MIcro Exam II – Lectures 7-9 – Flashcards
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| Review Chart on Gram+/- |
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| Review |
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| Pathogenic Gram + (cocci) |
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| Staph, Strep, Entero |
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| Pathogenic Gram + (spore formers) |
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| Bacillus, Clostridium |
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| Pathogenic Gram + (rods) |
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| Corynebacterium, listeria |
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| Spores |
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| Keratin coat, DPA (hallmark of spores, allows it to cluster Ca++), no metabolism. |
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| Gram - (rods) |
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| Neisseria (diplococcus), treponema and Borrelia (spirochetes) |
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| Gram - (Others) |
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| Chladydia, Rickettsiae - obligate intracellular parasites. |
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| Acid Fast |
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| Mycobacterium |
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| Mycoplasma |
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| No cell wall |
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| Function of Ca++ in spores |
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| Stabilize DNA, protect from oxidative dmg. |
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| Bacillus shape, oxygen |
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| Fac. aerobe, streptobacillus |
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| B. anthracis virulence factors |
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| Capsule (makes it slippery), spores, toxins |
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| B. anthraces Toxins |
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| Protective Antigen (PA), Edema Factor - which is PA+EF, allows fluid to accumulate, Lethal Factor (LF) Stimulates macs to release cytokines, which lyses the macs. |
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| How B. Anthracis causes damage |
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| Cutaneous, Inhalation, GI |
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| Cutaneous Anthrax |
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| Majority of cases, Red w/in 12-36 hrs, 20% mortality, progresses to sepsis. |
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| Inhalation Anthrax |
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| Alveolar macs ingest spores, 95% fatal. Can progress to hemorraghic meningitis. |
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| GI Anthrax |
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| Mortality near 100% |
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| Anthrax diagnosis |
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| DFA (direct Fluor. Antibody), Lysis w/ gamma phage (virus that only infects it), PCR |
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| Treatment of B. anthraces |
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| Ciproloxacin for cutaneous, could use penicillin and doxycycline but penicillin resistance has been reported, Cipro or doxycycline for inhalation |
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| B. cereus causes |
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| food poisoning, eye infections, spore former. |
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| 3 forms of B. cereus |
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| Emetic form - heat stable enterotoxin, Diarrheal form - infection not intoxication, Ocular form - less common - eye injury |
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| Autoclave indicator |
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| B. stearothermophilus |
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| Listera shape, oxygen preferences |
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| Fac. aneaerobe, rod. |
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| How to clear Listeria |
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| Need CMI, abs not effective. |
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| Listeria is a facultative intracullular ____ |
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| Parasite |
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| What forms actin rockets |
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| Listeria - won't be exposed to I/S. In lunch meat, dairy. |
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| Diseases caused by Listeria |
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| Food poisoning, at risk are elderly, prigs, newborns, CMI defects. |
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| Treatment of Listeria |
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| penicillin OR gentamicin + penicillin or ampicillin |
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| Where to find Listeria |
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| Lunch meat, dairy, soft cheeses, raw veggies. |
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| Corynebacterium is opportunistic (T/F) |
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| True, few are true pathogens. |
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| What causes Diphtheria |
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| Corynebacterium |
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| Symptoms of Diptheria |
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| Pseudo membrane in throat, bull neck, cardiac complication from A-B exotoxin. |
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| What type of toxin is diphtheria toxin? |
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| A-B toxin - 2 parts |
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| A-B toxin, explain |
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| A-Action - A subunit goes in and stops translation, B is for binding. |
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| What 2 cell types do B toxins bind? |
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| Heart, nerve |
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| Treatment of Diptheria |
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| Antitoxin, Ab - penicillin or erythromycin to remove bacteria. |
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| What kind of vaccine is for diphtheria? |
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| Toxoid |
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| Size/shape/Oxygen Pref. of mycobacterium |
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| Aerorbic acid fast rods |
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| Damage of mycobacterium is from what |
