11.21 Anaerobes – Flashcards
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| Bacterial requirements for growth in the human host. |
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| nutrients, optimal temperature (mesophiles), optimal pH, presence or absence of oxygen |
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| oxygen is required and are inhibited by absence of oxygen (cannot ferment)= |
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| obligate or strict aerobes |
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| What are examples of obligate or strict aerobes? |
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| legionella, pseudomonas aeruginosa, mycobacterium, bordetella pertussis |
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| organisms cannot grow in the presence of oxygen (ferment)= |
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| obligate anaerobes |
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| What are examples of obligate anaerobes? |
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| clostridium spp, bacterioides, peptostreptococcus |
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| Organisms able to grow in the presence/absence of oxygen? |
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| facultative anaerobes |
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| Examples of facultative anaerobes? |
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| staphylococcus spp, enterococci, E coli, listeria, yeasts, WBCs |
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| Microaerophils require oxygen at levels reduced to ___% of normal. |
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| 21 |
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| In addition to requiring reduced oxygen levels, many microaerophils also require... |
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| increased CO2 (they are capnophiles) |
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| Examples of microaerophils. |
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| neisseria spp., haemophilus spp, S. pyogenes, campylobacter jejuni, helicobacter pylori, borrelia bergdorferi |
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| Examples of aerotolerant anaerobes. |
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| clostridium perfringens, treponema pallidum |
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| Where in a test tube are facultative anaerobic bacteria found? |
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| most at the top but can be found throughout |
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| Where are microaerophiles found in a test tube? |
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| gather at the upper part of the test tube but not the very top |
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| How do you grow microaerophiles? |
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| put them in a candle jar |
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| Two basic groups of anaerobic bacteria: |
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| endogenous anaerobes-normal or transient flora, opportunistic pathogens exogenous anaerobes- spore formers, disease caused by vegetative form |
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| Where in the body do endogenous anaerobic bacteria NORMALLy inhabit? |
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| oxygen deficient area of body created by presence of facultative aerobic organisms (synergism) |
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| What allows an endogenous anaerobe to become pathogenic? |
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| tissue injury causes anoxia; indiscriminate use of broad spectrum antibiotics make conditions favorable to growth of anaerobes |
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| Name endogenous anaerobic bacteria that are gram positive cocci. |
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| peptostreptococcus, gemella |
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| Name the endogenous anaerobic bacteria that are gram positive bacilli. |
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| actinomyces, propionibacterium, mobiluncus, lactobacillis, eubacterium, bifodobacterium |
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| What are the endogenous anaerobic bacteria that are gram negative bacilli? |
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| bacteriodes, fusobacterium, porphyromonas, veilonella, prevotella |
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| Most common infections for anaerobic bacteria. |
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| oral, dental, pleuropulmonary, intraabdominal, female genital tract, skin, periodontal disease, soft tissue, and bone infections |
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| What pathogenic molecule do all anaerobes possess? |
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| enzymes (collagenase, neuraminidase, deoxyribonuclease, deoxyribonuclease [DNase], heparinase, and protease), that may play a role in pathogenesis by helping the organisms to penetrate tissues and to set up infection after surgery or other trauma |
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| The three most common disease causing anaerobes. |
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| bacteriodes, prevotella, fusobacterium together constitute 1/3 of all clinical isolates |
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| Light microscopy of bacterioides= |
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| most strains are encapsulated. Vaculoization or irregular staining common, particularly in broth media. Some pleomorphism may also be seen. gram-negative |
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| 90% of bacteriodes infections are located where? |
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| in the peritoneal cavity |
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| Does bacteroides use oxygen? |
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| anaerobic but they are aerotolerent and thus can survive in the abdominal cavity |
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| How does B fragilis become invasive? |
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| not overtly invasive, can cause intraabdominal infections when the mucosal wall of the intestine is disrupted. Like during GI surgery, perforated or gangrenous appendicitis, perforated ulcer, diverticulitis, trauma, and inflammatory bowel disease |
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| Which antibiotics are bacteroides resistant to? |
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| beta lactams, aminoglycosides, and recently many have acquired resistance to erythromycin and tetracycline |
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| Why is bacteroides antibiotic resistance a concern? |
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| bacteroides may become a reservoir for resistance in other, more highly pathogenic bacterial strains |
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| Benefits of having bacteroides. |
