Micro Final Review

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Micro Final Review
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Micro Final Review
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  1. What are resident microbiota?
    Microbes which can be repeatedly cultured from a given site over time
  2. What are transient microbiota?
    Microbes which may initially inhabit a site after exposure, but do not persist
  3. What does colonization by a microbe mean?
    Establishment of a microbial population in the animal host
  4. What does infection by a microbe mean?
    Colonization of an animal host by a pathogen (disease implied)
  5. What is a primary pathogen?
    Microbe capable of producing disease in a healthy human or animal host
  6. What is an opportunistic pathogen?
    Microbe capable of producing disease only in a host whose defenses have been compromised
  7. What is a microbe carrier?
    Individual colonized with a pathogen, but free of disease, who is capable of acting as a source of infection for others
  8. Culture of the skin shows the microbiota on this tissue are mostly anaerobic or aerobic?
    predominantly anaerobic
  9. Which group of oral microbiota is associated with endocarditis?
    • Viridans streptococci
    • (Staphylococcus aureus)
  10. What strains of oral microbiota are associated with dental caries?
    • Streptococcus mutans
    • Actinomyces viscosus
  11. What strains of oral microbiota are associated with gingivitis?
    • Porphyromonas gingivalis
    • Prevotella melaninogenicus
    • Fusobacteria
    • Treponema denticola
  12. What strains of oral microbiota are associated with dental caries and lung abscesses?
    Porphyromonas gingivalisPrevotella melaninogenicusFusobacteria
  13. What strains of oral microbiota are associated with brain and liver abscesses and bacteremia?
    Streptococcus milleri group
  14. What strains of oral microbiota are associated with cervicofacial abscesses?
    Actinomyces israeli
  15. What are the proposed mechanisms between oral microbiota and systemic health?
    • Induction of systemic inflammatory and immune responses
    • Asymptomatic bacteremia
    • Endotoxemia
    • Direct role of periodontal pathogens (Oral bacteria present in atherotic plaques)
  16. What type of bacteria (anaerobic vs. aerobic) are predominant in the colon?
    anaerobic
  17. What are some of the beneficial effects of resident bacteria in the colon?
    • Protection from pathogens
    • Stimulation of gut maturation (e.g. angiogenesis)
    • Stimulation of innate and adaptive immune systems
  18. What are the symptoms of bacterial vaginosis? Is it common? Which vaginal microbiota are dominant in bacterial vaginosis and which become overtaken?
    • symptoms: fishy odor (KOH test), white discharge, elevated vaginal pH
    • bacterial vaginosis is the most common vaginal infection

    • dominant bacteria:
    • anaerobic vaginal microbiota (Prevotella, Porphyromonas, Bacteroides, Mobiluncus, many others)
    • Gardnarella vaginalis
    • Atobobium vaginae

    absence of H2O2 –producing Lactobacillus species (L. crispatus and others)
  19. How is bacterial vaginosis diagnosed?
    • Nugent criteria (“gold standard”): scoring of Gram stain based on:
    • 1. Absence of large Gram-positive rods (Lactobacilli)
    • 2. Presence of small Gram variable coccobacilli (Gardnerella vaginalis) and Gram-negative rods (Bacteroides)
    • 3. Presence of small Gram-variable curved rods (Mobiluncus)

    • Amsel criteria: any 3 of the following
    • 1. observation of "clue cell" on microscopic examination of vaginal smear wet mount
    • 2. adherent grayish discharge
    • 3. production of volatile malodorous amines on addition of KOH (whiff test)
    • 4. vaginal pH > 4.5 (e.g. Femexam pH and amine test card)
  20. What would be the most appropriate antiobitic treatment for bacterial vaginosis?
    • antibiotics active against microbes
    • e.g. clindamycin
    • e.g. metronidiazole
  21. What are host defenses against bacterial infections?
    • intact epithelium
    • phagocytic cells (neutrophils, macrophages, monocytes)
    • antibacterial secretions: fatty acids (skin) (seminal fluid)
    • desquamation (skin)
    • lysozyme (conjunctiva)
    • normal microbiota
    • mucociliary clearance (respiratory epithelium)
    • alveolar macrophages (respiratory epithelium)
    • secretory IgA (respiratory epithelium, gut epithelium, urogenital epithelium)
    • peristalsis (esophagus, intestines)
    • acidity (stomach)
    • urine flow
    • ciliated epithelium of fallopian tubes
  22. What are the host defenses against bacteria in deeper tissue specifically?
    • The phagocytic cell - monocytes, macrophages, dendritic cells, neutrophils
    • Inflammation: recruitment of opsonins, phagocytic cells to site of infection
    • Complement: opsonization (most important), direct lysis (less important)
    • Phagocytosis: killing of bacterial cell (oxidative processes and antibacterial peptide-mediated membrane damage); processing and presentation of bacterial antigens

    • Innate Immunity
    • Alternative pathway of complement fixation
    • Mannan-binding lectin (MBL) pathway of complement activation
    • Pattern recognition of microbial components triggers innate immune responses
    • Toll-like receptor (TLR) – cell surface receptors
    • Nod-like receptor (NLR) – intracellular receptors

