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443 Cards in this Set
- Front
- Back
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What is the clinical presentation of an acute infection?
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rapid onset, short duration- on the order of "days"
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What is the clinical presentation of a chronic infection?
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slower onset, longer duration- on the order of weeks, months, years
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What are 6 general patterns of tissue reaction to infection by different organisms?
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three most common:
acute inflammation chronic inflammation granulomatous inflammation others: eosinophilia cytopathic changes widespread necrosis |
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What are the 4 classic signs of acute inflammation?
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rubor (redness)
calor (heat) tumor (swelling) pain |
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Tell me about pus
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an inflammatory oozing substance (exudate) containing neutrophils and protein rich fluid
pyogenic = pus producing |
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How is acute tonsilitis characterized?
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- red, swollen tonsils
- overlying pus |
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What organism often causes acute tonsilitis and how is it recognized?
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Group A streptococcus pyogenes
beta-hemolytic, gran positive cocci in pairs and chains |
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How is acute appendicitis characterized?
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- appendix is swollen, red, warm to touch (theoretically)
- pus - markedly thickened appendix wall- due to accumulation of fluid and inflammatory cells (like neutrophils, macrophages) |
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What are 3 possible outcomes of acute inflammation?
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- Normal healing (the usual outcome)
- Tissue destruction - Progression to chronic inflammation |
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What are 2 possible mechanisms of tissue destruction?
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- Abscess formation
- Scarring |
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What is an abscess?
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A focal lesion where the inflammatory response has resulted in local destruction and replacement with a collection of neutrophils (pus)
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What happens to an abscess over time?
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Becomes surrounded by a wall of fibrous tissue. All that is left is a collection of dead tissue and neutrophils.
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Are you more likely to see a lot of neutrophils in response to a bacterial infection or a viral infection?
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bacterial
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Are you more likely to see a lot of natural killer cells in response to a bacterial infection or a viral infection?
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viral
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Will you see pus with a bacterial infection or a viral infection?
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bacterial- because of the presence of neutrophils
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What kind of cell forms the initial immune response to a viral infection?
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Natural killer cell
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What organism would be likely to cause an infection that includes a chronic inflammatory infiltrate consisting of lymphocytes, macrophages, and plasma cells?
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an intracellular organism
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What is a granuloma?
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A collection of activated macrophages
Large cells with abundant pink cytoplasm often fuse to form giant cells. This is a special subtype of a chronic inflammation A delayed type of hypersensitivity reaction |
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How is a granuloma formed?
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Activated macrophages fuse to form giant cells form small clusters in an attempt to wall off an infection. This cluster is called a granuloma.
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What type of organisms elicit granulomatous inflammation?
What is one really important example? |
Poorly digestable intracellular organisms. Sometimes worms and fungi.
Most important: mycobacterium Tb |
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What kind of organisms do eosinophils defend us against?
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helminths (worms)
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What is "major basic protein" and what type of cell contains it?
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Eosinophils contain it. It is a toxic compound for helminths that also causes host tissue damage.
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What kind of organism induces "cytopathic changes"?
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virus
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What are some features of cytopathic changes?
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nuclear inclusions, cytoplasmic inclusions, multinucleated cells.
cellular enlargement, fusion with adjacent cells. |
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What cytopathic changes do you see with CMV?
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cellular enlargement
nuclear inclusions cytoplasmic inclusions |
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What cytopathic changes do you see with herpes simplex virus?
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multinucleated cells due to cell fusion
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What cytopathic changes do you see with infection by HPV?
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enlarged nucleus, binucleated, perinuclear halo
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What cytoplasmic changes do you see with infection by adenovirus?
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intranuclear inclusion
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What type of organisms cause extensive necrosis?
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toxin mediated (from bacteria and parasites)
viruses |
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What types of organisms cause pneumonia?
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A wide variety of bacterial, viral, fungal and parasitic agents
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What are the main bacterial causes of pneumonia?
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Streptococcus pneumoniae
Haemophilus influenzae Mycoplsma pneumoniae Staphylococcus aureus Legionella species |
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What are two methods by which successful pathogens circumvent complement (and how do they work)?
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O-antigen- sugar residues that prevent membrane attack complex from acting in proximity to cell membrane
Capsular polysaccharides - completely envelop and protect cell |
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What type of organism is the major cause of menningitis in newborns?
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encapsulated organisms - this helps the pathogen to pass through the blood-brain barrier
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Beyond two months of age, where do organisms responsible for meningitis typically originate
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nasopharynx
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Describe the physiology of streptococcus pneumoniae (gram, shape, hemolytic-ness, catalase)
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gram-positive
cocci, often shaped as diplococcus (in pairs) alpha-hemolytic catalase negative |
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When is streptococcus pneumoniae virulent?
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When it transits outside its niche to normally sterile spaces within respiratory tract (lung, middle ear), and following an invasive infection (blood, meningitis)
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What makes streptococcus pneumoniae adaptable and difficult to treat/prevent?
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antibiotic resistance- especially to penicillins. Resistance to beta-lactam antibiotics and others have been rising.
serotype shifts in response to introduction of vaccination antibody to CPS takes many days to develop- there are over 90 unique types of CPS |
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What is the most common location/pattern of streptococcus pneumoniae?
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lobar pneumonia- affects an entire lobe of the lung
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What do the alveoli look like during streptococcoc pneumonia infection?
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Filled with acute inflammatory cells, including neutrophils --> exudate. Alveolar walls have capillaries that are dilated and filled with RBCs. Structure of alveolie is maintained--> minimal residual damage.
Exudate gives rise to cough of yellow/rust colored sputum. |
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Describe the structure and physiology of Haemophilus influenzae (size, gram, shape, growth requirements)
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small, nonmotile
gram-negative coccobacillus (ie has both cocci, rod appearance) aerobic growth requires hemin, NAD |
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What types of infections does non-typable Haemophilus influenzae cause?
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In children:
Acute otitis media Conjunctivitis In adults: exacerbations of chronic bronchitis |
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How do people typically obtain immunity to type-b Haemophilus influenzae
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There is a vaccine for type b (but NOT for untypable H. influenzae)
Most people naturally acquire immunity via antibody to type b CPS |
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How is Haemophilus influenzae treated?