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| Your I/S. |
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| Clinical test for Mycobacterium? |
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| PPD, Acid Fast stain. |
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| Primary infection of Mycobacterium |
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| Taken up by macs - aerosolized transmission. Ghon's complex forms - inflammation, WBCs, tissue destruction. |
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| Secondary Infection of Mycobacterium |
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| Reactivation of infection, Pulmonary TB or miliary TB, Granulomas - inflammation, chronic fever, night sweats, weight loss, cough. |
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| Treatment of TB |
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| RIP, Rifamycins (inhibit transcription) Isoniazid (cell wall synthesis inhibitor), Pyrazinamide (unclear mode) |
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| Prevention of TB |
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| BCG vaccine. |
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| What causes leprosy |
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| Mycobacterium leprae |
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| What type of immunity is needed to clear M. leprae? |
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| CMI - it's an intracellular bacteria. |
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| Forms of Leprosy? |
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| Lepromatous leprosy - highly infectious, skin destruction, takes >1 yr. of treatment. Tuberculoid leprosy - Nerve damage, low infectivity, hypopigmented skin lesions. |
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| Which form of leprosy is the most serious? |
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| Lepromatous leprosy. |
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| Epidemiology of Mycobacterium avium? |
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| Pulmonary disease or disseminated disease, especially in immunocompromised, immunosuppressed people. |
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| Treatment of M. avium |
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| Prophylaxis in HIV patients - azithromycin, treat infections w/ refampin or isoniazid. |
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| Shape/oxygen prefs. of Clostridium? |
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| Gram + rods, mostly anaerobic |
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| Where does clostridium live? |
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| Soil, sewage, GI of humans and animals. |
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| C. Perfringens infection site… |
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| Wound infection/gas gangrene or gastroenteritis. |
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| C. perfringens infection site that is most severe |
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| Wound infection. Tissue destroyed – blood supply cut off – necrosis. Myonecrosis – spreads deeper and kills muscle. Diabetics get this in ischemic limbs (lack of blood flow and therefore oxygen). Treat by keeping wounds CLEAN and penicillin. High mortality for would infections because more than 12 toxins |
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| Lecithinase is associate w/ which bacteria |
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| C. perfringens - hydrolyzes host cell membranes and mediates massive cell destruction, tissue destruction, hepatic toxicity, and myocardial dysfunction. |
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| What disease does Clostridium tetani cause, and where? |
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| Tetanus, wound infections - fatal in newborns when umbilical stump gets infected. |
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| Where is C. tetani found? |
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| Soil and GI tracts of humans and animals. |
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| Two important toxins of C. tetani? |
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| Tetanolysin (hemolysin) and Tetanospasmin (A-B toxin, a neurotoxin). |
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| Treatment of C. tetani |
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| Wound debridement, Metronizadol, Antitoxin. |
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| Clostridium botulinum causes what? |
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| Food poisoning, wound botulism, and infant botulism. |
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| Why do you die with botulism? |
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| You can't work your lung muscles. |
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| Treatment of botulism? |
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| Removal from GI tract if it's there - metronizadole or penicillin, Can also use an antitoxin. |
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| Prevention of C. botulinum? |
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| Destroy spores in food, prevent germination, destroy the toxin. |
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| Clostridium dificile is a component of normal flora (T/F) |
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| True for 5% of the population. |
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| What causes Pseudomembranous colitis? |
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| C. dificile, due to clindamycin wiping out normal flora. |
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| Treatment of C. dificile? |
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| Stop antibiotic you were taking and switch to a safe one. |
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| Lactobacillus shape, oxy preferences, etc… |
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| Gram + rod, anaerobe, found in the mouth. |
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| Is Lactobacillus acidogenic or acidouric? |
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| Both, easy one. |
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| Actinomyces gram status, shape, oxy prefs |
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| Gram + Fac. anaerobe or strict anaerobe. |
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| Who has filamentous hyphae |
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| Actinomyces |
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| Does Actinomyces have a role in caries? |
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| Yes. A. israelii is part of normal flora but can be opportunistic, can find in plaque, gingivitis, granulomatous lesions. Treat w/ penicillin. Too much for one flashcard? |
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| Most Gram- are rods except... |