    • Acquired Immunity
    • Humoral: (antibody mediated)more efficient opsonization, complement fixation; neutralization of toxins; prevention of adherence to mucosal surfaces
    • Cellular: activation of monocytes/macrophages; killing of intracellular bacteria
  23. How may toxins made by bacteria in gut mucosa affect the host immune sytem?
    • toxins may act locally with tissue damage
    • toxins may act locally and directly affect epithelial function without tissue damage
    • toxins may be disseminated with systemic effects
  24. What are some bacterial strategies for pathogenesis?
    • non-invasive pathogens
    • invasive pathogens (routes of tissue invasion; strategies against phagocytic cells)
    • Mucosal Surface Colonization and Production of Toxins
    • Tissue Invasion
    • Penetration of intact epithelium
    • Penetration of compromised epithelium (physical trauma; arthropod vector)
    • Inflict damage to tissue prior to phagocytosis
    • Avoid phagocytosis
    • destroy phagocyte
    • antiphagocytic surface properties
    • inhibit phagocytic function by “injection” of effector proteins
    • Survive phagocytosis (escape from phagosome, prevent lysosomal fusion, survive in phagolysosome)
    • Escape from neutrophil extracellular traps (NETs) (dissolution of NETs by bacterial DNases)
  25. What are some types of tissue that can be tested for the presence of microbes?
    Blood, throat swab, sputum, urine, STD (cervical, urethral) CSF, other body fluids (pleural, ascitic, synovial, etc.)
  26. What are some diagnostic strategies for detecting microbes?
    • Direct microscopic examination
    • Direct antigenic detection techniques
    • Molecular diagnosis - Nucleic acid amplification/hybridization
    • Selection of appropriate media and conditions (Differential, selective media; Aerobic, microaerophilic, anaerobic incubation)
    • Isolation and microscopic examination
    • Antigenic tests
    • Molecular analysis
    • Biochemical analysis
    • Serology
  27. For which types of microbe is molecular diagnosis (Nucleic acid amplification/hybridization) particularly useful?
    • N. gonorrhoeae
    • Chlamydia
    • Mycobacteria
    • Rickettsia
    • Viruses
  28. For which types of microbe is diagnosis by serology particularly useful?
    • syphilis
    • Lyme disease
    • leptospirosis
    • Mycoplasma pneumoniae
    • Rickettsia sp.
    • viral (e.g. HIV, hepatitis)
  29. For which types of microbe is a diagnostic skin test particularly useful?
    • Mycobacterium tuberculosis
    • certain fungal pathogens
  30. Are viruses considered "living" in a scientific sense?
    NO: even though they contain matter capable of self-replication (i.e. nucleic acids), viruses do not independently self-replicate
  31. What are some qualities of murein (aka peptidoglycan)?
    • not synthesized by mammals
    • bag-shaped mesh-like structure
    • surrounds cell membrane
    • single cross-linked macromolecule
    • provides rigidity
    • glycan strings (backbone): muramic acid, glucosamine
    • (tetra)peptide side chains
    • inter-peptide cross-links
  32. Peptidoglycan removal results in:
    • Spheroplasts (partial removal)
    • Protoplasts (complete removal)
    • (both are stable only in highly osmotic solutions)
  33. What are some qualities of a bacterial cell envelope?
    • Cell membrane
    • + Peptidoglycan cell wall
    • (+ Outer membrane)
    • Anything else associated with the above
  34. What are the ordered steps in conducting a gram stain?
    • 1. heat/dry
    • 2. crystal violet stain
    • 3. iodine fix
    • 4. alcohol de-stain
    • 5. safranin stain
  35. Which specific components in a gram (+) bacteria's cell wall trigger neutrophil activation?
    • lipoteichoic acid (serves as adhesin)
    • teichoic acid (defines serotype; recognized by antibodies; cell wall digestion/synthesis)
  36. What are the "wall-less" (i.e. only possess single cell membrane) bacteria?
    • Mycoplasma
    • Chlamydia
  37. What is unique about Acid-Fast bacteria and what are some examples?
    • they are gram (+) bacteria but possess an outer cell membrane (arabinogalactan +; mycolic acid layer)
    • e.g. Mycobacterium
    • e.g. Nocardia
  38. What is the difference between a capsule and a slime layer of a bacterium?
    • a capsule is covalently attached and makes agar colonies appear smooth
    • a slime layer (or glycocalyx) is non-covalently attached
  39. What 2 types of bacteria are known particularly for their endospores?
    • Bacillus
    • Clostridium
  40. What is the difference between sterilization, disinfection, and sanitization?
    • Sterilization: killing of all microorganisms in a material or on the surface of an object.
    • Disinfection: reducing the number of viable microorganisms present in a sample
    • Sanitization: cleaning of pathogenic microorganisms from public eating utensils and objects
  41. What is the difference between a disinfectant and an antiseptic?
    • Disinfectant: a chemical or physical agent that is applied to inanimate objects to kill microbes (e.g. sink surface, dental tools)
    • Antiseptic: a chemical agent that is applied to living tissue to kill microbes (e.g. skin, oropharynx, conjunctiva)
  42. By what means does sterilization/disinfection kill bacteria?
    • Protein denaturation (heat; moist heat esp. for spores; alcohols, oxidizing agents, halogens
    • Membrane disruption (surfactants, organic acids, alcohols, phenolics
    • Nucleic acid damage (UV radiation, oxidizing agents
    • Inhibition of metabolism (ionizing radiation, heavy metals, oxidizing agents, alkylating agents)

    The killing of microorganisms occurs exponentially
  43. What is the rank order of microbes and microbrial components according to descending intrinsic resistance to antiseptics and disinfectants?
    • spores
    • mycobacteria
    • gram (-) bacteria
    • gram (+) bacteria
  44. Does the evolution of a microbe from planktonic form to biofilm-growth from increase or decrease its resistance to antiseptics/disinfectants?
    increases resistance
  45. What are the Acquired Bacterial Resistance Mechanisms to antiseptics and disinfectants?
    • Plasmid-encoded resistance:
    • Inactivation (enzymes, e.g. formaldehyde dehydrogenase)
    • Decreased uptake (resistant LPS or porins structure)
    • Efflux (pumping out)