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| 1)anaerobic production of butyrate, acetate and proprionate provides 70% of energy supply of colonic enterocytes. 2) enterohepatic bile acid recirculation and bile acid biotransformation. 3) competes with pathogenic bacteria (via deconjugating bile salts and changing the pH) 4) produces some vitamin K (menaquione, vitamin K2) |
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| Describe fusobacterium respiration, whether they form spores, shape, and gram stain. |
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| anaerobic, non spore forming, filamentous and gram negative bacillus |
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| Is Fusobacterium normal flora? |
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| yes, of mucosal surfaces of mouth, URT, GI tract and vagina. |
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| Which organism is the bridging organism in dental plaque? |
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| fusobacterium |
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| What diseases are associated with fusobacterium? |
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| F. nucleatum= periodontal diseases F. necrophorum= Lemierre's syndrome F. ulcerans= topical skin ulcer from animal/insect bite |
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| Throat diseases caused by fusobacterium necrophorum. |
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| 10% of all acute sore throats, 21% of re-occurring sore throats, 23% of peritonsillar abscesses |
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| What is Lemierre's syndrome? |
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| a form of thrombophelbitis caused by fusobacterium necrophorum that usually affects young healthy adults. "a forgotten disease" |
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| What is the mortality rate of Lemierre's syndrome? |
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| 90% before antibiotics, 5% with antibiotics |
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| What is the pathogenesis of lemierre's syndrome? |
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| after S. pyogenes infection causes peritonsillar abscess, abscess is infected with F. necrophorum which then migrates to the jugular vein and forms an infected clot. Thrombi can break off and become embedded in the lungs as an emboli, causing shortness of breath, chest pain and severe pneumonia, or may travel to the brain and joints |
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| What antibiotics are used to treat F. necrophorum? |
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| susceptible to beta-lactams, metronidazole, clindamycin and third generation cephalosporins. polymicroby usually exists so need more than one drug |
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| What is the disease caused by actinomyces bacteria? |
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| actinomycosis which is characterized by the development of chronic granulomatous lesions that become suppurative and form abscesses connected by sinus tracts. |
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| What is the presence of a actinomyces colony? |
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| yellow or orange due to the presence of sulfur granules |
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| How is actinomyces transmitted? |
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| from the soil or water; there is no person-person transmission. Also from colonized foreign bodies such as intrauterine devices |
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| What organ systems can get actinomycosis and how? |
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| cerviofacial (poor oral hygeine or dental trauma), thoracic actinomycosis, abdominal actinomycosis (GI surgery_, pelvic actinomycosis (infected intrauterine device), central nervous actinomycosis (spread from the lungs) |
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| What is the unique metabolism of proprionibacterium? |
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| able to synthesize propionic acid by using unusual transcarboxylase enzymes |
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| Does propionibacterium cause disease? |
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| primarily facultative parasites and commensals that live in and around the sweat and sebaceous glands. Ubiquitous and do not cause problems for most but can cause acne and other skin conditions as well as shunt infections |
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| T/F THe main etiologic agent of periodontal disease are aerobes. |
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| false, anaerobes! |
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| What is the ecological plaque hypothesis? |
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| natural plaque--> inflammation and increased gingival cervicular fluid flow --> utilized by Gram (-) anaerobes--> suppress growht of normal sepcies with shift to periodontopathic anaerobic flora (PAF) --> PAFs secrete proteases lipase, etc. that produce episodic tissue destruction--> periodontitis and gingivitis |
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| Healthy gingival flora= |
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| mainly gram (+) cocci with few spirochetes or motile rodes |
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| Bacteria in a mouth with chronic marginal gingivitis= |
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| about 55% of cells are gram positive with occasional spirochetes and motile rodes |
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| Dental flora in a mouth with chronic periodontitis= |
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| about 75% of cells are gram-negative (90% being strict anaerobes). Motile rods and spirochetes are prominent |
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| What is the bacteiral flora in a mouth with aggressive periodontitis |
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| about 65-75% are gram negative bacilli. Few spirochaetes or motile rods present |
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| Three bacteria that cause dentoalveolar infections? |
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| prevotella, porphyromonas, fusobacterium |
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| What are two ways endogenous anaerobes can become opportunistic pathogens with the environment becomes "less aerobic"? |
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| lowering environmental redox potential by either facultative anaerobes or inflammation OR tissue trauma |
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| In general, infections with anaerobic bacteria must be treated with... |
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| more than one antibioitc because often polymicrobic |
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| What causes disease in infection with anaerobes? |
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| tissue destruction by action of proteases and lipases (lack exotoxins) |
