes kennel cough. Occasionally causes respiratory or wound infections in humans. Current treatment Erythromyin – only effective in early stages of the disease before the toxin(s) have been released Vaccination P part of DPT (killed, encapsulated organism); a subunit vaccine has also been developed (purified pertussis toxin). 180 Diagnosis, Treatment, and Prevention Diagnosis Symptoms of pertussis are usually diagnostic Treatment Primarily supportive Antibacterial drugs have little effect on the course of the disease Prevention Immunization with the DPT vaccine Cases in the United States have increased due to a refusal by some parents to have their children immunized 181 DPT Vaccine The vaccine components include diphtheria and tetanus toxoids, and killed whole cells of the organism that causes pertussis. The usual course of childhood immunization is five doses between 2 months and 15 years. While vaccinations helped eradicate pertussis from the United States in the latter half of the 20th century, in recent years the disease resurfaced and resulted in fatalities. Many parents decline to vaccinate their children against the disease for fear of side effects. 182 Vaccine refusal contributes to whooping cough outbreaks The 2010 whooping cough outbreak in California may have been fueled by clusters of parents who refused to vaccinate their children, a new study suggests. Researchers found increased rates of whooping cough in children entering kindergarten with "non-medical" vaccine exemptions, meaning parents or guardians applied for an exemption from school policies requiring vaccines due to personal beliefs, rather than for medical reasons. In 2010, the year the state experienced a whooping cough outbreak that caused 9,120 cases and 10 deaths from the disease. 183 whooping cough San Diego County had a particularly high degree of pertussis cases. There were 980 pertussis cases in the county, and the area in and around Escondido, a city in San Diego County, had more than 5,100 exemptions. Although the overall rate of vaccination in California remained high (90 percent of kindergartners in 2010 were fully vaccinated), some regions had lower immunization rates. In 2010, some schools reported non-medical exemption rates as high as 84 percent. 184 NEXT TUESDAY We will start in the lab room and finish this lecture after dinner. Run a PCR and gel electrophoresis on your soil sample. Use your unknown organism to inoculate the following tubes and place them in the incubator to examine on the following Thursday. Just flame your loop once and do all of the inoculations with your unknown organism. There are 3 tubes total for each lab group. Glucose fermentation tube Lactose fermentation tube Sucrose fermentation tube Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 186 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Francisella tularensis Morphology and cultural characteristics Small, pleomorphic (various shapes) rods Non-motile Non-encapsulated Won’t grow on ordinary media – requires cysteine (an amino acid) for growth 187 Tularemia (“Rabbit Fever”) Found in rabbits and is transmitted to humans by hard ticks and deer flies. The disease is named after Tulare County, California, where it was first identified. From May to October 2000, an outbreak of tularemia in Martha's Vineyard resulted in one fatality. This is the only place in the world of a documented case of tularemia resulting from lawn mowing. 188 Francisella tulerensis Found living in water as an intracellular parasite of animals Causes the zoonotic disease tuleremia Spread to humans occurs mainly through the bite of an infected Dermacentor tick or by contact with an infected animal The bacteria can spread through unbroken skin and mucous membranes, making it highly infectious Tuleremia produces symptoms common to other bacterial and viral diseases and may be misdiagnosed 189 Francisella tularensis: Disease = Tularemia Tularemia has three possible forms: Cutaneous (ulceroglandular form) Ingestion (typhoidal form) Inhalation (pneumonic form) 190 Francisella Cutaneous: entry through skin abrasions (ulceroglandular form of the disease) - after ~ 48 hours a lesion occurs at the inoculated site. Symptoms Ulcer Headaches Pain, Fever Adjacent lymph nodes become enlarged. If not contained, this can progress to septicemia, pneumonia, and abscesses throughout the body. The organism survives for long periods of time inside phagocytic cells. 191 Francisella Ingestion (typhoidal form of the disease) the focus of infection is the mouth, throat, and GI tract. Inhalation (pneumonic form of the disease) This is the most severe form of the disease and it manifests as a pneumonia with a high mortality rate of 30% in untreated cases. Antimicrobial susceptibility Streptomycin or tetracycline An attenuated, live vaccine that protects against the inhalation form of the disease is available for those exposed to the organism. 