    • Mutation-acquired resistance:
    • Optimizing the ways to inactivate, decrease uptake or pump out.
  46. Which species of bacteria are able to use transformation as a means of genetic recombination?
    • Bacillus
    • Haemophilus
    • Neisseria
    • Streptococcus
    • S. pneumoniae
  47. What are some examples of virulence factors?
    • adhesins, fimbriae (binding to human tissues)
    • capsule (protection from immune system)
    • siderophores (iron acquisition - growth rate)
    • flagella (spread into new compartments)
    • TOXINS (damage to human cells)
  48. What are the major types of bacterial toxins?
    • Endotoxins – usually released by dead bacteria (LPS)
    • Membrane-bound toxins - act from the bacterial surface
    • Exotoxins – secreted out by live bacteria (mostly proteins)
  49. Which bacteria use a Type III injection system to deliver their toxins directly into a cell?
    • gram (-) bacteria only
    • Salmonella
    • Shigella
    • Diarheal E. coli
    • Yersinia
    • Pseudomonas
  50. Which bacteria have developed a resistance to penicillin via production of penicillinases/beta lactamases?
    • Staphylococcus aureus
    • Enteric bacteria
    • Neisseria gonorrhoeae
    • Haemophilus influenzae
  51. Which bacteria have developed a resistance to penicillin via production of altered penicillin binding proteins (PBP)?
    • Streptococcus pneumoniae
    • Staphylococcus aureus (MRSA)
    • Neisseria meningitidis
  52. Which bacteria have developed a resistance to penicillin via decreased permeability or active efflux?
    Pseudomonas aeruginosa
  53. Which bacteria is resistant to penicillin treatment?
    • Staphylococcus aureus
    • Enteric bacteria
    • Neisseria gonorrhoeae
    • Haemophilus influenzae
    • Pseudomonas aeruginosa
    • Streptococcus pneumoniae
    • Staphylococcus aureus (MRSA)
    • Neisseria meningitidis
  54. Which types of antibiotics interfere with cell wall synthesis?
    • beta lactams (e.g. penicillin, ampicillin, cephalosporins, etc.)
    • glycopeptide antibiotics (vancomycin, telavancin)
  55. Enterococci bacteria are becoming increasingly resistnat to which antibiotic?
    vancomycin
  56. Which antibiotics interfere with protein synthesis?
    • macrolides
    • mupirocin
    • linezolid
    • aminoglycosides
    • tetracyclines
    • clindamycin
    • retapamulin
    • synercid
  57. For which conditions and bacteria are macrolides (e.g. erythromycin,clarithromycin, azithromycin (Zithromax), telithromycin (ketolide) (Ketek)) useful against?
    • pneumonia
    • sinusitis
    • Chlamydia
    • atypical mycobacteria
    • Toxoplasma (parasite)
    • Streptococcus pneumoniae
    • acne (erythromycin)
  58. What are some aminoglycosides and what are they useful against?
    • e.g. streptomycin, gentamicin, tobramycin, neomycin
    • Synergistic with ß-lactam antibiotics for serious Gram-positive infections
    • Useful against Pseudomonas aeruginosa
    • Inactive against anaerobes
    • the most toxic of currently used antibiotics
  59. What are some tetracyclines and what are they effective against?
    • e.g. doxycycline, minocycline
    • Effective for intracellular pathogens (e.g. Chlamydia, Rickettsia)
  60. What are some antibiotics that interfere with nucleic acid synthesis?
    • quinolones: ciprofloxacin (gram (-)); levofloxacin (levaquin) (gram (+)); moxifloxacin (gram (+), gram (-) anaerobes)
    • rifampin
    • metronidazole
  61. What is the mechanism of the quinoilone class of antibiotics and what are they useful against?
    • disrupt topoisomerases and DNA gyrase of bacteria
    • useful against community acquired pneumonia
  62. Which group of antibiotics is associated with tendon rupture as a potential side effect?
    quinolones
  63. What is the mechanism of rifampin and what is it useful against?
    • disrupts nucleic acid synthesis: binds to bacterial RNA polymerase
    • useful only in prophylaxis or in combination
    • important in treatment of tuberculosis
    • prophylaxis of menigococcal disease
  64. What is metronidazole effective against and what is its mechanism of effectiveness?
    • DNA disruption
    • useful against all anaerobes
    • Trichomonis vaginalis
    • Entamoeba histolytica (protozoa)
  65. Which antimetabolite antibiotic is also effective against the fungus Pneumocystis jirovecii?
    Trimethoprim sulfamethoxazole
  66. What are some antimetabolite antibiotics?
    • sulfanamides
    • Trimethoprim
    • Trimethoprim sulfamethoxazole (Bactrim, Septra)
  67. What are some antibiotic combination therapies that capitalize on synergy?
    • ß-lactam + aminoglycoside for Pseudomonas
    • Trimethoprim + sulfamethoxazole for Enterococcus
  68. What are some appropriate uses for combination antibiotic therapy?
    • In some cases synergy offers clear advantage.
    • (ß-lactam + aminoglycoside for Pseudomonas, EnterococcusTrimethoprim + sulfamethoxazole)
    • To prevent emergence of resistance by mutation (e.g. tuberculosis).
    • To treat polymicrobial infections.
    • In empiric therapy to cover multiple pathogens (e.g. STDs)
  69. When is prophylactic antibiotic therapy warranted?
    • Appropriate when a specific antibiotic has been demonstrated to prevent a specific infection for which there is high risk.
    • Early treatment of asymptomatic infection, e.g. tuberculosis.
    • Recurrent urinary tract infections.
    • Prior to and following surgical procedures with high risk of infection.
    • Control of outbreaks of meningococcal disease
    • Travel
  70. Which antibiotics are useful against MRSA, VISA, and VRE?
    • Daptomycin
    • Clindamycin
    • Linezolid
    • Tigecycline
    • Synercid
    • Mupirocin
    • Retapamulin
  71. What is daptomycin's mechanism of action and what is it usefula against?
    • membrane depoloarization
    • useful for skin and subcutaneous infections caused by Gram-positive organisms
    • Staphylococcus (MRSA),
    • Streptococcus,
    • Entercoccus (VRE)
    • Staphylococcus aureus,
    • E. faecium bacteremia,
    • endocarditis
  72. What is the mechanism of action of clindamycin and what is it useful for?
    • inhibits protein synthesis
    • useful against community acquired MRSA, anaerobic infections
  73. What is the mechanism of action of linezolid and what is it useful for?
    • inhibits protein synthesis
    • Broadest spectrum drug available against Gram-positives
    • useful against MRSA, penicillin-resistant Streptococcus pneumoniae, and vancomycin-resistant enterococci (VRE)
  74. What conditions are associated with synercid toxicity?
    • arthralgia
    • myalgia
  75. What is the mechanism of action of mupirocin (Bactroban) and what is it useful for?
    • inhibits protein synthesis
    • Useful for eradication of nasal carriage of MRSA
    • treatment of skin infections caused by Staphylococcus aureus and Streptococcus pyogenes
    • topically applied
  76. Which antibiotics are useful against Mycobacterium tuberculosis?
    • Isoniazid – (mycolic acid synthesis) used for treatment of active tuberculosis in combination with other drugs, and alone for chemoprophylaxis
    • Pyrazinimide
    • Ethambutol
    • Rifampin (targets RNA polymerase)
  77. Which antibiotics are useless against multidrug resistant tuberculosis?
    • rifampin
    • isoniazid
    • resistance acquired by mutation
  78. What is fosfomycin used for?
    Used for single dose oral therapy of E. coli urinary tract infections
  79. What are the general characteristics of streptococci?
    • Gram (+) spherical/ovoid cocci, usually in chains
    • Form significant portion of normal flora
    • non-spore forming
    • Metabolism is anaerobic: some strict, some oxygen-tolerant
    • Most species rarely cause disease

