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Ch 14 bacilli
Gram positive bacilli
| Question | Answer |
|---|---|
| What is the structure of pathogenic bacillus | occur singly, in pairs, or in chains and may have central endospores |
| What is the physiology of pathogenic bacillus | facultative anaerobes, form central endospore |
| What is the species of pathogenic bacillus | bacillus anthracis bacillus cerus |
| B. anthracis epidemiology. where is it found and how is it transmitted | zoonotic, contracted from infected animal, transmitted via either inhalation of spores, inoculation of spores through break in skin, or ingestion of spores |
| -pathogenic B. anthracis pathogenesis | anthrax toxin |
| Anthrax toxin | Causes the cells to lose water and form an edema, may be lethal as it causes cells to undergo apoptosis and macrophage to secrete toxic levels of cytokines that can lead to shock and death |
| Protective antigen and adenylate cyclase | cause cells to lose water which causes and edema |
| Protective antigen and protease | cause cells to undergo apoptosis and cause macrophage to release toxic levels of cytokines |
| What disease does B. anthracis | causes anthrax, three clinical manifestations |
| What are the three clinical manifestations of anthrax caused by B. anthracis | Gastrointestinal anthrax, inhalation anthrax, and cutaneous anthrax |
| Gastrointestinal anthrax | Rare in humans, spores ingested |
| Inhalation anthrax | rare in humans, requires inhalation of airborne endospores, high mortality rate |
| Cutaneous anthrax | produces ulcer called an eschar, fatal in 20% of untreated patients |
| eschar | death of skin, black |
| Diagnosis of B. anthracis | large, nonmotile, gram-positive bacilli in lung or skin samples |
| Treatment of B. anthracis | many antimicrobials are effective against B. anthracis |
| Prevention of B. anthracis | Control of disease in animals, Effective vaccine available requires multiple doses and boosters |
| What disease is caused by B. cereus | secretes enterotoxins that can cause mild food poisoning |
| What is the structure of pathogenic listeria | bacilli in singles or pairs |
| What is the physiology of listeria | psychrotolerant, Facultatively anaerobic, produce flagella at 30C or below, organize actin filaments into propeller like tail that allow for motility in human host |
| What is the pathogenic species of Listeria | Listeria monocytogenes , only human pathogen from this genus |
| What is the epidemiology of L. monocytogenes | found in soil, water, and animals. Enters the body via contaminated food and drink |
| What is the pathogenesis of L. monocytogenes | migrates to stomach and to small intestines, then can migrate to liver and gallbladder by hepatocytes using internalin and survive inside macrophages in the gallbladder |
| What does listeriolysin help listeria with | avoid digestion by the host cell by allowing bacteria to breakout of endosome vesicles ( virulence is correlates with ability to live within cells) |
| What does listeria do after it multiplies? | develops actin motility that allows motility into bloodstream, then to the brain, and can also cross the placenta and infect embryos and fetuses |
| What disease does listeria monocytogenes cause | can cause meningitis in at-risk individuals |
| When women transmit listeria to fetus, what happens | can cause premature delivery, miscarriage, stillbirth, or meningitis in the newborn |
| how does listeria enter the body and cause disease pt I | enters body through contaminated drink/food, listeria triggers its own phagocytosis by host cell, in the cell it escapes the phagosome, bacteria reproduces in the phagocyte, bacteria polymerizes the host actin into tail |
| How does listeria travel across the body | tail propels bacteria into pseudopods, pseudopod is endocytosed by host cell, cycle repeats as bacteria reproduces in the new host cell, bacteria can travel to brain via blood and cause meningitis |
| How is L. monocytogenes diagnosed | presence of bacteria in the CSF for individuals w meningitis. rarely seen in gram stain preparations |
| treatment of L. monocytogenes | ampicillin and other antibiotics |