192 Prevention A vaccine is available to at risk individuals Preventing infection is done by avoiding the major reservoirs of the bacteria. 193 Gram positive exotoxins (no endotoxins) 194 Staphylococcus aureus Cytotoxins (TSS, NF, exfolatin), Neurotoxin, Enterotoxin Clostridium difficile Cytotoxin, Enterotoxin Clostridium perfringens Cytotoxin, Enterotoxin Clostridium botulinum Neurotoxin (botulism toxin) Clostridium tetani Neurotoxin (Tetanus toxin) Bacillus cereus Enterotoxin Bacillus anthracis Cytotoxin (Anthrax toxin) Corynebacterium diphtheriae Cytotoxin (Diphtheria toxin) These all have endotoxins, but what EXOTOXINS do they produce? E. coli (EHEC) Verotoxin, AB toxin E. coli (ETEC) Enterotoxin, heat labile and heat stable toxins Klebsiella pneumoniae Enterotoxin Campylobacter jejuni Enterotoxin Salmonella typhi Enterotoxin Shigella dysenteriae Shigatoxin Vibrio cholerae Cholera toxin Bordatella pertussis Pertussis toxin 195 What Diseases Do These Cause? Enterobacteriaceae E. coli Diarrhea, septicemia, UTI Enterobacter aerogenes Diarrhea, pneumonia, septicemia Klebsiella pneumoniae Pneumonia, septicemia Proteus vulgaris UTI, diarrhea, nosocomial wound infections Serratia marcescens UTI, wound infections (catheters), pink grout Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia Salmonella typhi Diarrhea and typhoid fever; feces on food, raw chicken, reptiles Shigella dysenteriae Bloody diarrhea from human feces Yersinia enterocolitica Diarrhea; lymph node inflammation Yersinia pestis Bubonic (black) plaque 196 What Diseases Do These Cause? 197 Neisseria gonorrhea Gonorrhea Neisseria meningitis Meningitis Vibrio cholerae Cholera Helicobacteri pylori Stomach and duodenal ulcers Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis Bordetella pertussis Whooping cough, kennel cough in dogs Francisella tularensis Rabbit Fever Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis 198 NOTE: All of the organisms on this slide are rods except Neisseria, which are cocci (diplococci). Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Brucella Classification Are all intracellular organisms Small, pleomorphic (various shapes) coccobacilli 4 species can infect humans B. abortus B. suis B. canis B. melitensis causes the most serious infections 199 Brucella Virulence factors Endotoxin (LPS) Clinical significance Has a tropism (preference) for erythritol Animal fetal tissues and placenta, other than those in humans, are rich in erythritol and, therefore, the organisms often cause abortions in these animals. 200 Brucella Causes Brucellosis or undulent fever in man following ingestion of contaminated milk or cheese from goats (B. melitensis), cows (B. abortus), pigs (B. suis), or canines (B. canis). Man can also acquire the organism via contact with infected animals. Clinical manifestations range from subclinical, to chronic with low grade symptoms of low fever and muscular stiffness, to acute with fever and chills. The fever typically spikes each evening and this coincides with the release of organisms from phagocytes (hence the name undulent fever). The patient may also experience malaise, weakness, enlarged lymph nodes, weight loss, and arthritis. 201 Brucella Antibiotic susceptibility Chemotherapy is difficult because of the intracellular survival of the organism. Tetracycline for 21 days, sometimes combined with streptomycin. 202 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 203 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Pseudomonas Gram-negative, aerobic bacilli Ubiquitous in soil, decaying organic matter, and almost every moist environment Problematic in hospitals because they can be found in numerous locations Opportunistic pathogens 204 Pseudomonas aeruginosa Rarely part of the normal microbiota Opportunistic pathogen of immunocompromised patients Common in ulcers and burn wounds…turns it green Can colonize almost every organ and system and result in various diseases Often infects the lungs of cystic fibrosis patients The bacteria form a biofilm that protects them from phagocytosis Increases the likelihood of death in these patients 205 Pseudomonas aeruginosa Diagnosis can be difficult as the presence of bacteria may represent contamination of the sample Treatment is difficult because P. aeruginosa is resistant to many antibacterial drugs. Silvadene cream on ulcers or burns is used. 206 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 207 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Rickettsias Extremely