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| Describe clostridia (spore forming?, utilize O2?, shape?) |
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| spore forming anaerobic bacilli |
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| The majority of exogenous anaerobic bacteria that cause disease all have which characteristics in common: |
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| gram positive, spore formers that cause disease either by the ingestion/inoculation of spores or products of the vegetative state in soil, water, food |
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| Name four claustridium spore formers. |
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| tetani, difficile, botulinum, perfringens |
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| Common characteristics of clostridial infections. |
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| forms spores (found in soil) and then germinate when they find an anaerobic environment in the body (wounds or GI tract). Virulence factors are exotoxins |
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| Are clostridium normal flora? |
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| can be transient or permanent members of normal flora of skin and GIT of humans and animals |
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| How do you control/treat clostridial infections? |
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| antibiotic therapy and tissue debridgement of necrotic tissue to decrease the anaerobic environment. Antitoxin therapy (passive immunity) and toxoid immunization is effective in controlling some clostridial infections that mediate disease via toxin production. |
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| Which clostridia cause disease by ingestion or innoculation with spores which then germinate in host? |
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| tetanus (C. tetani), infant or wound botulism (C. botulinum), gas gangrene (C. perfringens), and pseudomembranous colitis (C. difficile) |
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| Which clostridia cause disease by ingestion of toxins produced by vegetative cells growing outside the host? |
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| clostridial food poisoning (C. perfringens), or botulism (C. botulinum) |
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| What types of diseases does C. perfringens cause? |
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| necrosis in gas gangrene and food poisoning in enteritis necroticans or diarrhea |
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| Is C. tetani invasive? How does it cause disease? |
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| NO! it remains confined to the necrotic tissue where the vegetative cells of C tetani elaborate a toxin, tetanospasmin that then diffuses to neural cells. |
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| How does teatnus toxin get into nervous system? |
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| thru neuromuscular junction of alpha motor neurons. The toxin is then transported to the otehr neruons, most importantly presynaptic inhibitory cells where it is no longer accessible to be neutralized by antitoxin |
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| Once tetanus toxin gains access to inhibitory neurons, it blokcs the release of the neurotransmitters ____________. |
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| glycine and gamm-aminobutyric acid |
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| clinical term for symptoms of tetanus= |
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| spastic paralysis |
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| How much tetanus toxin is considered lethal? |
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| 130 ug |
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| The highest mortality rates of tetanus are in persons... |
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| unvaccinated or over 60 |
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| What are the four kinds of teatnus? |
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| generalized, localized, cephalic and neonatal |
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| What's another name for generalized tetanus? |
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| descending tetanus |
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| What percent of tetanus is generalized? |
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| 80% |
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| What are the symptoms of generalized tetanus? |
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| first sign= trismus (lockjaw) and risus sardonicus (facial spasms), followed by stiffness of the neck, difficulty swallowing and rigidity of pectoral and calf muscles. Eventually can get opisthotonos. Also= high temp, sweating, high bp, and episodic rapid heart rate. |
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| How long does tetanus last? |
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| 3-4 weeks and complete recovery, if any, may take months |
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| Localized tetanus is also called... |
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| ascending tetanus |
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| Is localized tetanus fatal? |
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| only 1% |
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| Who gets localized tetanus? |
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| inadequately immunized patients |
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| What is cephalic tetanus. |
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| rare form of the disease, occasionally occuring with otitis media in which C. tetani is present in teh flora of the middle ear. Or following head injuries. Involves cranial nerves, esp of face |
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| What is neonatal tetanus? |
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| form of generalized tetanus in newborns when mother lacks immunity and the umbilical stump becomes contaminated with C. tetani spores. |
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| How many infants die from neonatal tetanus? |
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| 14% of neonatal deaths in developing countries with a 90% mortality rate |
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| Why aren't you immune to tetanus after you've had it once? |
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| toxin is very potent so the amount released is too small to trigger immune mechanisms. Also, because the toxin binds firmly to neural tissue it may not interact effectively with teh immune system |
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| One-half of all cases of tetanus worldwide are of what type? |
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| neonatal tetanus |
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| What is the mortality rate of non-neonatal tetanus? |
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| 50% |