| Prevention of L. monocytogenes? | at risk individuals should avoid certain foods |
| What is the structure of Corynebacterium | Bacilli in singles, or pairs in palisades or "V" shaped arrangements |
| Palisades | V shaped arrangements |
| Physiology of Corynebacterium -What is their oxygen requirements -are they fastidious or non fastidious -can they move -how do they divide | Oblique aerobes Highly fastidious nonmotile divides by snapping fission, causing unusual division arrangements |
| What species of Corynebacterium exist | Corynebacterium diphtheriae |
| What is the epidemiology of Corynebacterium diphtheriae | found ubquitiously on plants and in animals/humans colonize the skin and respiratory, GI tract, urogenital tract |
| What is the pathogenesis of Corynebacterium diphtheriae | Produce diphtheria toxin |
| What disease does Corynebacterium diphtheriae cause | causes diphtheria |
| Diphtheria -what is it caused by -how is it transmitted | caused by Corynebacterium diphtheriae, endemic in developing parts of world with poor immunization -transmitted via respiratory droplets or skin contact |
| What virulence factor causes the signs and symptoms of Diphtheria | Diphtheria toxin inhibits polypeptide synthesis in eukaryotes |
| bacteria (ex. Corynebacterium diphtheriae) that do not produce diphtheria toxin are pathogenic or nonpathogenic | nonpathogenic |
| What are some signs of diphtheria and what makes it dangerous | formation of pseudomembrane at the back of throat that may cause suffocation. Surgery is needed to remove |
| How is Corynebacterium diphtheriae diagnosed | presence of pseudomembrane Elek test used to confirm diagnosis |
| How is Corynebacterium diphtheriae treated | antitoxin neutralizes effects of toxin penicillin or erythromycin kills the bacterium Surgery may be needed to open a blocked airway |
| How is Corynebacterium diphtheriae prevented? | immunization is the most effective way |
| Pathogenic Clostridium strucure | Single bacilli contain endospores at their terminal ends |
| What is the physiology of Clostridium | -obligate Anaerobic -forms terminal endospores -most are motile except clostridium perfringens |
| What four pathogenic species of Clostridium are there | C. difficile C. botulinum C. tetani C. perfringens |
| What is the epidemiology of Clostridium difficile | found ubiquitous in soil, water, and is a part of the resident microbiota in GI tracts of animals and humans, |
| What is the pathogenesis of Clostridium difficile | produces two toxins and enzyme hyaluronidase it is an opportunistic pathogen in pt's taking broad spectrum antimicrobial drugs |
| What diseases does Clostridium difficile cause | self-limiting explosive diarrhea in minor cases pseudomembranous colitis in severe , life-threatening cases. colon wall sloughs off and becomes infected by fecal bacteria |
| How is Clostridium difficile diagnosed | isolated from a fecal sample, toxins found in immunoassays |
| How is Clostridium difficile treated | Discontinued use of broad antimicrobials drugs for severe cases, treatment of antimicrobials used |
| How is Clostridium prevented | proper hygiene to limit nosocomial (HAI) infection |
| Clostridium botulinum epidemiology | Found in the soil, and freshwater and marine sediments may be found in improperly canned food |
| What is the pathogenesis of Clostridium botulinum | botulism leads to production of toxins, for this strain 7 deadly toxins are produced which bind neurons and prevent muscle contractions= paralysis |
| What is botulism | when endospores germinate and produce botulism toxins |
| What is the mechanisms of action for botulism toxins | B. toxins prevent the release of acetylcholine vesicles from the synaptic terminal ends into the synaptic cleft, preventing the contraction of neuromuscles |
| What diseases does Clostridium botulism lead to | three manifestations of botulism intoxication: Foodborne botulism Pediatric botulism Wound botulism |
| Foodborne botulism | caused by C. botulinum. death can result from asphyxiation slow recovery from growth of new nerve cell endings |
| Pediatric botulism | Results from ingestion of endospores paralysis and death are rare |