small (not much bigger than a smallpox virus) Appear almost wall-less due to the small amount of peptidoglycan present Obligate intracellular parasites Unusual because they have functional genes for protein synthesis, ATP production, and reproduction Five genera cause disease in humans Rickettsii, Prowasekii, Typhi, Orienta, Ehrlichia 208 Characteristics of Rickettsias 209 Table 21.1 Rocky Mountain Spotted Fever Symptoms usually develop about 2 to 14 days after the tick 210 bite. They may include: Chills & Fever Severe headache Muscle pain Mental confusion & Hallucinations Rash Abnormal sensitivity to light Diarrhea Excessive thirst Loss of appetite Nausea &Vomiting Spread by ticks Typhus vs. Typhoid Fever Typhus is any of several similar diseases caused by Rickettsia bacteria. The name comes from the Greek “typhos” meaning smoky or hazy, describing the state of mind of those affected with typhus. The causative organism, Rickettsia is an obligate parasite bacterium that cannot survive for long outside living cells. Typhus should not be confused with typhoid fever. While "typhoid" means "typhus-like", the diseases are distinct and are caused by different species of bacteria. Condition 211 Bacteria Vetor Epidemic typhus Rickettsia prowazekii Lice on humans Endemic typhus (murine typhus) Rickettsia typhi Fleas on rats Endemic Typhus Chills Cough Delirium High fever (104 degrees Fahrenheit) Joint pain (arthralgia) Light may hurt the eyes Low blood pressure Rash that begins on the chest and spreads to the rest of the body (except the palms of the hands and soles of the feet) Severe headache Severe muscle pain Stupor Spread by fleas 212 Epidemic Typhus Abdominal pain Spread by lice Backache Dull red rash that begins on the middle of the body and spreads Extremely high fever (105 - 106 degrees Fahrenheit), which may 213 last up to 2 weeks Hacking, dry cough Headache Joint pain (arthralgia) Nausea Vomiting Gram Negative Bacteria Enterobacteriaceae 214 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Not Enterobacteriaceae Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Chlamydias Do not have cell walls Have two membranes but without any peptidoglycan between them Grow and multiply only within the vesicles of host cells Have a unique developmental cycle involving two forms Both forms can occur within the phagosome of a host cell 215 Chlamydia trachomatis Has a limited host range One strain infects mice, all others infect humans Infect the conjunctiva, lungs, urinary tract, or genital tract Enters the body through abrasions and lacerations Clinical manifestations result from the destruction of infected cells at the infection site, and from the resulting inflammatory response 216 Chlamydia trachomatis Causes two main types of disease Sexually transmitted diseases Causes the most common sexually transmitted disease in the United States Symptomatic in women but not men Women can develop pelvic inflammatory disease if reinfected with C. trachomatis Ocular disease called trachoma Occur particularly in children Endemic in crowded, poor communities with poor hygiene, inadequate sanitation, and inferior medical care In the USA, All newborns receive silver nitrate drops in the eyes at birth to prevent this disease, which causes blindness. 217 Chlamydia—Rates by Sex, United States, 1990–2009 Rate (per 100,000 population) 600 Men Women Total 500 400 300 200 100 0 1990 1992 1994 1996 1998 2000 2002 2004 Year NOTE: As of January 2000, all 50 states and the District of Columbia had regulations that required chlamydia cases to be reported. 2006 2008 Trachoma Disease of the eye Leading cause of nontraumatic blindness in humans Bacteria multiply in the conjunctival cells resulting in scarring The scarring causes the eyelashes to turn inwards and abrade the eye that can eventually result in blindness Typically a disease of children who have been infected during birth Infection of the eye with bacteria from the genitalia can also result in disease 219 Diagnosis, Treatment, and Prevention Diagnosis Demonstration of the bacteria inside cells from the site of infection Treatment Antibiotics can be administered for genital and ocular infections Surgical correction of eyelid deformities from Trachoma may prevent blindness 220 Diagnosis, Treatment, and Prevention Prevention Abstinence and safe sex can prevent sexually transmitted chlamydial infection Blindness can only be prevented by prompt treatment with antibacterial agents and preventing reinfections 221 Gram Negative Bacteria Not Enterobacteriaceae Enterobacteriaceae 222 E. coli Enterobacter aerogenes Klebsiella pneumoniae Proteus vulgaris Serratia marcescens Campylobacter jejuni Salmonella typhi Shigella dysenteriae