    • Significant human pathogens:
    • Streptococcus pyogenes (GAS, group A strep)
    • Streptococcus agalactiae (GBS, group B strep)
    • Viridans streptococci
    • Streptococcus pneumoniae
  80. How are streptococci classified?
    • 1. hemolysis on blood agar (complete = beta; partial = alpha; none = gamma)
    • 2. serologic properties based on cell wall polysaccharides (Lancefield groups)
    • 3. biochemical/physiological properties
  81. Which strain of streptococci is resistant to bile and grows in high salt concentrations?
    enterococci
  82. Which streptococci strains conduct beta hemolysis of blood agar?
    • S. pyogenes (GAS)
    • S. agalactiae (GBS)
    • Groups C and G
  83. Which types of streptococci can undergo alpha hemolysis of blood agar?
    • S. pneumoniae (pneumococcus)
    • S. bovis (GDS)
    • Groups C and G
    • Viridans group
    • Milleri group
  84. For which streptococci groups is it possible not to see any hemolysis of blood agar in culture?
    • Groups C and G
    • S. bovis (GDS)
    • Viridans group
    • Milleri group
  85. What are the clinical signs of strep throat (Group A strep) infection?
    • exudative pharyngitis
    • palatal petechiae
    • "beefy" red throat
    • fever
    • sore throat, malaise
    • absence of cough
    • lymphadenopathy
    • lasts about 1 week
  86. What are some potential clinical indications and therapies of necrotizing fascitis?
    • Onset acute
    • severe pain out of proportion to exam findings
    • fever and chills
    • Rapid progression over hours - life-threatening

    • Prompt, aggressive surgical debridement of necrotic tissue
    • may require plastic surgery later
    • Intensive care: antibiotics, IV fluids, inotropic support
  87. What are the signs and symptoms of acute rheumatic fever?
    • Joint involvement: Migratory arthritis, large joints
    • O (♥): Carditis - inflammation of cardiac connective tissue, enlargement, heart failure; prolonged PR interval on EKG; valvular damage
    • Nodules, subcutaneous: bony surfaces, prominences
    • Erythema marginatum: advance at margins, clear at center
    • Sydenham’s chorea (St. Vitus’ dance): emotional lability, purposeless movements

    • onset 3 weeks post pharyngitis
    • recurs with repeat GAS infection
    • autoimmunity due to molecular mimicry
  88. What is the most common secondary infection to influenza?
    pneumonia by S. pneumoniae
  89. Which strain of streptococci is lancet-shaped?
    Streptococcus pneumoniae
  90. What are the 3 basic mechansims through with Group A strep avoids the host immune system?
    • 1. hyaluronic acid capsule (antiphagocytic, adhesion, camoflauge)
    • 2. M protein (adhesion, antiphagocytic)
    • 3. lipoteichoic acid (adhesion)
  91. What are the general characteristics of staphylococci?
    • Gram-positive, non-motile, non-spore forming
    • 0.5-1 μm diameter
    • Lab isolates grow in clusters (staphylo = bunches of grapes) - but not always seen in clinical specimens
    • Aerobes or facultative anaerobes
    • Grow best on blood-enriched media
    • β-hemolytic
    • Grow at 18-40 C
    • Can grow in 10% NaCl
    • Catalase-positive; S. aureus coagulase-positive
  92. Which staphylococci strains are catalase and/or coagulase positive?
    • Coagulase positive: S. aureus
    • Catalase positive: S. aureus, S. epidermidis, S. saprophyticus
  93. What is the most common general clinical presentation of each of the 3 major staphylococci strains?
    • S. aureus: most virulent
    • S. epidermidis: foreign body infections
    • S. saprophyticus: UTI
  94. What is the function of catalase?
    neutralizes oxidative burst of phagocytes
  95. What is the function of coagulase?
    converts fibrinogen to fibrin by binding prothrombin
  96. What is a superantigen and which group of bacteria is associated with it?
    • superantigen:
    • Distinct class of bacterial (or viral) antigens that bind to MHC class II receptors in a distinctive way
    • Activate T cells without processing by antigen-presenting cell
    • Stimulates massive cytokine production by CD4+ cells
    • resulting in toxicityIL-1:
    • high feverTumor necrosis factor
    • interferon gamma
    • associated with staphylococci
  97. What is pelvic syndrome and what bacteria is associated with it?
    • Pelvic syndrome: arthritis + osteomyelitis + myositis + septic thrombophlebitis + necrotizing pneumonia + sepsis
    • associated with S. aureus
  98. What are the most common bacteria strains that infect people with CF?
    • Pseudomonas aeruginosa (#1)
    • S. aureus
  99. What risk behavior is right-sided endocarditis associated with? What types of bacteria can cause endocarditis?
    associated with IVDU

    • gram (+) cocci:
    • S. aureus
    • S. epidermidis
    • Viridans strep
    • Groups C and D strep
    • enterococci

    • gram (-):
    • Haemophilus aphrophilus
    • Actinobacillus actinomycetemcomitans
    • Cardibacterium hominus
    • Eikenella corrodens
    • Kingella kingae

    other random bacteria: chlamydia, legionella, etc.