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About 70-80% still sensitive to penicillin.
When there is resistance, it's usually due to beta-lactamase --> cephalosporins are effective |
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Describe the structure and physiology of Neisseria meningitidis (gram, shape, distinguishing characteristics)
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Gram-negative
bean-shaped diplococcus prominent antiphagocytic polysaccharide capsule |
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What are the most important serogroups of Neisseria meningitidis?
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Names are based on CPSs:
A,B,C,Y,W-135 |
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What are the 2 presentations of Neisseria meningitidis?
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meningococcemia, characterizes by petechiae (minute hemorrhagic spots on skin) or purpora (larger hemorrhages on skin)
acute bacterial meningitis |
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What is meningococcemia characterized by?
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sudden and severe sepsis
rapidly progressive multisystem involvement high mortality |
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What is meningococcal meningitis characterized by, and what are some symptoms?
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bacteremic spread, but less overwhelming sepsis than meningococcemia.
--> more treatable, prolonged symptoms include fever, altered mental status, headache, nausea, vomiting, photophobia |
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How is Neisseria meningitidis treated?
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Penicillin or a third-generation cephalosporin
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Interesting epidemiological aspects of Neisseria meningitidis
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high risk groups include people in close contact --> antibiotic prophylaxis recommended in this case
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Problems with polysaccharide vaccines (for encapsulated pathogens)
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stimulated thymus-independent antibody response -->
lack of memory response lack of affinity maturation impaired class-switching ineffective in children < 2 years old there is also a rise of vaccine-resistant bacteria |
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Describe the physiology and structure of Bordtella pertussis (size, ana/aer, gram, shape)
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small
aerobic gram-negative coccobacilli |
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Where does bordtella pertussis become pathogenic?
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localized infection of ciliated surfaces of upper respiratory tract following person-person transmission
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What does pertussis toxin do to host?
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Pertussis toxin has a subunit that interferes with cell signalling --> overproduction of cAMP --> promotes respiratory secretions and interfere with neutrophil functions involved in clearance.
Also mediates binding to epithelial cells, blocking activitiy of immune effector cells --> lymphocytosis (abnormal increase in amount of lymphocytes in blood) |
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What are the exotoxins produced by Bordetella pertussis?
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pertussis toxin
adenylate cyclase toxin tracheal cytotoxin |
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What does tracheal cytotoxin do?
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Secreted by Bordetella pertussis, it inhibits ciliary beating --> inhibits clearance by mucociliary elevator
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What is the major clinical disease caused by Bordetella pertussis?
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Whooping cough
(characterized by big "whoop"- inspiration- at end of coughing spurt) |
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Who gets whooping cough?
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Young children- can be deadly
Also- young adults can get it when immunity wains |
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Epidemiology of Bordetella pertussis
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highly contagious
person-person spread causes outbreaks, including in hospitals older children, adults can be a source of spread in population high morbidity and mortality in first 6 months of life |
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What are the 3 stages of infection with Bordetella pertussis?
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1. Catarrhal stage- indistinguishable from URI
(catarrh = excessive discharge or buildup of mucus in nose or throat) 2. Paroxysmal stage- episodic paroxysmal coughing- may or may not have "whoop" 3. Convalescent stage- could take weeks |
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How is Bordetella pertussis diagnosed?
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flourescent antibody or culture from nasopharyngeal swab.
PCR is preferred method when available |
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How is Bordetella pertussis treated?
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erythromicin or other macrolides, but usually too late to stop toxin-mediated damage.
DTaP vaccine includes pertussis toxin Booster shots of vaccine used in teenagers and adults now |
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What is unusual about the structure of mycoplasma pneumonia?
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it lacks a cell wall
(therefore is not affected by penicillins and beta-lactams) |
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Describe the symptoms of mycoplasma pneumonia?
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Insidious onset of fever, headache, malaise, cough.
Chest x-ray generally shows interstitial infiltrate that is patchy, involves multiple lobes. Described as "walking pneumonia" b/c less severe |
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How is mycoplasma diagnosed in a lab?
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Not in routine culture, does not take up gram stain.
diagnosis by serology or PCR |
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Describe the physiology and structure of Pseudomonas aeruginosa (gram, shape, an/aer)
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gram negative
rod aerobic motile with polar flagella |
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Where does Pseudomonas aeruginosa like to live?
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likes wet, aerobic, warm environments
ubiquitous --> becomes an opportunistic infection where there is damage minimal growth requirements so can live in many environments likes to make biofilms on medical equipment |
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How is Pseudomonas aeruginosa recognized?
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aside from structure (gram negative, rod):
produces pigments forms mucoid colonies on culture plates easily grown in lab for diagnosis and characterization of antibiotic resistance patterns oxidase-positive, non-lactose fermenting sweet odor |
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What type of patients get chronic lung infection with Pseudomonas aeruginosa?
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patients with cystic fibrosis are very susceptible
also burn victims, corneal damage, ventilator associated pneumonia |
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What are three non-encapsulated pathogens of the human respiratory tract?
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Bordtella pertussis
Mycoplasma pneumoniae Legionella pneumophilia |
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Problems with treating Pseudomonas aeruginosa
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resistant to many antibiotics, antiseptics due to:
- beta-lactamases - mutations in porins reduce uptake - exchange of plasmas encoding resistance - reduced susceptibility of biofilms |
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Approaches to treating Pseudomonas aeruginosa
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do sensitivity testing is useful
anti-pseudomonal penicillins 4th generation cephalosporins fluoroquinolones combinations of antibiotics removing catheters |
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Describe the structure and physiology of Legionella pneumophila (gram, size, shape)
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gram-negative but does not stain well with gram stain
small coccobacilli has flagella |
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What is the metabolism of Legionella pneumophila
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nutritionally fastidious - doesn't grow on routine bacteriologic media
non-fermentative gets energy from amino acids |
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Why does Legionella pneumophila stain poorly with Gram stain?
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Has unusual phospholipid content in cell envelope
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What is the typical host of Legionella pneumophila?
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Thought to be amoebae.