Yersinia enterocolitica and pestis Neisseria gonorrhea and meningitis Vibrio cholerae Helicobacteri pylori Haemophilus influenzae Bordetella pertussis Francisella tularensis Brucella Pseudomonas aeruginosa Rickettsia spp Chlamydia spp Legionella Bartonella spp Pasturella multocida Legionella pneumophila Aerobic, slender, pleomorphic bacteria Universal inhabitants of water Humans acquire the disease by inhaling the bacteria in aerosols from various water sources Intracellular parasites 223 Legionella pneumophila Causes Legionnaires’ disease Results in pneumonia Immunocompromised individuals are more susceptible Elimination of the bacteria is not feasible but reducing their number is a successful control measure What you should know about this disease: http://fxn.ws/Ou9EGv 224 Bartonella Gram-negative aerobic bacilli Found in animals but only cause disease in humans 3 species are pathogenic Bartonella bacilliformis Bartonella quintana Bartonella henselae 225 Bartonella bacilliformis Bartonellosis -Carrión’s Disease Transmitted by blooding-sucking sand flies Acute phase: (Carrion's disease) fever pallor, malaise, nonpainful hepatomegaly, jaundice, lymphadenopathy, splenomegaly. This phase is characterized by severe hemolytic anemia and transient immunosuppression. • The case fatality ratios of untreated patients exceeded 40% but reach around 90% when opportunistic infection with Salmonella occurs. • • • • • • • • 226 Sand Fly This looks like a mosquito, except its body is hairy and the wings are feathery. Remember, Leishmaniasis (a protozoan) is another disease transmitted by this insect. 227 Bartonella quintana Trench fever Spread person to person by human body lice Also causes disease in immunocompromised patients The disease is classically a five-day fever of the relapsing type 228 Bartonella henselae Cat scratch fever Introduced into humans through cat scratches or bites 229 Pasteurella multocida Normal flora in cats that can infect others if bitten. Causes avian cholera (deadly) in birds In humans, causes septicemia, endocarditis, menigitis 230 Family Sues Petco After Son's Death from Rat-Bite Fever A San Diego family is suing Petco following the death of their 10-year-old son from a bacterial infection that they say he contracted from his pet rat. Aidan became sick two weeks after the family bought the rat, and died the next day, hours after being rushed to the hospital with severe stomach pains. The San Diego County Medical Examiner's Office ruled the cause of death was streptobacillus moniliformis infection, commonly known as rat-bite fever, after exposure to an infected rat. A breeder would have to test eight rats to be 95 percent certain a colony of 100 rats or more did not have the disease. The test costs $40 per rat, and a rat costs between $6 and $11 at Petco. 231 What Diseases Do These Cause? Enterobacteriaceae E. coli Diarrhea, septicemia, UTI Enterobacter aerogenes Diarrhea, pneumonia, septicemia Klebsiella pneumoniae Pneumonia, septicemia Proteus vulgaris UTI, diarrhea, nosocomial wound infections Serratia marcescens UTI, wound infections (catheters), pink grout Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia Salmonella typhi Diarrhea and typhoid fever; feces on food, raw chicken, reptiles Shigella dysenteriae Bloody diarrhea from human feces Yersinia enterocolitica Diarrhea; lymph node inflammation Yersinia pestis Bubonic (black) plaque 232 What Diseases Do These Cause? 233 Neisseria gonorrhea Gonorrhea Neisseria meningitis Meningitis Vibrio cholerae Cholera Helicobacteri pylori Stomach and duodenal ulcers Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis Bordetella pertussis Whooping cough, kennel cough in dogs Francisella tularensis Rabbit Fever What Diseases Do These Cause? 234 Brucella Undulant fever, abortions Pseudomonas aeruginosa Infects ulcers and burns, cellulitis, otitis Rickettsia spp Rocky Mt spotted fever, endemic and epidemic typhus Chlamydia spp STD and trachoma Legionella Legionnaires’ disease (pneumonia) Bartonella spp Carrion's disease, Trench Fever, Cat Scratch Fever Pasturella multocida Bird Cholera Spirochetes Treponema pallidum Borelia burgdorferi and other spp. 235 Spirochetes Spirochetes are Gram negative, but they are too small to be seen with a light microscope after a Gram stain. They are best seen with a dark field microscope, in which Gram stain does not show up. Unlike other Gram negative bacteria, they do not have endotoxin in their cell walls. Spirochetes seen with dark field microscopy 236 Spirochetes Thin, tightly coiled, helically shaped bacteria Moves in a corkscrew fashion through its environment This movement is thought to enable pathogenic spirochetes to burrow through their