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| Neisseria (diploccus) and Treponema and Borrelia (spirochetes) |
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| Gram- have what in their cell wall |
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| Lipopolysaccharide. |
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| What is the mechanism of LPS? |
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| Endotoxin, released when bacteria lyse, active at the site of infection, reacts w/ macs and causes shock in large quantities. |
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| Which is unstable, toxic in tiny amounts, small, and specific to a cell (exotoxin or endotoxin) |
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| Exotoxin. |
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| Which is needed in higher doses, stable, can't be converted to a toxoid, causes a fever (endotoxin or exotoxin)? |
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| Endotoxin |
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| Shape, arrangement, gram status of Neisseria? |
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| Gram-, aerobic diplococci. |
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| What diseases does Neisseria cause? |
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| N. gonorrhea (STD), and N. meningitides (meningitis). |
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| What diseases cause meningitis in < 6 mos.? |
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| Listeria, E. coli, S. agalactiae. |
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| What diseases cause meningitis in > 6 mos. people? |
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| S. pneumoniae, M. mengitides, H. influenzae. |
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| Who is most at risk of N. meningitides? |
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| Children and young adults. Mortality near 100% if not treated. |
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| What is the mortality of meningitis? |
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| Near 100%. |
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| What is the disease process of N. meningitides? |
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| Exposure through close contact with secretions, May lead to colonization, Bacteria engulfed by epithelial cells of the mucosa, Penetrate into blood vessels then cross blood brain barrier, Grow in CSF, Symptoms: fever, sore throat, headache, fever, stiff neck, convulsions, Bacteria shed endotoxin into circulation and macs are stimulated, Cytokines lead to vascular hemorrhage and coagulation, IF they recover 10%-20% of patients will have lasting cognitive impairment |
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| What is the diagnosis/treatment of N. meningitides? |
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| Spinal tap, treat w/ penicillin, also rifampin, ciprofloxacin, tetracycline. |
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| Is there a N. meningitides vaccine? |
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| Yes, mostly for high risk people - military, students, kids <2. |
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| What are the virulence factors of N. meningitides? |
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| Capsule, Endotoxin - LPS, Pili, Adhesins, IgA protease, Transferrin binding protein (iron for the bug), LOS - lipooligosaccaride - which inflames the innate I/S. |
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| What is the 2nd most prevalent STD in the US? |
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| Gonorrhea (1st is Chlamydia). Incidence exceeds reported cases b/c of asymptomatic carriers. |
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| What are the symptoms of gonorrhea? |
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| Pelvic inflammatory disease, septic arthritis, conjuctivitis and blindness in newborns. |
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| What are the stages of infection of N. gonnorrhea? |
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| Direct contact – only short term survival on fomites, Attach to epithelial surface with fimbriae, pili and Opa protein, Invade underlying connective tissue, 2-6 days you get inflammatory reaction that may or may not lead to symptoms, asymptomatic in 10% of men and 50% of women, asymptomatic carriers are the reservoir, Stimulate complement, but do not produce lasting immunity |
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| What is the diagnosis of N. gonorrhea? |
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| Diagnosis of Gram- diplococci (possibly IN neutrophils) from exudates. |
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| What is the treatment of gonorrhea? |
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| Cephalosporins, and not penicillin. |
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| What are the virulence factors of N. gonorrhea? |
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| NO CAPSULE, fimbriae, pili, and Opa protein. IgA, B-lactamase, lactoferrin-binding proteins, Por protein, LPS and LOS |
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| Does N. gonorrhea have a capsule? |
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| NO |
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| Which bacteria exhibits the Por Protein? |
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| N. gonorrhea. |
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| Describe the gram status, oxy. prefs and shape of Enteobacteriaceae family? |
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| Gram- rods, aerobic, or fac. anaeorbes. |
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| What is the common site of infection of enterobacteriaceae? |
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| GI tract. Can also be in CNS, lower resp. tract, blood stream, UTI |
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| What family contains lactose fermenters? |
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| Enterobacteriacae. |
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| What is the shape/oxy prefs, gram status of E. coli? |
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| Fac. anaerobic rod, gram-. |
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| What is ETEC/EHEC? |
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| E.coli, ETEC – enterotoxigenic E. coli Not person-person spread. Very large amt. needed for infection. EHEC – enterohemorrhagic E. coli – E. coli 0157:H7, for example. Small amt. needed for infection - ~100 bacteria. Low infection dose = easy to cross-contaminate. |
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| What bacteria is most associated with UTI? |
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| E. coli. |
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| What is the most common cause of Gram negative sepsis? |
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| E. coli. |