Bacteria falsely recognizes macrophages in humans as its natural host |
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How does Legionella pneumophila use the macrophage environment to proliferate?
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Able to survive in intracellular vacuole, multiply and spread
Regulates host phagosome biogenesis and transport to suit the organism |
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Epidemiology of Legionella pneumophila
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outbreaks associated with water systems
- spreads by acquisition of contaminated water into respiratory tract by aspiration no person-to-person transmission |
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What are the 2 clinical diseases associated with Legionella pneumophila
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Legionnaires' disease
- cough, high fever, pneumonia - can get cardiac, GI, neuromuscular, renal complications - mortality > 15% Pontiac fever - acute, flu-like illness |
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Treatment of Legionella pneumophila
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macrolides
fluoroquinolones antibiotics must be able to penetrate into host cell --> beta-lactams are ineffective |
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How is Legionella pneumophila diagnosed?
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Samples from sputum, lower respiratory aspirates or biopsy
Fluorsecent antibody stain Urine antigen test Difficult to grow in culture |
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How are mycobacteria identified in a lab?
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Acid-fast stain is used.
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Are mycobacteria gram positive or negative?
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Classified with a gram positive group, but they do not respond to gram stain
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Describe the physiology and structure of mycobacteria
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Non-spore forming
Non-motile Rods Slow rate of replication Obligate aerobes |
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Describe the mycobacterial cell envelope
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- Waxy, lipid rich outer layer made of mycolic acids that act as a barrier to small molecules (this is why gram stain can't get in)
- Space b/w mycolic acids and cytoplasmic membrane - Thin layers of peptidoglycan and arabinogalactan - Porin channels |
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What are three distinctive properties related to the mycolic acids on the mycobacterial cell envelope?
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- imparts resistance to gram staining
- waxy coating provides resistance against drying, which is important for airborn transmission - mycolic acid biosynth is the target of one of the most important drugs for TB: INH |
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Where do mycobacteria like to grow and replicate?
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Within macrophages
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How do mycobacterium tuberculosis avoid being killed by their host cell?
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Mycobacterium tuberculosis stays within the phagocytic vesicle and prevents the vesicle from fusing with lysosomes
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Describe the immune response to mycobacterium tuberculosis
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Inflammatory aggregates of macrophages and T-cells called granulomas.
- might represent an attempt to "wall off" infection - caseous "cheese-like" necrosis often develops in the centers of the granulomas |
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What types of cells does an effective response to mycobacterium tuberculosis depend on?
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Cell-mediated immunity, since it's an intracellular pathogen.
Need TH1, CD4 cells, cytokines. |
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What types of immune system defects increase susceptibility to mycobacterium tuberculosis?
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defects in CD4+ responses, TNF blockade, and INF-gamma receptor defects
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About what fraction of the world's population are infected with mycobacterium tuberculosis?
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1/3.
Most are asymptomatic, have ~10% chance of developing active TB at some point |
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Epidemiology Main Points About TB
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- TB in the US increased with the AIDS epidemic
- Drug resistance is an increasing problem - Resistance to isoniazid and rifampin constitutes multi-drug resistance - Risk factors for TB include poverty, malnutrition, homelessness, institutional settings - Transmission by inhalation of aerosol droplet nuclei which remain airborne for prolonged periods |
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Describe the process of primary TB infection
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With coughing, tiny droplets are aerosolized from deep within the lung. They are small enough that liquid evaporates before they settle, leaving droplet nuclei that can remain suspended for hours. These small particles deposit deep into the lung in alveoli. There, it infects resident macrophages and recruits new macrophages to infect. From there, spread to lymph nodes by macrophages.
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What are the usual symptoms of a primary TB infection?
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Usually there are no signs/symptoms other than a positive PPD test
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Describe Latent Tuberculosis Infection
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- controlled primary infection w/o clinical disease
- no evidence of active TB in chest x-ray - not contagious - may get reactivated with aging or weakening of immune system |
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Where is the most common site for TB reactivation?
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Apices of the lungs
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What type of necrosis does TB typically cause in the lungs?
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Caseous necrosis. These regions coalesce to become cavities, where mycobacterium tuberculosis replicates to high concentrations. This makes them highly infectious.
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What are the symptoms of pulmonary TB?
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cough, sputum production (often with blood), shortness of breath
fever, chills, night sweats, fatigue, weight loss |
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What is miliary TB?
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progressive, disseminated TB, spread in lungs through blood. Causes a diffuse, millet-seed-like infiltrate on chest X-ray
systemic disease not limited to lungs, often fatal |
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What are some extrapulmonary expressions of TB?
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meningitis
GI infection lymphadentitis genitourinary disease skeletal TB |
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How is TB tested for today?
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tuberculin skin test (3-9 weeks after exposure)
IGRA testing |
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Describe TST
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measures a cell-mediated delayed hypersensitivity reaction to TB, but is subject to false positives and false negatives
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Describe IGRA
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more specific than TST but still may not be positive in patients with weakened immunity who have TB
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How is diagnosis of TB made in a lab?
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It takes 2-3 weeks to grow a colony.
Can use acid-fast stains on a smear |
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What principles do you need to keep in mind when treating TB?
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- prolonged course of therapy required (usually 6 months)
- drug resistance evolves readily in patients on monotherapy or are non-adherent (always use at least 3 drugs- usually use 4) |
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4 first-line drugs for TB and what they target
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Isoniazid - inhibits mycolic acid synthesis
Rifampin - inhibits RNA polymerase Pyrazinamide - inhibits recycling of stalled-ribosomes Ethambutol - inhibits cell well arabinogalactan synthesis |
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What are toxicities associated with Isoniazid?
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Hepatitis, peripheral neuropathy
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What are side effects associated with Rifampin?
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orange discoloration of bodily fluids, hepatitis, interactions with many other drugs
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What are side effects associated with Pyrazinamide?
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hepatitis, polyarthalgia (joint pain)
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What are side effects associated with Ethambutol?