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| How long does the tetanus vaccine protect you for? |
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| 10 years |
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| HTIG will only neutralize toxin that is... |
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| unbound |
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| How do you treat tetanus? |
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| vaccine, HTIG, local debridgement. Suprotive measures (resp assistance and IV fluids). Benzodiazepines (diazepam=valium). Penicillin historically but may act synergistically with tetanospasm so use metronidazole |
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| What is the difference between infant botulism and food poisoning due to botulism? |
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| infants get sick due to germination of ingested spores. Adults get food poisoning due to ingestion of preformed toxin. |
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| Is wound botulism due to infection with spores or toxin? |
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| spores |
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| Adult form of intestinal C. botulinum colonization is very rare but can occur when... |
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| typically related to abdominal surgical procedures. Can be seen in older children and adults with abnormal bowels |
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| What is injection botulism? |
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| seen in patients injected with inappropriately high ammounts of therapeutic neurotoxin (botox) |
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| What is inhalation botulism? |
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| occurred in laboratory personnel who work with neurotoxins |
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| Nervous system symptoms of botulism= |
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| blurred or double vision, dry mouth, difficulty swallowing, muscle weakness, muscle paralysis, and slurred speech. Can cause respiratory paralysis and death |
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| Describe the neurotoxin of botulism? |
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| 7 serologically distinct neurotoxins (A-G) with A being one of the most potent neurotoxins. Secreted as inactive toxin and must be cleaved by either bacterial or host protease. |
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| C. botulinum causes a _________ paralysis. |
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| flaccid |
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| T/F C. botulinum spores produce 7 serologically distince neurotoxins. |
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| False. toxins only produced by vegetative state |
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| What is the pathophysiology of botulism toxin? |
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| toxin cleaves the polypeptides on synaptobrevins which are essential in triggering the release of acetylcholine into the synapse |
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| How long does botulism paralysis last? |
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| permanent; muscle cell can only contract again in two to four months after the axon replaces the damaged nerve terminal |
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| Long term sequale of botulism poisoning= |
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| fatigue and shortness of breath for years. longterm therapy may be needed to aid recovery |
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| Which botulism toxins are the worst? why? |
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| Mort rate= A>E>B, which reflects the affinity of the toxins for neural tissue |
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| Fatality rates of botulism is directly proportional to... |
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| infectious dose |
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| typical foods that give you botulism food poisoning= |
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| used to think was only associated with contaminated meat, esp sausage. but now know that it can grow well in vegitables, fish, fruits, and condiments. Most due to inadequate sterilization technique in home canning. |
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| Which is more resistant to degredation botulism toxin or spores? |
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| spores are heat resistant and can survive 100 degrees C for hours |
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| When do symptoms of foodborne botulism develope? |
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| 12-36 hours after ingestion of contaminated food |
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| Which toxins are most frequently associated with infant botulism? |
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| A or B |
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| At what age are you susceptible to infant botulism? |
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| 2 weeks to 6 months |
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| What are the symptoms of infant botulism? |
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| constipation, lethargy, sleepy, suck and gag reflexes diminish and dysphagia becomes evident with drooling. Head control is lost and infant becomes flaccid |
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| Food implicated in infant botulism? |
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| honey; no longer recomended for infants under 1 year of age. Also, soil and dust |
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| How do you treat infant botulism? |
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| antitoxin not routinely given. Use immune globulin called BabyBIG (botulism immune globulin), given IV. |
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| C. botulinum can replicate in adult intestinal tract due to 2 common things... |
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| antibiotic therapy or achlorhydria |
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| How do you treat botulism food poisoning? |
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| antitoxin that blocks the action of neurotoxn circulating in the blood. Some advocate antibiotic therapy. Removal of whatever contaminated food is left in gut via enema or vomiting. Surgically cleanse wound. Good supportive care |
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| What toxins is botulism antitoxin against? |
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| A, B and E= trivalent antitoxin from CDC A, B, C, D, E, F, and G= heptavalent from US army or FEMA |
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| What is the mortality rate of botulism? |
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| 60% in 1940s to 10% today |
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| Therapeutic botox is used for... |