    (fungi)
  100. What are some examples of commensule microbes?
    • Entamoeba coli (protozoan; GI tract)
    • Giardia lamblia (can be commensulate or pathogenic)
  101. What is an example of a microbe that can be either commensule or pathogenic?
    Giardia lamblia
  102. What are some common examples of ectoparasites?
    human body louse (Pediculus humanus)
  103. What are some common examples of endoparasites?
    Strongyloides stercoralis
  104. What are the definitive and intermediate hosts of Schistosoma mansoni?
    • definitive host = human
    • intermediate host = snail
  105. Dogs may function as definitive host for which parasites? As a reservoir host?
    • definitive host:
    • Leishmania spp. (also reservoir host)
    • Toxocara canis
    • Echinococcus spp.
  106. Humans serve as incidental hosts for which parasites? Carrier hosts?
    • incidental host:
    • Trichenella spiralis (muscle)

    • carrier host:
    • Cutaneous Larva migrans
  107. What is the main vector for malaria? Is it a biological or mechanical vector?
    malaria vector = female anopheles mosquito = biological vector
  108. What is a common vector for Entamoeba histolytica? Is it a biological or mechanical vector?
    Entamoeba histolytica vector = housefly = mechanical vector
  109. What are some examples of parasites that gain entry into the body via ingestion?
    • Giardia
    • Entamoeba histolytica
    • Toxoplasma
    • Cryptosporidia
    • Cestodes
    • some Nematodes
    • Trematodes (except Schistosomes)
    • Taenia solium (cystercerci in measly pork)
  110. What are some examples of parasites that gain entry into the body via arthropod bite?
    • Malaria
    • Babesia
    • Filaria
    • Leishmania
    • Trypanosomes
  111. What are some examples of parasites that gain entry into the body via parasite directed penetration?
    • Hookworm
    • Strongyloides
    • Schistosomes (Cercaria)
  112. What are some examples of parasites that gain entry into the body via sexual contact?
    Trichomonas
  113. What are some examples of parasites that utilize destructive enzymes as a pathological mechanism?
    • Anasakiasis
    • schistosome cercariae
    • hookworms
  114. What are some examples of parasites that utilize amoebic pores as a pathological mechanism?
    Entamoeba histolytica
  115. What are some examples of parasites that utilize endotoxins as a pathological mechanism?
    • African Trypanosomes
    • malaria
  116. What are some examples of parasites that utilize catabolites as a pathological mechanism?
    Trypanosomes
  117. What are some examples of parasites that utilize blockage of internal organs as a pathological mechanism?
    • Ascaris (appendix)
    • tapeworms
    • schistosomes
    • filaria
  118. What are some examples of parasites that utilize pressure atrophy as a pathological mechanism?
    • Echinococcus spp. (liver)
    • Cysticerci (measley pork)
  119. What are some examples of parasites that utilize migration through tissue as a pathological mechanism?
    Helminth larvae (Toxocariasis)
  120. Which parasites cause pathological damage via anaphylactic (antigen + IgE/histamine) mechanisms?
    helminthic infections
  121. Which parasites cause pathological damage via cytotoxic (antigen on host cell; complement/ADCC) mechanisms?
    Trypanosoma cruzi
  122. Which parasites cause pathological damage via immune complex (antibody complexes with extracellular antigen) mechanisms?
    • malaria
    • schistosomiasis
  123. Which parasites cause pathological damage via cell mediated (sensitized T cells; cytokines) mechanisms?
    • leishmania
    • schistosomiasis
  124. What are some examples of how parasites interfere with immune defenses?
    • Antigenic Variation: African trypanosomes, malaria
    • Molecular Mimicry: trypanosomes, schistosomes
    • Concealment of antigens: schistosomes, hydatid cyst
    • Intracellular location: malaria, toxoplasma, leishmania, Trypanosoma cruzi
    • Immunosuppression: trypanosomes, malaria
  125. What parasite kills the most people every year and what are the two commonest ways it kills?
    • malaria kills the most people every year
    • common mechanisms: anemia, immune system evasion
  126. How does malaria evade the immune system and how does partial immunity ensue?
    • immune system evasion: constant rearrangment of PfEMPs on infected RBC
    • partial immunity: PfEMP antibodies; G6PD deficiency; no Duffy-blood (FyFy) markers; sickle-cell trait
  127. What’s the most common protozoan infection in the world? How is it acquired and how does it cause disease?
    • Toxoplasma gondii causes the most common protozoan infection (toxoplasmosis) world-wide
    • acquisition: (feline) fecal oocysts; oocysts in raw meat (lamb, pork, some beef); transplacental
    • pathogenicity: fecal/tissue oocysts --> trophozoites --> disemmination: lympthadenopathy, inflammation
  128. What parasites require tests usually used for tuberculosis for detection (i.e. Acid-Fast stains)?
    • microspora
    • Coccidia:
    • Cyclospora
    • Crytposporidium
    • Isospora belli
  129. What are some examples of sporozoa?
    • Apicomplexa
    • Coccidia