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Decreased red-green color discrimination, decreased visual acuity
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Other Important Info About Treatment for TB
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- Sputum cultures may remain positive for several weeks, even if therapy is working
- LBTI treatment consists of a single drug (Isoniazid- aka INH) for 9 months to prevent reactivation - Resistance to first-line drugs is increasing - There are several second-line drugs, but they don't work as well |
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What is the typical treatment (with specific drugs) for TB?
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- Use all 4 drugs (INH, RIF, PAZ, EMB) for 2 months, followed by 4 months of INH and RIF
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Key Points About the BCG vaccine
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-Bacille Calmette-Guerin is a live attenuated vaccine for TB
- BCG provides poor protection against TB and can give a false-positive TST - BCG not given in US, but IS given in most other countries |
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Key Points About Nontuberculosis Mycobacteria
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- Encompasses a broad range of mycobacteria except Mycobacterium tuberculosis complex and mycobacterium leprae
- Prevalent in environmental sources such as soil, vegetation, and water - Some grow faster than mycobacterium tuberculosis, but still slower than many other pathogens - diseases include pulmonary infections, disseminated infections, cervical lymphadenitis, and cutaneous ulcers - treatment requires prolonged courses of several drugs |
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What are some challenges with studying mycobacterium leprae?
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It grows extremely slowly and cannot be cultured in vitro
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How is mycobacterium leprae transmitted?
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By nasal secretions or respiratory droplets
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What diseases does mycobacterium leprae cause?
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multibacillary leprosy
paucibacillary leprosy |
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How is multibacillary leprosy characterized?
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Lesions with many bacteria and few lymphocytes. Immune response is primarily TH2 cells, which are not very effective. These patients develop characteristic facial appearance of leprosy.
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How is paucibacillary leprosy characterized?
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Lesions with few bacteria and many lymphocytes. These patients mount a more effective TH1 response, and have well-formed granulomas and less severe disease.
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How is leprosy treated?
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Therapy with rifampin, dapsone, clofazimine.
Takes years. |
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What are GI Tract defenses against bacteria?
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mucus layer (protects from chem, phys damage; adhesions for microbes; ejection of microbes with peristalsis; has IgA)
acidic environment peristalsis secretion of bile salts indigenous flora antimicrobial peptides (nonspecific defense) |
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What are some parts of body that have lots of bacteria?
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GI tract, oral cavity, vagina
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What are some parts of body that are relatively sterile?
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urinary tract, lung, brain
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What are some roles of indigenous microbes?
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Exclusion of exogenous pathogens
Development of immune function Tissue and organ differentiation, dev Provision of nutrients, vitamins Detoxification of harmful dietary contents Prevention of bowel cancer? |
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Important Point
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Any organism can become a pathogen out of context
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Three examples of GI Bacteria that do not cause diarrhea
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Bacteroides fragilis
Helicobacter pylori Enterococcus |
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Describe Bacteroides fragilis (gram, size, shape, an/aer)
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gram negative
rod varying size and shape obligate anaerobe polysaccharide capsule |
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What is the function of Bacteroides fragilis's polysaccharide capsule?
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Adherence to peritoneal surfaces
Protection from phagocytosis Synergistic action with E. coli in abscess formation Increases populations of Th17 cells --> diminishes T-cell response (this can be good- might diminish IBD and therefor cancer) |
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What is the significance of LPS in Bacteroides fragilis?
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Lacks lipid A group --> not seen well by toll-like receptor --> immunologically impotent
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Epidemiological points about Bacterial fragilis
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- universally present in microbiota of humans
- associated with ruptured viscus associated infections |
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How is Bacteroides fragilis diagnosed in a lab?
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Grows readily in anaerobic culture
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What clinical diseases does Bacteroides fragilis cause?
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Polymicrobial infections causing peritoneal, intraabdominal, liver abscesses
Gynecologic abscesses |
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How is Bacteroides fragilis treated?
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Metronidazole
Beta-lactam with beta-lactamase inhibitor Carbapenem |
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What is the physiology and structure of Helicobacter pylori?
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gram negative
spiral rods highly motile with polar flagellae |
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What is the pathogensis of Helicobacter pylori?
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moves through mucin by decreasing viscosity --> attaches to mucosa, populates mucosal surface
tends to cause long, slow, persistent infection |
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How does Helicobacter pylori cause a long term infection?
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disrupts tight junctions of epithelial cells, allowing nutrients to leak into mucus layer.
IL-8 production attracts neutrophils, which further disrupt tight junctions |
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What diseases are caused by Helicobacter pylori?
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About 95% of all peptic ulcer disease
Atrophic gastritis Gastric cancer (from chronic gastritis) MALT lymphoma |
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How is Helicobacter pylori diagnosed in a lab?
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Difficult to culture. Use antigen detection immunoassays in stool.
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What is the treatment for Helicobacter pylori?
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Proton pump inhibitors
Macrolide antibiotic Beta Lactam antibiotic |
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What is the physiology and structure of enterococcus?
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gram positive cocci in pairs and short chains
alpha and gamma hemolytic facultative anaerobes (don't need O2) able to live in high NaCl and bile salt concentrations |
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What are the two major species of enterococcus?
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Enterococcus faecium
Enterococcus faecalis |
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How does enterococcus acquire resistance to vancomycin?
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detection of vancomycin triggers operon which replaces an amino-acid sequence with a different one
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What antibiotics does enterococcus have resistance to?
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Intrinsic resistance:
cephalosporins, oxacillin, trimetroprim-sulfamethoxazole Acquired resistance: vancomycin, aminoglycosides |
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How is enterococcus typically transmitted?
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In hospital, often involving catheters
Infections are from self or transmitted |
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What are risk factors for enterococcus infection?
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Broad spectrum antibiotics, especially cephalosporins and vancomycin
Immunocompromise Prolonged hospitalization |
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How does pathogenesis of enterococcus by catheter typically happen?
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commonly found in GI tract, but antibiotics leads to colonization of skin --> gains access to blood stream or urinary tract by catheter
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What kind of diseases does enterococcus cause?
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Cather-related (CLABSI)
UTI Endocarditis (inflammation of lining of heart) Hardware infections (prosthetic joints, spinal fusions) DOES NOT CAUSE PNEUMONIA |
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How is enterococcus diagnosed in lab?