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| What are the virulence factors of E. coli? |
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| Pili, enterotoxins, endotoxins, shiga toxins. |
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| What is the shape/gram status, oxy prefs of salmonella? |
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| Gram-, fac. anaerobes, rod. |
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| Where is salmonella found? |
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| Animals and animal products. Transmitted oral/fecal, contaminated food/water. |
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| What causes Typhoid Fever? |
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| Salmonella typhi. Most serious in the genus, severe diarrhea. |
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| What is the treatment for Salmonella typhi? |
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| Chloramphenicol - binds ribosome and stops protein synthesis. |
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| Which is more serious - Salmonella typhi or Salmonella typhimurium? |
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| Typhi. Typhimurium - found in poultry/eggs. |
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| What are the toxins of salmonella? |
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| Enterotoxins, Fimbriae, cytotoxin, survive intracellularly. |
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| What is the shape/oxy prefs, gram status of shigella? |
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| Gram-, fac. anaerobic rods. |
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| How is shigella spread? |
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| Fecal/oral. |
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| What is the most severe form of shigella? |
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| Shigella dysenteriae. |
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| Which is more invasive - Salmonella or Shigella? |
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| Salmonella - Shigella has Endotoxin, Shiga toxins, |
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| What is the shape/oxy prefs gram status of Yersinia? |
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| Fac anaerobic rods, Gram-, causes zoonotic disease. |
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| What causes the bubonic plague? |
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| Y. pestis. CDC cat. A. bioweapon. 75% mortality if not treated. |
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| What are the reservoir/vector of bubonic plague? |
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| Rodents are the reservoir, fleas are the vector. |
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| What causes the pneumonic plague? |
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| Y. pestis, aerosol variant of bubonic plague. 90% mortality. |
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| What is the reservoir of Y. enterocolitica? |
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| Farm animals. |
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| Rank Y. pestis, Y. enterocolitica, and Y. pseudotuberculosis? |
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| Pestis/Entero/Pseudo. |
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| What does Klebsiella pneumoniae cause? |
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| UTI, wound and soft tissue infections, pneumonia. Gram- rods. |
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| What has the enzyme urease? |
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| Proteus mirabilis. Causes UTIs, gram- rods. Urease splits CO2 and ammonia, causing pH balance problems in pee. |
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| Describe shape, gram status and oxy prefs. of Vibrio cholerae? |
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| Gram-, Fac. anaerobic curved rods. |
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| What disease does Vibrio cholerae cause? |
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| Cholera, aka butt urine. 20L/day. Results in hypovolemic shock. |
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| How is V. cholerae transmitted? |
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| Contaminated shellfish, water. |
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| What is the treatment for cholera? |
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| Oral vaccine - multiple doses per year. Hygiene is KEY. Treat w/ fluids and electrolytes. |
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| Place the virulence of the following in order...Y. pestis, Vibrio and Salmonella, Strep Pneumoniae, Shigella. |
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| Vib/Sal, Shigella, Strep Pneum., Y. pestis. |
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| Describe the shape, and oxy prefs of Campylobacter... |
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| Vibrio (spiral), microaerophiles. |
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| Name the 2 Camylobacter species that cause gastroenteritis in the US... |
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| C. jejuni - major foodborne illness in developed countries, zoonotic (sheep/chickens), water, milk, meat. Rehydration is sufficient. C.coli - associated w/ pork. |
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| What is the association between Campylobacter and Guillain-Barre (pronounced Gil-ayn Bare) Syndrome? |
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| Antigenic crossreactivity btw LPS and peripheral nerve gangliosides. Causes peripheral nerve dmg, auto-immune disease. |
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| Describe gram status and shape of Helicobacter? |
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| Gram-, pleomorphic rods. |
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| What is the transmission of Helicobacter? |
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| Fecal-oral, humans are the reservoir (40-50% of adult stomachs have it) flies can be vectors. Zoonotic from cats, dogs, other mammals. |
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| How does helicobacter survive the conditions in the stomach? |
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| Urease - causes peptic ulcers. Can cause esophageal carcinomas. |
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| How is helicobacter treated? |
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| Antibiotics clarithromycin and proton pump inhibitors. |
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| What is the gram status, shape and oxy prefs of Pseudomonas? |
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| Gram-, obligate aerobe rods. |
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| Where is pseudomonas normally found? |
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| Soil, water, hospitals - drinking fountains, sinks, soap, dishes. |