    • Plasmodia
    • Toxoplasmodia
    • Cryptosporidia
    • Isospora
    • Cyclospora
  130. What are the 5 most common species of plasmodia in humans?
    • Plasmodium falciparum: causes most fatalities, drug resistance common, predominant in tropics
    • Plasmodium vivax: relapsing, common in subtropics and temperate
    • Plasmodium ovale: relapsing, found in W. Africa
    • Plasmodium malaria: uncommon, temperate or subtropics
    • Plasmodium knowlesi: primate malaria in SE Asia (Malaysia), now in humans, appearance like P. malaria, but more serious/fatal
  131. What are some differentiating characteristics of the major malaria species?
    • P. falciparum: rings in early trophozoite; high parasitimia; banana gametocyte
    • P. vivax: rings and schizont; no need for Duffy-blood; hypnozoites
    • P. ovale: lots of merozoites in late trophozoite; no need for Duffy-blood; hypnozoites
    • P. malaria: line through cell; rosette schizont
    • P. knowlesi: primate malaria --> human (severe) malaria
  132. Which stages in the RBC development do different malaria species prefer?
    • P. vivax, P. ovale: reticulocytes
    • P. malaria: senescent cells
    • P. falciparum: all stages
  133. Which parasite species makes superficial parasitopherous vacuoles in the GI tract?
    Cryptosporidium
  134. Which parasite species make vacuoles in the GI tract?
    • Cyclospora cayatanensis
    • Cryptosporidium (superficial parasitopherous)
  135. What are some common features between Cyclospora cayatanensis and Isospora belli?
    • coccidia that infect upper small bowel
    • cause diarrhea
    • oocysts in stool (AFS)
  136. What parasite causes bloody diarrhea and may cause a liver abscess months later?
    Entamoeba histolytica
  137. What parasite can “eat” your eye if it gets in your contact lens?
    Acanthameba
  138. What parasite can “eat” your brain after waterskiing?
    Naeglaria fowleri
  139. What’s the most common STD parasite?
    Trichomonas vaginalis
  140. Which sporozoa have their sporogony and schizogony phases in the same host? different hosts?
    • same host: Toxoplasma gondii; Isospora spp.
    • different host: Plasmodium spp.
  141. What are some general characteristics of genitourinary tract parasites?
    • a. Trichomonas vaginalis
    • b. Direct (venereal) spread
    • c. Trophozoite infective agent
    • d. Worldwide
  142. What are some general characteristics of gastrointestinal tract parasites?
    • a. Entamoeba histolytica, Giardia lamblia, Balantidium coli
    • b. Indirect (fecal-oral) spread
    • c. Cyst infective agent
    • d. Found in areas of poor sanitation
  143. What are some general characteristics of blood/tissue parasites?
    • a. Plasmodium sp., Trypanosoma sp., Leishmania sp.
    • b. Arthropod vector
    • c. Tropical and subtropical areas
  144. What pathogenic mechanisms does Entamoeba histolytica employ to cause cell/tissue damage?
    • proteases
    • amoeba pores
    • phospholipases
    • release of toxic PMN contents
  145. What is the major protein that Entamoeba histolytica uses for adhesion?
    Galactose-inhibitable adherence protein (GIAP lectin)
  146. What are some examples of luminal and hemo- flagellates?
    • Luminal Flagellates:
    • Trichomonas vaginalis
    • Giardia lamblia

    • Hemoflagellates (Trypanosomatids):
    • Trypanosoma brucei (African trypanosomiasis)
    • Trypanosoma cruzi (American trypanosomiasis)
    • Leishmania spp
  147. Which ameba causes encephalitis in normal hosts? Immunocompromised hosts?
    • encephalitis in normal hosts: Naeglaria fowleri
    • encephalitis in immunocompromised: Acanthameba
  148. What’s the best way to protect from giardiasis: filtration or chlorination?
    filtration
  149. What’s the ciliated protozoan that can cause diarrhea in children?
    Balantidium coli
  150. How do you distinguish pathogenic from non-pathogenic Entamoeba?
    presence of GIAP lectin
  151. What is the “face-eating” form of Leishmaniasis?
    L. braziliensis
  152. What are the vectors of Leish, T. cruzi and T brucei? What way does the T cruzi vector transmit disease that’s different from the rest?
    • Leishmania vector = sandfly
    • T. cruzi vector = reduviid bug
    • T. brucei vector = tsetse fly

    T. cruzi: transmitted by vector's urine/feces contaminating a wound/mucosa (not direct infection by bite)
  153. What is the most common cause of heart disease and GI malfunction in rural South America?
    Chiga's disease (Trypanosoma cruzi infection)
  154. What causes sleeping sickness?
    Trypanosoma brucei (rhodesiense, gambiense)
  155. Which Leishmaniasis species cause cutaneous, mucosal, or visceral infection?
    visceral: L. donovani

    • cutaneous:
    • L. tropica
    • L. major
    • L. mexicana
    • L. braziliensis

    • mucosal:
    • L. braziliensis
  156. What are the different classes of trematodes and what tissue do they generally infect?
    • Blood Trematodes (Blood Flukes):
    • Schistosoma spp.

    • Tissue Trematodes (Tissue Flukes):
    • Paragonimus spp. - lung
    • Clonorchis/Opisthorchis spp. - liver
    • Fasciola spp. - liver