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grows easily on blood agar and chocolate agar
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How is enterococcus treated?
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Ampicillin
If resistant to ampicillin, vancomycin If vancomycin resistant. linezolid or daptomycin, chloramphenicol |
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3 Diseases Caused by Vector Borne Bacterial Agents
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Lyme Disease
Rocky Mountain Spotted Fever Plague |
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What is the typical vector transmission of a pathogen?
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between vector and a main reservoir
humans are accidental hosts, and usually a dead end for the pathogen |
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What is the infectious agent of Lyme disease?
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Borrelia burgdorferi
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How does expression of outer surface proteins of Borrelia burgdorferi change when a tick is feeding and when it isn't
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In unfed ticks, expression of OspA (outer surface protein A) is high, helping Borrelia bind to tick midgut
During tick feeding, OspA production decreases, and the pathogen migrates to tick salivary glands During tick feeding, OspC production increases. The hypothesis is that OspC, with tick Salp15, have immunosuppressive effects on the mammal the tick is feeding on. This allows the bacteria to spread to the mammal. |
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What are the vectors for Lyme disease?
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A black legged tick
Ixodes scapularis (deer tick) in NE, N-Central US Ixodes pacificus on Pacific Coast |
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Why is it important to remove ticks within 24 hours?
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The chance of becoming infected with Lyme disease is much higher after the tick has fed for 2-3 days
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When do most cases of Lyme disease occur and why?
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Summer
Nymph form of the tick is most likely to transmit bacteria to humans, and it feeds during late spring, early summer |
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What are the life stages of a tick and when does it take blood meals?
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Larvae --> nymphs --> adults --> lay eggs
eats a blood meal at each stage |
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What's going on with Lyme disease and tick vectors on the West coast?
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On West Coast:
I. neotomae is main vector for Borrelia burgdorferi, but does not usually bite humans. I. pacificus do bite humans, but usually are not infected b/c they feed on lizards, which are immune to Borrelia burgdorferi. However, if they can't find lizards, they feed on woodrats, which do get infected. |
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Where is Lyme disease most often found in the US?
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NE and mid-Atlantic states
Upper north-central states NW California |
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What is the structure and physiology of Borrelia burgdorferi
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Spirochete (corkscrew)
Gram negative Have flagella, highly motile Extracellular pathogens Do not produce toxin |
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What is significant about the Borrelia burgdorferi genome?
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Much of it is on plasmids
Huge proportion is dedicated to lipoproteins, many of which are on bacterial surface. - This shows how important attachment is to Borrelia's life cycle |
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How does Borrelia burgdorferi cause disease?
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Probably by migrating through tissues, adhering to host cells, evading host immune system
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Where does Borrelia burgdorferi attach in mammalian host?
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a variety of tissues, including: lymphocytes, platelets, epithelial cells, endothelial cells, neuroglia, maybe more. can bind to cell and ECM.
Uses a different set of binding proteins in mammalian host. |
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What are the early clinical manifestations of Lyme disease?
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bull's eye rash on 70-80% of patients (called erythema migrans)
rash usually appears 7~14 days after tick bite accompanied by fever, fatigue, headache, muscle ache |
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How does Lyme disease get disseminated early on?
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By cutaneous, lymphatic, blood-borne routes
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What are signs of early disseminated Lyme disease?
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secondary rash, facial palsy, muscle aches, headaches, fever, fatigue
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What are symptoms of late disseminated Lyme disease?
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intermittent swelling, pain of one or a few joints (often knee)
could also get neurological disease: ataxia, memory loss, mood changes, sleep disturbances - happens weeks or months after the tick bite |
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How does Borrelia burgdorferi persist for a long time in the host?
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-SalP15 (from tick) and OspC (from bacteria) work to protect bacteria during initial transmission to mammal from antibodies
- avoidance of complement-mediated killing by binding a host negative regulator, protein H, of the complement cascade. Borrelia produces a family of CRASPs (complement regulator- acquiring surface proteins) to assist with this. Since it is coated with protein H, it avoids complement. - antigenic variation of surface molecules - hiding in immune privileged sites |
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How is Lyme disease diagnosed?
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- Bull's eye rash
- Headache, muscle, or joint pain in summer (w/o GI or respiratory symptoms) - Laboratory confirmation of infection with ELISA followed by Western blot |
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What is the downside of using an antibody test to check for an infection?
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- It takes time before body has made an immune response
- Positive antibodies does not distinguish b/w someone who has been exposed and someone with an active infection |
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How is Lyme disease treated?
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Doxycycline for early/disseminated infection
Amoxicillin is 2nd choice IV antibiotics for late disseminated disease involving neurologic abnormalities |
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What is treatment resistant arthritis due to Lyme disease?
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About 10% of Lyme arthritis patients experience persistent joint pain for months or years after it seems that the bacteria is gone. This may be caused by an autoimmune reaction.
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What is the pathogen that causes Rocky Mountain Spotted Fever?
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Rickettsia rickettsii
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Is Rickettsia rickettsii gram positive or gram negative and what is its shape?
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gram negative bacillus
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Where does Rickettsia rickettsii like to live inside the host?
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obligate intracellular pathogen
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When do most cases of Rocky Mountain Spotted Fever occur?
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Summer
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Where do most cases of Rocky Mountain Spotted Fever Occur?
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US, southeast
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How is Rickettsia rickettsii transmitted to humans?
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The pathogen is spread by ticks. Small wild animal rodents serve as the reservoir, with humans as accidental hosts.
Infection of the mammalian host starts when bacteria deposited on the skin as the tick feeds. The bacteria gains entry from the host scratching the site. |
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What are the symptoms of Rocky Mountain Spotted Fever?
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Sudden headache
fever chills muscle aches Characteristic spotted red rash that starts on the periphery of body and spreads to trunk |
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How does Rickettsia rickettsii spread through the host body?
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Via the blood stream.
The bacteria attach to vascular endothelial cells and induce their own uptake. They can spread into adjacent endothelial cells or exit by lysing the cell. |
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How are the characteristic spotted red spots of Rocky Mountain Spotted Fever created by the pathogen?
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Damage to the cell membrane of vascular cells when Rickettsia rickettsii lyses the cells leads to leakage of red blood cells, which cause the spots.