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| Pseudomonas doesn't form biofilms - T/F? |
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| False - it does form biofilms. |
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| What produces a greenish pus, sweet smelling infection? |
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| Pseudomonas. |
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| Is pseudomonas part of the normal flora? |
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| No. |
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| Typical pseudomonas infections? |
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| UTIs, swimmers ear, wound infections in burn patients, pneumonia, sepsis, osteomyelitis. |
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| What are the Virulence factors for Pseudomonas? |
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| Capsule, pili, LPS, exotoxins, elastase, hemolysins, ABX resistance. |
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| T/F - Monotherapy is effective in treating Pseudomonas. |
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| False - almost always ineffective. |
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| What is the shape/gram status/oxy prefs of Haemophilus? |
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| Pleomorphic Gram- rods, often form long filaments. |
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| T/F Haemophilus infleunzae causes the flu. |
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| False - meningitis. |
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| T/F Haemophilus influenzae is the most common cause of meningitis 3 mos-3 yrs int he US. |
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| False - most common in the world, but we vaccinate. |
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| Other diseases caused by Haemophilus influenzae? |
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| Pharyngitis, pneumonia in adults, conjuctivitis, sinusitis, cellulitis. |
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| What is unique about the HiB vaccine? |
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| Conjugate polysaccharide (capsule) + protein (helps improve response to the vaccine in kids). |
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| What is the gram status/shape of Bordetella pertussis? |
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| Gram- coccus, strict aerobe. |
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| What causes whooping cough? |
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| Bordetella pertussis. |
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| How is B. pertussis transmitted? |
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| Aerosol - highly contagious. Increasing in the US in older kids and adults. |
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| T/F pertussis toxin is an A-B toxin. |
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| True. |
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| What is the mechanism of damage of whooping cough? |
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| Bacterium attach to epithelial cells by fimbria. |
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| How is B. pertussis infections treated/prevented? |
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| Toxoid vaccine (pertussis toxin) and macrolides (like erythromycin) - protein synthesis inhibitors. |
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| T/F Legionella pneumophilia is person-to-person spread. |
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| False - common src (like cooling towers, A/C). Sporadic worldwide occurrence from aerosols. |
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| What type of immunity do you need to recover from Legionella pneumophilia? |
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| CMI - it's intracellular. 75% mortality if immunocomrpomised, 15% if healthy. |
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| What diseases does Legionella pneumophila cause? |
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| Legionnaire's disease (pneumonia) and Pontiac fever (flu-like, no pneumonia). |
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| T/F Legionella pneumonia is a facultative intracellular parasite. |
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| True - need CMI to clear. |
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| Describe shape/oxy prefs/gram status of Legionella pneumophila. |
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| Gram- rods, fastidious obligate aerobes. |
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| How is Legionella pneumophila treated? |
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| Macrolides and fluroquinolones. |
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| What is gram status/oxy prefs/shape of Bacteroides? |
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| Gram- pleomorphic rod shaped anaerobes. |
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| T/F Bacteroides is normal flora of the GI tract and oral cavity. |
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| True - some can cause disease in oral cavity. |
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| T/F Bacteroides produces colleganes. |
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| True - important in progression of periodontal disease. |
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| What causes trench mouth? |
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| Bacteroides. |
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| How is Bacteroides treated? |
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| Clindamycin. |
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| B. fragilis causes anaerobic infection in the peritoneal cavity - T/F. |
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| True. Causes abcesses. |
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| What is the most common source of infection in the blood? |
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| Bacteroides. |
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| What is the gram status/oxy prefs/shape of Porphyromonas gingivalis? |
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| Gram- anaerobe rod. |
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| What is the role of Porphyromonas gingivalis in periodontal disease? |
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| Degrades collagen in perio disease. |
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| Which has higher virulence - Porphyromonas gingivalis or Prevotella inermedia? |
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| P. gingivalis. |
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| What is black when grown on blood agar? |
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| Prevotella intermedia and Porphyromonas gingivalis. |
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| Name the genus that contains oral spirochetes. |