hosts’ tissues 3 genera cause human disease Treponema, Borrelia, and Leptospira 237 Treponema pallidum Cannot survive in the environment Lives naturally only in humans as an obligate parasite Causative agent of syphilis Syphilis occurs worldwide Transmission is almost solely via sexual contact Endemic among sex workers, men who have sex with men, and users of illegal drugs Can also be spread from an infected mother to her fetus Often results in the death of the fetus or in mental retardation and malformation 238 Treponema pallidum • Syphilis can proceed through three stages – Primary-symptoms associated with the initial infection: painless chancer (ulcer) – Secondary-related to spread of the organisms away from the site of the original infection (spotted rash) – Tertiary syphilis - invades brain and also causes gummas (large invasive ulcers) 239 Primary Syphilis • Symptoms include: – Chancre that should • 240 heal by itself in 3-6 weeks • painless – genitals – Mouth – Skin – rectum Enlarged lymph nodes near the chancre Secondary Syphilis Spotted rash all over Fever general ill feeling loss of appetite muscle aches joint pain enlarged lymph nodes hair loss may occur. 241 Tertiary Syphilis Cardiovascular syphilis causes aneurysms or valve disease Central nervous system disorders (neurosyphilis) Infiltrative tumors of skin, bones, or liver (gumma) 242 Diagnosis, Treatment, and Prevention Diagnosis Primary, secondary, and congenital can be readily diagnosed with antibody tests against bacterial antigens Tertiary syphilis is difficult to diagnose Treatment Penicillin is the drug of choice except with tertiary syphilis which is a hyperimmune response and not an active infection Prevention Abstinence and safe sex are the primary ways to avoid contracting syphilis 243 Borrelia • Lightly staining, Gram-negative spirochetes • Cause two diseases in humans – Lyme disease – Relapsing fever 244 3D Image of Lyme Disease Spirochete Lyme Disease Borrelia burgdorferi is the causative agent Bacteria are transmitted to humans via a tick bite Hard ticks of the genus Ixodes are the vectors of Lyme disease 246 247 Transmission Transmitted by the Ixodes Tick Tick saliva carries the spirochete during blood feedings Usually goes unnoticed because tick is in nymphal stage and is very small Roughly only 1% of tick bites results in Lyme Disease (CDC 2012) Spirochete is problematic Lyme Disease Pathology Shows a broad range of signs and symptoms 3 phases of disease in untreated patients In most cases an expanding red “bull’s eye” rash occurs at the site of infection Neurological symptoms and cardiac dysfunction Severe arthritis that can last for years Pathology of this stage is largely a result of the body’s immune response 249 3 Stages of Lyme Disease There are 3 stages of Lyme disease Stage 1 is called early localized Lyme disease. The infection is not yet widespread throughout the body Stage 2 is called early disseminated Lyme disease. The bacteria have begun to spread throughout the body Stage 3 is called late disseminated Lyme disease. The bacteria have spread throughout the body Risk Factors Doing outside activities that increase tick exposure (for example, gardening, hunting, or hiking) in an area where Lyme disease is known to occur Having a pet that may carry ticks home Walking in high grasses Important Facts In most cases, a tick must be attached to your body for 24 - 36 hours to spread the bacteria to your blood. Blacklegged ticks can be so small that they are almost impossible to see. Many people with Lyme disease never even saw a tick on their body. Most people who are bitten by a tick do not get Lyme disease. To remove a tick, cover its body and legs with Vaseline so it cannot breathe. Wait for it to back out on its own. Bull’s Eye Rash Erythema Chronicum Migrans Symptoms Stage 1 Body-wide itching Bull’s-eye rash (erythema chronicum migrans) Thought to occur in 80% of infections Fever General ill-feeling Headache Light-headedness Myalgia Stiff neck Symptoms Stage 2 (early disseminated Lyme Disease) Paralysis or weakness in the muscles of the face Muscle pain and pain or swelling in the knees and other large joints Heart problems, such as palpitations and arrhythmias Symptoms Stage 3 (Late disseminated Lyme Disease) Abnormal muscle movement Muscle and joint pain Muscle weakness Numbness and tingling Speech problems Detection Blood test can be performed to detect antibodies to the bacteria that cause Lyme Disease Called the ELISA for Lyme Disease Test ELISA stands for “Enzyme-linked immunosorbant assay” Other tests include: Electrocardiogram Echocardiogram to look at the heart Spinal tap (lumbar puncture to examine spinal fluid MRI of the brain Treatments Most