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What happens if Rocky Mountain Spotted Fever is untreated?
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The bacteria destroy the blood vessels and patient dies
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How does Rickettsia rickettsii move to the periphery of the host cell and make finger-like projections?
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Using the host cell's actin
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How is Rocky Mountain Spotted Fever Treated?
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tetracycline, chlroamphenicol, or fluoroquinolones
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What is the pathogen that causes the Plague?
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Yersinia pestis
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Is Yersinia pestis gram positive or gram negative?
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gram negative
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Where does yersinia pestis like to grow?
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Capable of intracellular survival and replication in macrophages
Also grows extracellularly, especially late in infection |
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What does yersinia pestis look like in blood?
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safety pins
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What is the main vector for yersinia pestis?
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oriental rat flea
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What happens to a flea when it is infected with yersinia pestis?
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Yersinia colonizes the mid-gut of the flea and grows in high numbers there, forming a biofilm. It blocks the ability of the flea to ingest blood, making the flea hungry, which makes it try to feed more often.
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How does a flea infect a mammalian host with yersinia pestis?
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When an infected flea feeds on mammalian blood, it regurgitates the blood back into the wound.
Normally fleas feed on rodents, but if the rodents die they may turn to people. |
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What happens in humans soon after infection with yersinia pestis?
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The bacteria travels to lymph nodes, causing them to swell and become hemorrhagic within a week after initial infection.
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What are symptoms of the plague?
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swollen, infected lymph nodes called buboes
high fever chills headache extreme exhaustion |
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What happens in humans if infection with yersinia pestis is untreated?
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The bacteria can spread through the blood stream, producing a systemic infection that is very dangerous and often fatal.
If the bacteria reach the lung, you get pneumonic plague, which can be passed directly to humans by airborne transmission. Pneumonic plague results in dangerous epidemic conditions. |
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Describe Yersinia pestis's virulence factors
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When Yersinia transitions to a mammalian host, the increase in temperature triggers the production of virulence factors which allow it to grow extracellularly while avoiding phagocytosis.
Virulence factors include: - production of capsule - Type Three Secretion System |
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What is type three secretion system?
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A way for yersinia pestis to inject bacterial effector molecules directly into the cytosol of the host cell. These proteins prevent phagocytosis and siow the inflammatory response of the host cell.
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How is plague diagnosed?
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Gram stain of buboes, blood, spinal fluid
Fluorescent-antibody test against unique envelope antigen |
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How is plague treated?
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Streptomycin or tetracycline
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What are the 3 most common enteric pathogens?
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Campylobacter (most common)
Salmonella Shigella |
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What are the 3 general pathogenic mechanisms for development of bacterial gastoenteritis?
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- Ingestion of preformed toxin with rapid onset of illness
- Ingestion of organisms that produce toxins in vivo that cause disease - Infection by enteroinvasive organisms with delayed onset of illness |
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How do bacteria trigger a pro-inflammatory response in intestinal epithelial cells?
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- Bacteria can be detected by epithelial cells through cell-surface receptors or endocytosis of microbial products.
- This leads to a signalling cascade which leads to transcription of pro-inflammatory genes |
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How does staphylococcus aureus cause food poisoning?
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Ingestion of preformed toxin.
There are 24 staphylococcal enterotoxins- they are highly stable and resist degradation in intestinal tract |
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What is the clinical presentation of Staphylococcus aureus food poisoning?
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sudden onset of vomiting and diarrhea within hours. usually self-limited and lasts < 24 hours
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What is the morpholoy of Baciulls cereus?
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gram positive
rods spores facultative anaerobe |
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How is Bacillus cereus diagnosed?
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catalase positive
beta hemolytic motile test by culture of food samples, detection of toxins in food |
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How does Bacillus cereus cause food poisoning?
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Ingestion of preformed toxin or ingestion of large number of organisms followed by toxin production
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What are the symptoms of Baciulls cereus GI infection?
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- preformed toxin causes: nausea, vomiting within 1-6 hours of ingestion. lasts <24 hours
- ingestion of organism causes diarrhea, cramps, vomiting within 8-16 hours. May last several days. Both are self limited illnesses. |
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What is the morphology of Clostridium perfingens
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gram positive
rods spores obligate anaerobe |
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How is Clostridium perfingens diagnosed in a lab?
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beta-hemolytic
test by culture of food samples, detection of toxins in food |
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How does Clositridium perfingens cause GI infection?
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ingestion of organism followed by production of enterotoxin (Type A), damages intestinal epithelium --> electrolyte imbalance and fluid accumulation
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What are the symptoms of infection with Clostridium perfingens?
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diarrhea, cramps, vomiting within 8-16 hours
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What is the structure of Shigella species?
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gram negative
rods facultative anaerobe |
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How is Shigella diagnosed in a lab?
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oxidase-negative
non-motile non-lactose fermenter test by stool culture |
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How does Shigella cause GI infection?
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crosses M cells of Peyer's patches, apoptosis of macrophages
this lets bacteria escape into tissues, followed by cell-cell spread using actin low infectious dose (ie, highly infectious) affects primarily the distal colon, causing acute mucosal inflammation and erosion and purulent exudate |
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What are the symptoms of Shigella GI infection?
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abdominal cramps, bloody, mucoid diarrhea, high fever, vomiting within 1-3 days
segment of infected colon has pale, granular, inflamed mucosa with patches of coagulated exudate |
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What is the epidemiology of Shigella?
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3rd most common enteropathogen in US
higher risk in day care centers and crowded areas Most infections in US are caused by S. sonnei |
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What is the structure of Salmonella?
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gram negative
rods facultative anaerobe |
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How is Salmonella diagnosed in a lab?
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oxidase negative, motile, non-lactose fermentor,
test by stool culture |
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What are the two species of Salmonella and which contains the most important human strains?
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S. enterica (subspecies I has the most important human strains)
S. bongori |
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How does Salmonella cause GI infection?
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crosses M cells, apoptosis of macrophages causes inflammation
within macrophages, modifies vacuoles to support survival invades epithelial cells basolaterally/ disseminates systematically, enters epithelial cells directly or through dendritic cells large infectious dose |
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What is the epidemiology of Salmonella infection?