| wound botulism | contamination of a wound by endospores symptoms like foodborne botulism |
| How is C. botulinum diagnosed | symptoms are usually used to diagnose |
| How is C. botulinum treated | intestinal wash used to remove pathogen neutralizing antibodies used against botulism toxin antimicrobial drugs in infand and wound botulism cases |
| How is C. botulinum prevented | properly canning food and infants under 1 yr should not eat honey |
| Clostridium tetani epidemiology | ubiquitous in soil, dust, and GI tract of animals and humans |
| Clostridium tetani pathogenesis | tetanus, occurs when endospore germinate and produce tetanus toxins |
| Tetanospasmin toxin | synonymous with tetanus toxin, released by C. tetani cells when they die potent neurotoxin causes continuous muscle contractions by blocking release of muscles relaxing neurotransmitters |
| What disease does C. tetani cause? What are the signs and symptoms | Tetanus: jaw and neck muscle tightening (lockjaw), spasms and contractions spread to other muscles, contraction of diaphragm may cause death, recovery requires growth o new neuronal terminals |
| How is C. tetani diagnosed | Characteristic muscular contraction |
| How can C. tetani be treated | 1. cleansing of wounds to remove endospores 2. immunoglobulin against tetanus toxin 3.antimicrobial drugs 4. active immunization w/tetanus toxoid for those who are not immunized |
| What is the pathogenesis of C. perfringens | two toxins: enterotoxins and cytolytic toxins |
| What is the epidemiology of C. perfringens | Grows in the GI tract of animals and humans |
| What disease does C. perfringens cause | food poisoning and gas gangrene |
| C. perfringens food poisoning | [ abdominal cramps and water diarrhea. self limiting0- |
| C. perfringens gas gangrene | endospore introduced into body through trauma endospores germinate and cause necrosis gas produced and create ruptures in skin |
| How is C. perfringens diagnosed | a minimum bacterial load in food or feces appearance of gas gangrene |
| How is C. perfringens treated | gas gangrene requires removal of dead tissue and administration of antitoxins and penicillin |
| how is C. perfringes prevented | refrigeration of foods and proper cleaning of wounds |
| Pathogenic mycobacterium is what type of pathogen | Gram-positive, acid bacilli bacteria |
| What is the structure of pathogenic mycobacterium | single or paired bacilli, cell wall contains mycolic acid (a waxy lipid) |
| What is the physiology of mycobacterium | obligate aerobes nonmotile mycolic acid in cell wall: slow growth, protections from lysis after phagocytosis, capacity for intracellular growth, protection from desiccation, resistance to gram staining, detergents, and many antimicrobial drugs |
| What are the species of Mycobacterium | Mycobacterium tuberculosis and Mycobacterium Leprae |
| What is the epidemiology characteristic of Mycobacterium tuberculosis | - Found in soil and human carriers -transmitted by inhalation of respiratory droplet -cases most common in Asia and Africa -Muti-drug-resistant and extensively drug resistant strains have developed - |
| What is the pathogenesis of Mycobacterium tuberculosis | -low virulence, spreads via respiratory droplets, growth allowed by preventing formation of phagolysosome, causes inflammation in alveoli, formation of tubercles, |
| What are tubercles | structures formed from various proteins and cell debris |
| When does disease occur with individuals infected with Mycobacterium tuberculosis | when alveolar cells inside the tubercles begin to die off |
| What disease does Mycobacterium tuberculosis cause | Three types of tuberculosis 1. primary tuberculosis 2. secondary or reactivated tuberculosis 3. Disseminated tuberculosis |
| Primary tuberculosis | results from initial infections with M. tuberculosis |
| Secondary or reactivated tuberculosis | reestablishment of active infection after period of dormancy |
| Disseminated tuberculosis | bacteria released from infected alveoli and migrate to other sites of the body (kidney, spleen, long bones, brain, meninges) |