common treatment is 2-4 week course of antibiotics Controversy surrounds treatment for Post-treatment Lyme disease syndrome or “PTLDS” Persistent symptoms after 2-4 weeks treatment of antibiotics Long-term IV antibiotics are used despite the Infectious Disease Society of America’s guideline strictly prohibiting such treatment Many physicians view PTLDS as an accumulation of diseases rather than long-term Lyme disease Lyme Disease Pathology The increase of cases is a result of humans coming in closer association with ticks infected with Borrelia Antimicrobial drugs can effectively treat the first stage of Lyme disease Treatment of later stages is difficult because symptoms result from the immune response rather than the presence of bacteria Prevention is best achieved by taking precautions to avoid ticks 259 Prevention Avoid wooded or bushy areas, or areas with high grasses and leaf litter. Walk in the center of trails. Check yourself and your pets frequently during and after your walk or hike. Erythema Migrans Erythema Migrans Erythema Migrans The first stage of Lyme disease is a target shaped rash like this, which appears 3-30 days after the bite. Erythema Migrans When to get treatment for tick bite Just because you get a tick bite does not mean the tick was carrying a disease. The only tick that carries Lyme disease is a deer tick. They are tiny and have a red abdomen (the tick on the penny). The engorged tick is on the far right picture. If it was not engorged when you removed it, it will not have transmitted the disease. 265 Only ticks that are attached and have finished feeding or are near the end of their meal can transmit Lyme disease. After arriving on the skin, the tick that spreads Lyme disease usually takes 24 hours before feeding begins. Even if a tick is attached, it must have taken a blood meal to transmit Lyme disease. At least 36 to 48 hours of feeding is required for a tick to have fed and then transmit the bacterium that causes Lyme disease. After this amount of time, the tick will be engorged (full of blood). An engorged tick has a globular shape and is larger than an unengorged one.The risk of acquiring Lyme disease from an observed tick bite, for example, is only 1.2 to 1.4 percent, even in an area where the disease is common. 266 The Infectious Diseases Society of America (IDSA) recommends preventive treatment 267 with antibiotics only in people who meet ALL of the following criteria: Attached tick identified as an adult or nymphal I. scapularis (deer) tick Tick is estimated to have been attached for =36 hours (based upon how engorged the tick appears or the amount of time since outdoor exposure)If the person meets ALL of the above criteria, the recommended dose of doxycycline is a single dose of 200 mg for adults and 4 mg/kg, up to a maximum dose of 200 mg, in children = 8 years. If the person cannot take doxycycline, the IDSA does not recommend preventive treatment with an alternate antibiotic for several reasons: there are no data to support a short course of another antibiotic, a longer course of antibiotics may have side effects, antibiotic treatment is highly effective if Lyme disease were to develop, and the risk of developing a serious complication of Lyme disease after a recognized bite is extremely low. Antibiotic treatment can begin within 72 hours of tick removal The local rate of tick infection with B. burgdorferi is =20 percent (known to occur in parts of New England, parts of the mid-Atlantic states, and parts of Minnesota and Wisconsin) The person can take doxycycline (eg, the person is not pregnant or breastfeeding or a child <8 years of age) Relapsing Fever Relapsing fever is a vector-borne disease caused by infection with certain 268 bacteria in the genus Rickettsia and Borrelia, which are transmitted through the bites of lice or soft-bodied ticks. People get sick 1-2 weeks after they are bitten. Symptoms include fever, headaches, and muscle or joint aches. The symptoms continue for 10 days, then disappear. This cycle may continue for several weeks if the person is not treated. It is easily cured with antibiotics. Relapsing fever caused a series of plagues in late-medieval and early-renaissance England. At the time, they were called sweating sicknesses. Relapsing Fever The diagnosis of relapsing fever can be made on blood smear as evidenced by the presence of spirochetes. Other spirochete illnesses (Lyme disease, syphilis, leptospirosis) do not show spirochetes on blood smear. 269 Louse-borne Epidemic Relapsing Fever Along with Rickettsia prowazekii and Bartonella quintana, Borrelia recurrentis is one of three pathogens of which the body louse is a vector. Louse-borne epidemic relapsing fever is more severe than tick-borne endemic relapsing fever. Louse-borne epidemic relapsing fever occurs in epidemics amid poor living conditions, famine and war in the developing world. It is currently prevalent in Ethiopia and Sudan. 