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2nd most common enteropathogen in US
typhoidal and non-typhoidal strains transmitted through fecal-oral route |
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What are the symptoms of Salmonella infection?
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gastroentiritis within 1-3 days
enteric fever, bacteremia, endovascular infection, osteomyelitis (bone/bone marrow infection), abscess, typhoid fever non-typhoidal is usually self-limited- fever generally resolves within 48-72 hours, diarrhea within 4-10 days |
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What are the clinical symptoms of typhoidal Salmonella?
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abdominal pain, rash (rose spots on trunk and abdomen)
there may be hepatosplenomegaly, intestinal bleeding and perforation, secondary bacteremia, peritonitis |
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What is the structure of Campylobacter jejuni?
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gram negative
curved rods microaerobic (5% O2) |
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How is Campylobacter jejuni diagnosed in a lab?
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oxidase positive
catalase positive test by stool culture, gram stain of stool sample |
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How does Campylobacter jejuni cause GI infection?
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acute inflammatory enteritis, edema in mucosa
in small intestine, appendix and colon: causes villus blunting, multiple superficial ulcers, mucosaal inflammation, purulent exudate |
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What are the symptoms of Campylobacter jejuni?
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fever, cramps, diarrhea within 1-3 days, lasting several days - 1 week
Guillain-Barre syndrome is a rare complication infection is generally self-limited |
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What is the most common cause of Traveler's diarrhea?
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enterotoxigenic E. Coli (ETEC)
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What are the six types of diarrheagenic E. Coli?
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Enterotoxigenic E. Coli (ETEC)
Enteropathogenic E. coli (EPEC) Enterohemorrhagic E. coli (EHEC) Enteroinvastive E. coli (EIEC) Enteroaggregative E. coli (EAEC) Diffusely adhering E. coli (DAEC) |
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What is the structure of E. coli?
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gram negative
rods |
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How is E. Coli diagnosed in a lab?
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oxidase negative
lactose fermenter grows on blood agar test by stool culture to detect specific toxin for some strains EHEC can be detected using cultue and immunologic assays Some strains are difficult to diagnose outside research settings |
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What is the pathology of Enterotoxigenic E. Coli?
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adheres to small intestine enterocytes
produces a cholera-like-heat-labile (easily destroyed by) and/or heat-stable enterotoxins |
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What is the epidemiology of Enterotoxigenic E. coli?
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contaminated water, food, childhood diarrhea in developing countries, causes travelers' diarrhea
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What are the symptoms of Enterotoxigenic E. coli?
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watery diarrhea
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What is the pathology of Enteropathogenic E. coli?
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adheres to small intestine enterocytes
destroys microvilli pedestal formation (when attaches to the surface of a cell, they modify the surface and form a very firm attachment, which looks like a pedestal - the membrane of the cell extends upwards, and forms a base to which the organism is attached) |
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What is the epidemiology of Enteropathogenic E. coli?
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person-person spread
causes infantile diarrhea |
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What are the symptoms of Enteropathogenic E. coli?
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severe watery diarrhea and vomitting
may be persistent |
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What is the pathology of Enterohemorrhagic E. Coli?
|
adheres to large intestine
Shiga toxin- systemic ingestion of this can cause life-threatening complications |
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What is the epidemiology of Enterohemorrhagic E. Coli?
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contaminated water or food, person to person contact, major cause of bloody diarrhea in develped countries
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What are the symptoms of Enterohemorrhagic E. Coli?
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watery, bloody diarrhea for up to 5 days, hemolytic uremic syndrome (toxic substance destroys RBCs, causing kidney injury)
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What is the pathology of Enteroaggregative E. coli?
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adheres to small and large intestine epithelia, forms biofilm, enterotoxins
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What is the epidemiology of Enteroaggregative E. coli?
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contaminated food, outbreaks in developed countries
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What are the symptoms of Enteroaggregative E. coli?
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watery diarrhea
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What is the pathology of Enteroinvasive E. coli?
|
invades colonic epithelial cell, moves from cell to cell using actin
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What is the epidemiology of Enteroinvasive E. coli?
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chronic diarrhea in developing countries
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What are the symptoms of Enteroinvasive E. coli?
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persistent mucoid diarrhea, sometimes bloody
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What is the pathology of diffusely adhering E. coli?
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signal transduction in small intestine enterocytes, growth of cellular projections
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What is the epidemiology of diffusely adhering E. coli?
|
diarrhea in older children in developing countries
mode of transmission unknown |
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What is the structure of Clostridium dificile?
|
gram positive
rods spores obligate anaerobe |
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How is Clostridium dificle diagnosed in a lab?
|
Tcd A is detected in stool samples using an immunoassay
TcdB can be detected in immunoassay or bioassay |
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What is the pathology of Clostridium dificile?
|
2 enterotoxins, called TcdA and TcdB, target Ras proteins, causing cytopathic effects
Both toxins disrupt tight junctions of epithelia and enhance migration of neutrophils into intestines |
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What is the epidemiology of Clostridium dificile?
|
Common cause of antibiotic-associated diarrhea in hospital setting, also community acquired.
Antibiotics often open a spot for C. dificile to get in- it's an endoginous infection |
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What are the symptoms of Clostridium dificile?
|
There is a wide spectrum of illness.
mild-to-severe watery diarrhea, fever, cramps, leukocytosis, pseudomembranous colitis, toxic megacolon |
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How is Clostridium difficile treated?
|
oral vancomycin - but many patients experience relapse
metronidazole many alternative strategies including treatment with probiotics |
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What is blood agar used for diagnostically?
|
To determine if an organism is alpha (partially), beta (fully), or gamma (not at all) hemolytic
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What is MacConkey agar used for diagnostically?
|
isolates common enteric gram-negative bacteria (gram-positive can't grow on it)
Differentiates b/w lactose fermentors (produce pink colonies) and non-lactose fermentors (colorless) |
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What is Hektoen enteric agar used for diagnostically?