    • Intestinal Trematodes (Intestinal Flukes):
    • Fasciolopsis spp.
  157. What is schistomiasis most commonly caused by?
    • Schistosoma mansoni
    • Schistosoma haematobium
    • Schistosoma japonicum
    • (S. mekongi [SE Asia], S. intercalatum [C&W Africa])
  158. What causes swimmer's itch? What are its reservoir hosts?
    • Schistosoma dermititis
    • reservoir host = water fowl, migratory birds, muskrats
    • (other hosts: snails, humans)
  159. What are some general characteristics of Schistosoma mansoni?
    • Africa, S. America; ova large lateral spine
    • Infects inferior mesenteric vein, perirectal area
    • Colitis, liver disease (pipestem fibrosis), all above
  160. What are some general characteristics of Schistosoma haematobium?
    • Africa, Middle East; ova terminal spine
    • Infects peri-vesicular (around bladder) veins
    • Bladder damage, obstruction, bleeding, bladder transitional cell cancer
  161. What are some general characteristics of Schistosoma japonicum?
    • Asia; produces most ova, diminutive lateral spine; water buffalo reservoir host
    • Infects superior mesententeric veins, small bowel
  162. How is schistosomiasis diagnosed?
    • Eosinophilia
    • serology
    • ova in biopsies or stool (mansoni or japonicum) or urine (haematobium)
  163. Which worm disease causes the most morbidity and mortality? What are its general presenting symptoms of infection?
    • Schistosomiasis
    • Clinical: Early: ‘swimmers itch’; 6 weeks: Katayama fever @ oviposition (serum sickness/allergic); Late: bowel, bladder damage, liver disease (eggs swept to liver, pipestem fibrosis), portal hypertension, hepatosplenomegaly, GI bleeds, pulmonary fibrosis and pulm. hypertension, rarely perispinous vein infection gives transverse myelitis and LE paralysis
  164. Which worm is responsible for the most morbidity and mortality?
    Schistosomas
  165. What worm can cause you to vomit blood until you die?
    Schistomiasis mansoni
  166. What worm can make you to be unable to pass urine?
    Schistosomiasis haematobium
  167. What worm can cause biliary cancer?
    Clonorchis sinensis (clonorchiasis)
  168. What worm acts like tuberculosis and lung cancer?
    Paragonimus spp.
  169. Why should you feel bad for bees after they’ve stung you but not wasps?
    • bees: lose their venom apparatus in act of stinging then die
    • wasps: can sting repeatedly without dying, also can bite
  170. What’s the difference between a hobo spider sting and a black widow sting?
    • Black widow sting: neurotoxic venom
    • Hobo (recluse) spider sting: necrotic venom
  171. What arthropod burrows into your skin?
    mites (Scabies: Sarcoptes scabei, Chigger: Tunga penetrans)
  172. What arthropod hangs onto hair?
    lice
  173. What maggots live in human skin (myiasis)?
    • Dermatobium hominis
    • Cordylobia anthropophaga (Tumbu fly)
  174. Link the vector to the type of infectious diseases they transmit:

    tsetse fly
    mosquito
    reduviid bug
    Lutzomyi phlebotomine fly
    simulian (deer) fly
    louse
    Ioxodes (soft) tick
    Hard tick
    flea
    • tsetse fly: Trypanosoma brucei (African Sleeping Sickness)
    • mosquito: Malaria, lymphatic filariasis, yellow fever, dengue fever, numerous other viruses (JEV, EEV, VEV, etc)
    • reduviid bug: Chiga's disease (T. cruzi)
    • Lutzomyi phlebotomine fly: leishmaniasis, bartonellosis, viruses
    • simulian (deer) fly: loiasis
    • louse: relapsing fever, ricketsial disease
    • Ioxodes (soft) tick: Lyme disease, babesiosis, anaplasmosis (HGA)
    • Hard tick: RMSF, ehrlichiosis (HME), colorado tick fever
    • flea: Yersinia Pestis
  175. What are the tick-borne diseases?
    • Hard ticks: RMSF, (HME) ehrlichiosis, colorado tick fever
    • Soft ticks (Ornithodorus): relapsing fever
  176. Stings and bites cause damage by:
    • by increased blood supply
    • increased capillary permeability
    • leukocyte ingress
    • hypersensitivity reactions: immediate or delayed
    • neurotoxic venoms (e.g. Widow spiders [Latrodectus spp.] and scorpions)
    • necrotic venoms (e.g. recluse and hobo spiders)
  177. Which arthropods give hymenoptera stings?
    • bees
    • wasps, hornets, yellow jackets
    • stinging fire ants (S.E. USA)
    • harvester ants (W. USA)
  178. Itchy butt? What worm might be causing it?
    pruritis ani: Enterobius Infections: Enterobius vermicularis (Pinworms)

    (larva currens: Strongyloides stercoralis)
  179. Trichuris: Key Concepts
    • Trichuris trichuria, whipworm, small nematodes, widespread in warm places, disproportionately affect children
    • Transmitted through fecal contamination of ova in soil, 1-3 week embryonation period required, then contamination of food or water
    • Clinical: generally symptomatic only in children, then abd pain, diarrhea, rectal prolapse
    • Therapy: albendazole, mebendazole
  180. Hookworms: Key Points
    • Necator americanus, Ancylostoma duodenale:
    • Infection by larvae penetrating skin in fecally contaminated areas, warm, poor-sanitation
    • Pass through lungs (loeffler’s pneumonia) and move to small bowel where attach and suck blood
    • Clinical:Anemia (iron-deficiency)
    • Less common: abd pain, protein loss
    • Diagnosis: O&P of stool: ova 40x80 uM, thin shell, 2-4 cells
    • Therapy: albendazole, mebendazole, pyrantel pamoate
  181. What is the “Count Dracula” of parasites?
    DRACUNCULIASIS (Guinea Worm Infection): Dracunculus medinensis


    (hookworm: causes iron deficiency anemia)
  182. What worm can turn a butt inside-out?
    • Trichuriasis
    • Trichuris trichuria (whipworm)
  183. Trichinosis: Key Concepts
    • Trichinella spiralis:
    • Acquired by eating undercooked meat of carnivores (in past, pigs, recently bear/cougars)
    • Clinical: Replicate in intestine, sometimes GI symptoms
    • Release larvae that disseminate to muscles, causing edema (periorbital), myalgias, encephalitis, eosinophilia about 1-3 wks after ingestion
    • Diagnosis: eosinophilia, serology, muscle bx.
    • Treatment: Steroids for severe symptoms; Mebendazole, Albendazole (esp. if still in intestinal phase)
  184. What worm might crawl out of the nose during anesthesia?
    Ascaris lumbricoides
  185. Which worms have to go through the lungs to get to the bowels?
    • Ascaris lumbricoides
    • Ascaris suum