270 Tick-borne Endemic Relapsing Fever Tick-borne endemic relapsing fever is found primarily in Africa, Spain, Saudi Arabia, Asia in and certain areas of Canada and the western United States. Borrelia hermsii is the most common cause of Endemic relapsing fever in the United States. 271 Relapsing Fever 2 types of relapsing fever Epidemic relapsing fever (lice) Endemic relapsing fever (ticks) 272 Don’t confuse this with epidemic and endemic typhus! Epidemic Relapsing Fever Mortality rate is 1% with treatment; 3070% without treatment Transmitted by lice 273 Endemic Relapsing Fever Several Borrelia species can cause this disease Transmitted to humans by soft ticks of the genus Ornithodoros 274 Relapsing Fever Both types of relapsing fever are characterized by recurring episodes of fever and septicemia separated by symptom free intervals Pattern results from the body’s repeated efforts to remove the spirochetes, which continually change their antigenic surface components 275 Relapsing Fever Observation of the spirochetes is the primary method of diagnosis Successful treatment is with antimicrobial drugs Prevention involves avoidance of ticks and lice, good personal hygiene, and use of repellent chemicals 276 What Diseases Do These Cause? Enterobacteriaceae E. coli Diarrhea, septicemia, UTI Enterobacter aerogenes Diarrhea, pneumonia, septicemia Klebsiella pneumoniae Pneumonia, septicemia Proteus vulgaris UTI, diarrhea, nosocomial wound infections Serratia marcescens UTI, wound infections (catheters), pink grout Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia Salmonella typhi Diarrhea and typhoid fever; feces on food, raw chicken, reptiles Shigella dysenteriae Bloody diarrhea from human feces Yersinia enterocolitica Diarrhea; lymph node inflammation Yersinia pestis Bubonic (black) plaque 277 What Diseases Do These Cause? 278 Neisseria gonorrhea Gonorrhea Neisseria meningitis Meningitis Vibrio cholerae Cholera Helicobacteri pylori Stomach and duodenal ulcers Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis Bordetella pertussis Whooping cough, kennel cough in dogs Francisella tularensis Rabbit Fever What Diseases Do These Cause? 279 Brucella Undulant fever, abortions Pseudomonas aeruginosa Infects ulcers and burns, cellulitis, otitis Rickettsia spp Rocky Mt spotted fever, endemic and epidemic typhus Chlamydia spp STD and trachoma Legionella Legionnaires’ disease (pneumonia) Bartonella spp Carrion's disease, Trench Fever, Cat Scratch Fever Pasturella multocida Bird Cholera Review 280 For the Lecture 3 Exam The whole test is matching. Be able to match the following with their description: Virulence factors/enzymes The three hemolysis patterns Disease terms Toxins Match the disease (or characteristic symptom) to the organism Know which diseases have which vectors 281 Virulence Factors Adhesins (to adhere) • Enzymes Invasins (to get into cells) Endotoxin (LPS, LOS, and Lipid A) Exotoxins Cytotoxins (kills cells) Enterotoxin (GI upset) Neurotoxins (disrupts nerves) H Ag (flagella allows motility) K Ag (capsule) • • • • • • • • • β lactamase (deactivates penicillins) Ribosylase (causes diarrhea) Catalase (deactivates H2O2) Coagulase (causes blood clots) Staphylokinase (dissolves blood clots) Streptokinase (dissolves blood clots) IgA or IgG protease (deactivates Ab’s) Hyaluronidase (can move thru tissues) SOD (superoxide dismutase; deactivates WBC lysosomes) Angiotrophic ability (pulls blood vessels close) Facultative intracellular pathogens (can survive with and without O2) MDR plasmids (genetic drug resistance) PG (prostaglandins; promotes inflammation) Hemolysis Hemolysin Patterns: (alpha hemolysis; partially breaks down RBC membranes. Turn blood agar green) (beta hemolysis; completely ruptures RBCs. Turns blood agar clear) (gamma hemolysis is no RBC lysis; no color change on blood agar) 283 Disease Terms Furuncle (boil; infected hair follicles) Carbuncles (mass of boils) Cellulitis/ soft tissue infections. Scalded Skin Syndrome exfolatin toxin from Staph aureus Necrotizing Faciitis: destroys muscle and fat tissue Toxic Shock: Bacteremia (bacteria in blood) and multisystem failure Enterointoxication (enterotoxin-mediated diarrhea). This is Dz, not 284 infection. Pneumonia (fluid in the lungs) Osteomyelitis (bone infection). Requires 6-8 weeks of iv antibiotics Renal Abscess infarcts (seeds from renal artery, forms abscess, clots blood beyond that site) Endocarditis (heart valve infection) --> destruction of valve --> blood clot