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| Treponema - suspected to be main causer of perio disease. |
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| Describe the shape/gram status/oxy prefs of Treponema. |
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| Gram- anaerobes, spirochetes. |
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| What causes Syphilis? |
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| Treponema pallidum. #3 STD in the US. |
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| How is T. pallidum visualized? |
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| Dark field microscopy. DFA test also used to diagnose. |
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| How is syphilis treated? |
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| Pen G(injected). |
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| What is the 1st stage of syphilis? |
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| Canker at site of infection. |
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| What is the 2nd stage of syphilis? |
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| Bacteremia w/ rash. |
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| What is the 3rd stage of syphilis? |
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| Organ damage, neurological dmg - granulomas called GUMMAS. |
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| What is congenital syphilis - and dental ramifications? |
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| From mom to baby - crosses placenta. Hutchinson's incisors and Mulberry Molars. |
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| What is the shape/oxy prefs/arrangement of Borellia burgdorferi? |
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| Gram- spirochetes. |
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| What causes Lyme disease? |
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| Borellia burgdorferi. |
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| Where does Lyme disease occur mostly? |
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| Endemic in US, NE and mid-atlantic states. |
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| Fleas are the vector for Lyme disease - T/F. |
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| False - ticks. |
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| What are the symptoms of Lyme disease? |
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| Rash at bite, neuro symptoms if not treated, cardiac dysfunction, arthritis. |
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| How is Lyme disease treated - what about late stage? |
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| amoxicillin, doxycycline, tetracycline. Late stage is penicillin. |
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| What is the gram status of Mycoplasmas? |
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| Trick question - no cell wall so no gram status. |
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| What does Mycoplasma cause? |
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| Pneumonia. |
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| How is Mycoplasmas treated? |
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| Erythromycin, tetracycline, fluoroquinolone. |
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| Describe the gram status and shape of Rickettsia. |
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| Gram- cocci, obligate intracellular parasites. |
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| T/F Mycoplasma can't make ATP on its own. |
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| False - Rickettsia can't. |
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| What is the vector for Rickettsia? |
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| Arthropods (I think later it says no vector - air). |
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| What causes typhus, Rocky Mtn. Spotted Fever, Q fever? |
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| Rickettsia. |
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| What causes typhus? |
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| Rickettsia prowazekii. |
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| What is the vector for Rickettsia prowazekii? |
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| Louse. |
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| What are the symptoms of typhus? |
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| Rash everywhere BUT face. Fever, headache, fatigue. |
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| How is typhus treated? |
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| Tetracycline. |
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| What causes Rocky Mtn. Spotted Fever? |
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| Rickettsia rickettsii. |
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| Where is Rocky Mtn. Spotted Fever found? |
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| SW US and Eastern seaboard. |
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| How is Rocky Mtn. Spotted Fever spread? |
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| Humans via ticks. |
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| Where does Rocky Mtn. Spotted Fever grow in the cell? |
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| The nucleus. |
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| How is Rocky Mtn. Spotted Fever treated? |
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| Tetracycline (same for all Rickettsia). |
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| T/F Chlamydia is an obligate intracellular parasite? |
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| True. |
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| What is the leading STD in the US? |
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| Chlamydia - may have co-infection w/ gonorrhea. |
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| What is infected in Chlamydia? |
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| Urethra/Fallopian Tubes, also eye infections (but rare in US, treatable). |
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| What does Chlamydia trachomatis cause? |
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| Chlamydia. |
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| What does Chlamydia pneumoniae cause? |
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| Pneumonia. |
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| Which bacteria have A-B toxins? |
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| B. pertussis, Clostridium, Vibrio, Corynebacterium. |
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| Which bacteria has 12 toxins? |
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| C. perfringens |
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| Large drift, small drift (Influenza A/B/C). |
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| A/B |