    Hookworms (Ancylostoma duodenale, Necator americanus, A. ceylanicum)

    Strongyloides stercoralis

    Toxocara canis or T. cati
  186. What nematode is associated with Hyperinfection Syndrome?
    Strongyloidiasis (rhabditiform larvae)
  187. Strongyloidiasis: Key Concepts
    • Strongyloides stercoralis:
    • Found in warm, poor-sanitation areasAcquired by penetration of filariform larvae from fecally-contaminated soil
    • Larvae pass through to lungs, breakout, up trachea and swallowed into small bowel where 1-2 mm adults find each other and start producing rhabditiform larvae, small % autoinfect making infection persistent for decades
    • Clinical: Early: rarely ground-itch at penetration and loeffler’s
    • Later: Abdominal discomfort, skin manifestations (hives, etc), larva currens (track like movement that may start in peri-rectal region
    • Immunocompromised: hyperinfection syndrome, fever, pulmonary infiltrates, sepsis (often polymicrobial) due to increased invasion of larvae
    • Diagnosis: rhaditiform larvae in stool, filariform larvae in sputum in hyperinfection, eosinophilia unless steroids/cytotoxic agents given, serology
    • Therapy: Ivermectin, Albendazole
  188. Which worm can threaten your life after immunosuppression, decades after you get it?
    Strongyloidiasis (rhabditiform larvae)
  189. What roundworms can penetrate the unbroken skin if you’re walking around barefoot?
    • hookworms:
    • Ancylostoma duodenale
    • Necator americanus
    • A. ceylanicum
  190. Toxocariasis: Key Concepts
    • Toxocara canis & cati:
    • Caused by accidental ingestion of ova from dog and cat ascariids in fecally contaminated soil (e.g. sandbox ingestion)
    • Larvae migrate in tissues, without proper development, causing eosinophilic inflammation
    • Clinical:
    • Visceral (Age 1-4)Fever, enlarged liver and spleen, skin rash, pneumonia, convulsions, neurologic defects
    • Ocular (Age 7-8)Exudative endopthalmitis, mimics retinoblastoma
    • Diagnosis: eosinophilia, serology, occ. Biopsies
    • Therapy: Albendazole + corticosteroids
  191. What worm can mimic cancer of the eye?
    Toxocara canis & cati
  192. Cutaneous Larva Migrans: 
Key Concepts
    • Ancylostoma braziliense:
    • Caused by dog and cat hookworm larvae
    • Humans carrier host (carry larvae without further development)
    • Filariform larvae penetrates skin and crawls, leaving red linear rash
    • Skin exposure in warm damp areas where pet feces soil environment, e.g. beach in Jamaica, crawling under houses in Fl.
    • Diagnostic: no specific diagnosticTherapy: Ivermectin, albendazole
  193. Filariasis: Key Concepts
    • Onchocerciasis (river blindness): Onchocerca volvulus
    • Vector: blackflies (Simulium spp.): Africa, C/S America
    • Eosinophilia, nodules, skin changes, microfilariae in eye and skin, blindness
    • Dx: skin snips, serology, Mazzotti reaction
    • Rx: ivermectin every six months

    • Lymphatic filariasis (elephantiasis): Wucheria & Brugia
    • Vector: mosquitos (often night biting): much of the tropics
    • Clinical: nocturnal fevers, pulmonary symptoms, retrograde lymphangitis, lymphedema
    • Dx: blood microfilaria at night or after DEC
    • Rx: diethylcarbamazipine

    • Loaiasis: Loa loa
    • Transmitted by deer flies (Chrysops): West Africa ONLY
    • Conjunctival or dermal migration (Calabar Swellings)
    • Dx: demonstration of worm or serology
    • Rx: diethylcarbamazipine
  194. What worm can cause Optic Atrophy, "hanging groin", and Schlerosing Keratitis?
    Onchocerciasis (filariasis)
  195. What worm can cause blindness?
    Filariasis: onchocerciasis (river blindness)
  196. What worm can make a testicle larger than both legs?
    Filariasis (lymphatic): Wucheria bancrofti
  197. What worm can you get from sushi that gives you the worst belly pain of your life?
    Anisakiasis (nematode)

    (Diphyllobothriasis (tapeworm); Nanophyetiasis (trematode))
  198. What are the 3 basic types of helminths?
    • nematodes (round worm)
    • cestodes (tapeworms)
    • trematodes (flukes)
  199. What worm gets attention when it squiggles across the eye?
    Filariasis: Loaiasis
  200. Nematodes (Intestinal vs. Tissue):
    Intestinal Nematodes: Presence of the adult worm in intestine responsible for major disease manifestation(s)

    Tissue Nematodes: Produce disease by migration of larvae or adult worms through tissues of definitive host
  201. Enterobiasis: Key Concepts
    • Pinworms (Enterobius vermicularis): 1-2 mm nematodes, worldwide, esp. children, oral-fecal transmission
    • Auto-reinfection and group infections common
    • Clinical: Pruritis ani
    • Diagnosis: perirectal cellophane tape test in AM
    • Therapy: Albendazole, Mebendazole, Pyrantel pamoate
  202. Ascaris: Key Points
    • Ascaris lumbricoides, transmitted by fecal ova, embryonated in soil >3 wks, contaminating food or water, large nematode adults (15-40 cm)
    • Larvae from ova hatch in intestine, move through circulation to lungs, break into alveolae, crawl up to trachea, swallowed back down and 2 mos after infection adults reside in upper intestine by muscular force (6-18 mo life span)
    • Clinical: Early: loeffler’s eosinophilic pneumonia; Later: abdominal pain, worm obstruction of orifice
    • Diagnosis: ova (mammilated) in stool, adult worm passed
    • Therapy: Albendaole

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