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| involuntary muscle spasms (strabismus and certain focal dystonias), wrinkle remover |
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| What type of toxin is in botox? |
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| type A |
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| Which animals have cycles of botulism? |
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| avain botulism |
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| What GI diseases are caused by C. Difficile? |
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| spectrum of intestinal disease from uncomplicated antibiotic associated diarrhea to severe, possibly fatal, antibiotic associated colitis known as psuedomembranous colitis |
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| Where is C. difficile found in the environment?/How is it spread? |
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| everywhere! soil, air, water, human and animal feces; inadequate handwashing |
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| T/F C. difficile is a part of the normal GI flora. |
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| a small number 3% of healthy people naturally carry C diff in their large intestine but mostly C diff causes disease |
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| Which antibiotics most often cause C diff infection? |
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| flouroquinolones, cephalosporins, clindamycin |
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| What is pseudomembranous colitis? |
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| C diff infection that forms patches of raw tissue that can bleed or produce pus in the colon |
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| What are the signs/symptoms of severe c diff infection? |
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| watery diarrhea 10-15x/day, abdominal cramping and pain, fever, blood or pus in stool, nausea, dehydration, loss of appetite, weight loss |
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| What is the mort rate of pseudomembranous colitis? |
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| 10% |
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| How does C diff cause disease? |
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| produces toxin A and B (TcdA and TcdB). TcdA binds to apical side of the cell and after internalization cuases cytoskeleton changes that results in disruption of tight junctions and lossening of epithelial barrier. This allows TcdA and B to cross the epithelium. TcdB binds preferentially to the basolateral cell membrane. Both toxins are cytotoxic and induce the release of various immunomodulatory mediators from epithelial cells, phagocytesand mast cells, resulting in inflammation and PMNs. |
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| What is a potential complication of C diff toxins entering the blood stream? |
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| TcdB has a tropism for cardiac tissue |
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| Which group of people can have large numbers of Cdiff in their feces and still be healthy? |
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| infants (50% of neonates are carriers). Toxins are also present in the infants stools in the same amounts associated with adult disease but toxins typically have no adverse effect in infant, probably b/c they lack specific intestinal receptors for Cdiff toxins. |
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| C diff manifests in AIDS patients as... |
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| chronic diarrhea |
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| How long does a Cdiff infection last? |
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| 1-14 days after offending antibiotic is dicontinued. Supportive therapy needed to compensate for severe fluid and electrolyte loss |
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| Suspect C diff in anyone with diarrhea who has... |
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| taken antibiotics in the past two months or when diarrhea develops a few days after hospitalization |
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| How do you diagnose C diff? |
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| look for toxins in stool (most use EIA test=fast but inspecific, with tissue culture assay=slow but accurate). Also colon examination for inflammation/pseudomembranes. CT can also show thickening of wall of colon |
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| HOw do you treat C diff? |
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| stop taking antibiotic. Take metronidazole for moderate dz or vancomycin for severe disease. Take probiotics (saccharomyces boulardii). Surgical removal of diseased colon. |
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| Treatment of C diff that has recurred= |
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| antibiotics, probiotics (S. boulardii), stool transplant |
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| Besides antibiotics what other drugs can cause C diff? |
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| antacids and proton pump inhibitors (losec) |
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| What causes recurrent C diff diarrhea? |
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| 50% d/t reinfection; 50% d/t relapse |
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| What increases your risk of C diff diarrhea recurring if you've had it once? |
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| age >65 and exopsure to additional antibiotics |
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| How does clostridium perfringens stain? is it sporeforming? |
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| gram positive spore former |
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| Where in the environment is C. perfringens found? |
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| intestines of humans and animals and everywhere else in the environement |
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| What diseases are caused by C. perfringens? |
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| gas gangrene, anaerobic cellulitis, endometritis, and food poisoning |
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| What is gas gangrene? |
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| acute dz with poor prognosis d/t trama compromising oxygen to tissues and subsequent growth of anaerobic bacteria |
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| What are the symptoms of gas gangrene? |
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| initial= fever and pain in infected tissue; later= local tissue necrosis and systemic toxemia, purple mottling of infected muscle, edema and foul smelling exudate; gas bubbles form from products of anaerobic fermentation |
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| How does C perfringens cause gas gangrene? |