forms, breaks off, travels as a septic embolism ENDOTOXINS (GRAM NEGATIVE ONLY) O Antigen Inner plasma membrane LPS Cell Wall Lipid A (endotoxin) 285 LPS (LOS is LPS with smaller or missing O antigen) Outer plasma membrane Exotoxins and their classification Cytotoxins Verotoxin (Shigella-like toxin; E. coli EHEC) AB toxin (Kills colon epithelium; E. coli EHEC) Toxic Shock Syndrome toxin (Staph aureus) Exfolatin (Scalded Skin Syndrome; Staph aureus) Necrotizing Fasciitis Toxin (group A Strep) Anthrax Diphtheria Pertussis and tracheal cytotoxin Enterotoxins Neurotoxins Botulism Tetanus 286 Gram positive exotoxins (no endotoxins) 287 Staphylococcus aureus Cytotoxins (TSS, NF, exfolatin), Neurotoxin, Enterotoxin Clostridium difficile Cytotoxin, Enterotoxin Clostridium perfringens Cytotoxin, Enterotoxin Clostridium botulinum Neurotoxin (botulism toxin) Clostridium tetani Neurotoxin (Tetanus toxin) Bacillus cereus Enterotoxin Bacillus anthracis Cytotoxin (Anthrax toxin) Corynebacterium diphtheriae Cytotoxin (Diphtheria toxin) These all have endotoxins, but what EXOTOXINS do they produce? E. coli (EHEC) Verotoxin, AB toxin E. coli (ETEC) Enterotoxin, heat labile and heat stable toxins Klebsiella pneumoniae Enterotoxin Campylobacter jejuni Enterotoxin Salmonella typhi Enterotoxin Shigella dysenteriae Shigatoxin Vibrio cholerae Cholera toxin Bordatella pertussis Pertussis toxin 288 What Diseases Do These Cause? Enterobacteriaceae E. coli Diarrhea, septicemia, UTI Enterobacter aerogenes Diarrhea, pneumonia, septicemia Klebsiella pneumoniae Pneumonia, septicemia Proteus vulgaris UTI, diarrhea, nosocomial wound infections Serratia marcescens UTI, wound infections (catheters), pink grout Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia Salmonella typhi Diarrhea and typhoid fever; feces on food, raw chicken, reptiles Shigella dysenteriae Bloody diarrhea from human feces Yersinia enterocolitica Diarrhea; lymph node inflammation Yersinia pestis Bubonic (black) plaque 289 What Diseases Do These Cause? 290 Neisseria gonorrhea Gonorrhea Neisseria meningitis Meningitis Vibrio cholerae Cholera Helicobacteri pylori Stomach and duodenal ulcers Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis Bordetella pertussis Whooping cough, kennel cough in dogs Francisella tularensis Rabbit Fever What Diseases Do These Cause? 291 Brucella Undulant fever, abortions Pseudomonas aeruginosa Infects ulcers and burns, cellulitis, otitis Rickettsia spp Rocky Mt spotted fever, endemic and epidemic typhus Chlamydia spp STD and trachoma Legionella Legionnaires’ disease (pneumonia) Bartonella spp Carrion's disease, Trench Fever, Cat Scratch Fever Pasturella multocida Bird Cholera What Diseases do these cause? Gram Positive bacteria Gram Positive Cocci Staphylococcus poisoning, scalded skin syndrome, impetigo, folliculitis, furuncles, S. aureus Food toxic shock, bacteremia, endocarditis, pneumonia, osteomyelitis, MRSA S. haemolyticus Skin infections S. epidermidis Wound and internal fixation devices infections S. saprophyticus UTI Streptococcus Strep throat, Scarlet fever, Impetigo, Toxic Shock Group A (Strep. Pyogenes) Syndrome, Necrotizing fasciitis, Rheumatic fever Group B (Streptococcus agalactiae) neonatal sepsis and meningitis in infants Group D (Enterococcus faecalis) Nosocomial infections Viridins (Steptococcus pneumoniae) Pneumonia, meningitis, endocarditis, cavities, sinus and ear infections 292 What Diseases do these cause? • Gram Positive Rods • Bacillis cereus Food poisoning anthrax • Bacillis anthracis • Clostridium perfringins Food poisoning, gas gangrene • Clostridium difficile Diarrhea from antibiotics, pseudomembranous colitis • Clostridium botulinum Botulism • Clostridium tetani Tetanus • Listeria Food poisoning • Proprionibacterium acnes acne • Corynebacterium diptheriae Diphtheria • Nocordia asteroides Pneumonia, wounds, CNS infections • Actinomyces israelii Maxillary osteomyelitis, human bite wounds • Acid-fast bacteria Tuberculosis • Mycobacterium tuburclulosis • Mycobacterium leprae Hansen’s disease • Non-acid-fast, non-gram staining Walking pneumonia • Mycoplasma pneuomoniae 293 Vectors and their Diseases 294 Organism Francisella tularensis Disease Tularemia (“Rabbit Fever”) Rickettsia rickettsii Rocky Mountain Spotted Fever Vector Dermacentor ticks (hard tick) and deer flies Ticks Rickettsia typhi Endemic typhus Fleas Rickettsia prowazekii Epidemic typhus Lice Bartonella bacilliformis Carrión’s Disease Sand flies Borrelia burgdorferi Lyme Disease Ixodes ticks (hard tick) Borrelia recurrentis Epidemic Relapsing Fever Lice Borrelia hermsii Endemic Relapsing Fever Ornithodoros (Soft tick) Yersinia pestis Bubonic plague Fleas How do you eat an elephant? 295 296