| How is Mycobacterium tuberculosis diagnosed | tuberculin skin test identifies possible exposure chest XR identify individuals with active disease |
| How is Mycobacterium tuberculosis treated | -most common antimicrobials are ineffective because of mycolic acid, so Isoniazid, ethambutol, and rifampin are used -combination therapy |
| How is Mycobacterium tuberculosis prevented | immunization with BCG vaccine avoid inhaling respiratory droplets from TB patients |
| What is the epidemiology of Mycobacterium leprae | humans and armadillos are only hosts optimum growth at 30C, so infects superficial layers of body tissues transmitted via person to person or break in skin causes nerve and tissue destruction |
| What disease does Mycobacterium leprae cause | two forms of Leprosy aka (Hansen's disease) -tuberculoid leprosy -lepromatous leprosy |
| tuberculoid leprosy | nonprogressive form, due to strong cell-mediated immune response |
| lepromatous leprosy | virulent form, due to weak cell-mediated immune response |
| How is Mycobacterium leprae diagnosed | using the signs and symptoms of disease |
| How is Mycobacterium leprae treated | combination of antimicrobial drugs and lifelong treatment |
| How is Mycobacterium leprae prevented | limiting exposure to pathogen and BCG vaccine may provide some protection |
| What is the structure of pathogenic nocardia | Filamentous microscopic appearance, cell wall contains mycolic acid |
| What is the physiology/oxygen requirements of Nocardia | obligate aerobe |
| What pathogenic species of Nocardia are there | Nocardia asteroides |
| What is the epidemiology of Nocardia asteroides | common inhabitants of soil rich organic matter |
| What is the pathogenicity pf Nocardia | produces opportunistic infections in numerous sites |
| What diseases does Nocardia create | 3, Pulmonary infections, cutaneous infections, and central nervous system infections |
| Nocardia asteroides pulmonary infections | develop from inhalation of the bacteria |
| Nocardia asteroides cutaneous infections | results from introduction of the bacteria into wounds may produce a mycetoma |
| Nocardia asteroides central nervous infection | results from spread of bacteria in the blood |
| Nocardia asteroides diagnosis | presence of Nocardia in samples is usually diagnostic |
| Nocardia asteroides treatment | six-week course with sulfonamides immunocompromised patients have poor prognosis |
| How is Nocardia asteroides prevented | avoiding exposure to bacterium in the soil |
| What is the structure of pathogenic mycoplasma | lacks cell wall, pleomorphic, smallest free-living microbes, most have sterols in their cytoplasmic membranes |
| Pleomorphic | has no defines shape |
| What is the physiology of Pathogenic Mycoplasma | lack cytochromes, require host growth factors, colonize mucous membrane respiratory and urinary tract, |
| What are the pathogenic species of Mycoplasma | Mycoplasma pneumoniae main one although there are other species |
| What is the epidemiology of Mycoplasma pneumoniae | found in humans, animals, and soil |
| What is the pathogenesis | Attaches to ciliated epithelial cells lining human respiratory tract, stops beating, buildup of mucous in RT which promotes growth types of other bacteria that irritates RT |
| What disease does Mycoplasma pneumoniae cause | primary atypical pneumonia (walking pneumonia): not severe enough for hospitalization, spread by nasal secretions , common in children 5 to 15 years old |
| Mycoplasma pneumonia diagnosis | Mycoplasma are small and difficult to detect, and grow slow in culture |
| Mycoplasma pneumonia treatment | Macrolides, doxycycline, or fluoroquinolones |
| Prevention of Mycoplasma pneumonia | patients are typically asymptomatic but infectious prevented with proper hygiene and avoidance of aerosols and contaminated fomites |
| Other Mycoplasmas | Often colonize urinary and genital tracts of newborn girls, cause nongonococcal urethritis, may cause pelvic inflammatory disease in women (PID), |
| How can other Mycoplasmas be prevented | abstinence and safe sex |
| How can other Mycoplasma infections be treated | with various antibiotics |
Created by:
Acrob89
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