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| multiply in wound and make various exotoxins (hemolysins, collagenases, proteases, and lipases that are liberated into the surrounding tissue causing more local tissue necrosis and systemic toxemia. |
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| Which muscle groups are more frequently affected by gas gangrene? |
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| those in the extremities served by one or two major blood vessels |
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| List chronic, systemic diseases that increase your risk of gas gangrene. |
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| atherosclerosis, chronic alcoholism, corticosteroid use, diabetes, GI malignancy, HIV, hypoalbuminemia, IVDU, malnutrition, obesity, PVD |
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| What are the different types of C perfringens? |
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| five different types: A, B, C, D, E |
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| Name important toxins of C perfringens. |
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| alpha toxin and theta toxin |
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| Describe alpha toxin. |
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| toxin of c perfringens that is a lecithinase also called phospohlipase C. that lyses cell membrane lecithins, disrupting cell membranes and causing cell death |
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| Describe theta toxin. |
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| contributes to rapid tissue destruction in C perfringens infection by several mechanisms. Is an oxygen labile cytolysin that promotes direct vascular injury. Lower toxin concentrations activate PMNs and endothelial cells by promoting distal vascular injury. Causes leukostasis, thrombosis, decreased perfusion and tissue hypoxia. Also mediates production of shock |
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| How does C perfringens cause shock? |
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| theat toxin mediates production of shock through induction of inflammatory mediators such as platelet activating factor, tumor necrosis factor, interleukin 1 and interleukin 6 |
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| Describe C. perfringens endometriitis. |
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| necrotic products of conception in uterus can facilitate growth of C perfringens with subsequent infection of the endometrium. Necrosis and bactermia with intravascular hemolysis due to theta toxin may ensue. Very common after illegal abortion and the use of non-sterile instruments |
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| Describe anaerobic cellulitis caused by C. perfringens. |
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| a milder form of gas gangrene with prominent gas formation |
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| Describe immune response to clostridial wound infections. |
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| ineffective with no protective immunity. Conditions almost always fatal |
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| How do you treat C. perfringens infection? |
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| debridgement, amputation, hysterectomy. Massive doses of penecillin and broad spectrum cephalosporins. Also, hyperbaric oxygen chamber |
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| How does hyperbaric oxygen chamber help with c. perfringens infection? |
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| slows bacteria growth, toxin production, and oxidizes theta toxin |
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| What are common sources of C perfringens food poisoning? |
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| beef, poultry, gravies, and dried or pre-cooked foods |
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| What is the time frame and symptoms of C perfringens? |
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| incubation for 8-24 hours after ingestion of contaminated food. Symptoms are diarrhea, cramps, and abdominal pain. (rarely= fever, nausea, and vomiting). Lasts for 24 hours |
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| What species of C perfringens causes food poisoning? |
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| type A makes an enterotoxin that affects the permeability of the plasma membrane of mammalian cells |
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| What is the mortality rate of C. perfringens food poisoning? |
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| essentially zero but elderly and ICX patients should be closely supervised |
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| How do you diagnose C perfringens food poisoning? |
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| detect bacterial toxin in feces or by tests to determine the number of bacteria in the feces. At least 106 spores/gram of stool wtihin 48 hours of when illness began to dx infection |
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| Wound contamination by clostridium spores which germinate in situ to produce toxins= |
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| either C tetani producing tetanus or C. perfringens producing gas gangrene |
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| Contamination of food with clostridia spores which germinate under anaerobic conditions= |
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| either C botulinum producing flaccid paralysis or C perfringens producing diarrhea or enteritis necroticans |
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| ingestion of spores in honey which germinate= |
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| c. botulinum in infant botulism |
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| Which clostridium species is an opportunistic pathogen? |
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| c diff causing pseudomembranous colitis |
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| Special considerations of anaerobic infection laboratory diagnosis: |
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| 1) slow growth of organism, 2) contamination free specimen, 3) protect specimen from O2, 4) often members of normal flora, 5) polymicrobic |
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| How do prevent tissue sampels from O2 exposure? |
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| placed into a degassed bag and sealed or into a glassed out screw top vial that may contain oxygen free pre-reduced culture medium, tightly capped and plated as rapidly as possibly onto culture media that has been prepared for anaerobic transport and culture |
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| THe BBL vacutainer anaerobic specimen collector is media free because... |
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| this helps to minimize sample dilution |
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| HOw do you know you're anaerobic jar is actually anaerobic? |
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| methylene blue strip is only blue in the presence of oxygen. Will be colorless if jar is anaerobic |