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detects Salmonella and Shigella
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What is Sorbitol-MacConkey agar used for diagnostically?
|
detects E. Coli O157 (a subspecies of EHEC)
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What is unique about the conditions under which a culture is incubated to look for Campylobacter jejuni?
|
The plates are incubated in an environment containing 5% oxygen
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Which bacterial agent that causes diarrhea would you want to do a gram stain in order to detect?
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Campylobacter jejuni, because it has a distinctive shape
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What is mycosis?
|
a fungal infection in or on a part of the body; a disease caused by a fungus
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What are some cellular properties of fungi?
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eukaryotes
not plants (no chloroplasts/chlorophyll) have cell walls cell walls made of chitin and glucan (NOT peptidoglycan) no cholesterol- instread have ergosterol grow more slowly than bacteria larger than bacteria |
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What is a yeast?
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A unicellular fungus
oval shaped or round reproduces by budding or fission |
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What is a mold?
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A multicellular fungus
Grow as thin, threadlke structures called hyphae Makes spores Septae are walls between adjoining cells |
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What is a dimorphic fungus?
|
Exists as a mold in nature
Exists as a yeast at 37 degrees Celsius in animals |
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Where do molds elongate?
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At this tips
(this is where new cell wall material is produced, and a good target for drugs) |
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How do molds reproduce?
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Generate special structures with spores at tips. These tips can easily become airborne, are quite stable, and can spread wide distances and be inhaled
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What are the two typical approaches to diagnosing a fungus in a lab?
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- Growing a culture of the organism (most sensitive but can take awhile)
- Looking under a microscope (useful, since fungi have distinctive shapes) |
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What are the three main targets for antifungal therapy?
|
Cell membrane - generally targets ergosterol
DNA synthesis Cell wall- obvious target since mammals don't have cell walls |
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What are polyene antibiotics?
|
They bind directly to ergosterol, forming channels in the cell membrane that disrupt osmotic integrity of the cell
Tend to be fungicidal |
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What are the two most important polyene drugs?
|
Amphotericin B
Nystatin (used topically) |
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Tell me about Amphotericin B
|
Has very broad activity
Fungicidal Poor penetration into joints, CNS VERY TOXIC- used it when you have something very bad Administered by IV Lipid-formulated version: much more expensive but reduced side effects |
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What are the two classes of drugs that target the fungal cell membrane?
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polyenes
triazoles |
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What do triazoles do to fungi?
|
they prevent the synthesis of ergosterol
tend to be fungistatic |
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What are the two most commonly used triazoles?
|
fluconazole- used a lot!
voriconazole - a newer drug |
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What are echinocandins?
|
Class of antifungals that target the cell wall
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What is the most important echinocandin?
|
Caspofungin
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How does Caspofungin damage the fungal cell wall?
|
It inhibits the enzyme that produces glucan, a major constituent of the cell wall
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Tell me about Capsofungin
|
administered as IV only
most common side effects are infusion related generally well-tolerated |
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What is flucystosine?
|
An antifungal that inhibits DNA synthesis
Our cells lack the enzyme it acts on |
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What are side effects of prolonged use of flucystine?
|
bone marrow suppression, hair loss, abnormal LFTs
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What are dermatophtes?
|
Fungi that cause cutaneous infections
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What are two "true" (ie, not opportunistic) fungal pathogens?
|
Histoplasmosis (Ohio Valley Fever)
Coccidiomycosis (San Joaquin Valley Fever) |
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How do primary fungal pathogens gain entry into human hosts?
|
They are inhaled as spores and initially infect the lung
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What are two kinds of primary fungal pathogens?
|
Histoplasma capsulatum
Coccidiodes immitis |
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How do superficial mycoses spread from host to host?
|
skin to skin contact with contaminated skin. chronically moist skin is a risk factor
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How do virulence factors in fungi generally differ from virulence factors in bacteria?
|
In fungi, the tissue damage usually results from the immune response
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What are three opportunistic fungal pathogens, and which is the most frequent?
|
Candida - the most common- a yeast
Cryptococcus neoforman - a yeast Aspergillus - a mold- very nasty |
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What parts of the innate and adaptive immune system are most important for protection from fungi?
|
innate- integrity of barriers, respiratory cilia
adaptive- cell mediated immunity |
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What is the structure of Candida?
|
a yeast, but can form hyphae
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Where and when does Candida cause disease?
|
Candida is frequently found as normal flora in mouth and gut.
Immunosuppression can lead to disease. If Candida gets into bloodstream, can form microabcesses anywhere- lesions in retina often happen Causes oral thrush in mouth/throat, esophageal, and vulvovaginal infection |
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What are the typical clinical features of Candida albicans infection?
|
fever, skin lesions, retinitis, endocarditis, microabcessses in any organ.
get a thick white growth with oral thrush |
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How is Candida treated?
|
flucanazole
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What is the structure of Cryptococcus neoformans?
|
has a polysaccharide capsule that is quite large, giving it a halo appearance under the microscope
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Where does Cryptococcus neoformans like to grow?
|
Likes nitrogen rich areas, such as soil and bird droppings
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How do humans typically get infected with Cryptococcus neoformans?
|
It is inhaled. Not very virulent, so the amount of infection matters.
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What are the symptoms of Cryptococcus neoformans infection?
|
Often relatively asymptomatic- can cause respiratory symptoms like cough, fever
Inflammatory response might cause formation of nodules ***If it gets in bloodstream, it likes to go to the CNS and causes meningitis. This is fatal if not treated. Symptoms of this include: stiff neck, mental status changes, visual and hearing loss**** |
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How is Cryptococcus neoformans diagnosed in a lab?
|
Can do direct microscopic examination if you have tissue.
Can do a serologic test to detect antibodies to bits of polysaccharide capsule that have broken off. |
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How is Cryptococcus neoformans treated?
|
treatment for systemic infection requires amphotericin B and flucytosine for two weeks, followed by longterm fluconazole
AIDS patients often take fluconazole as a prophylaxis for it |
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What is the structure of Histoplasma?
|
dimorphic- so it is a mold in nature where it produces spores to be inhaled, and a yeast in humans
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Where in humans does Histoplasma like to grow?
|
in macrophages
this is unusual- it is the only significant intracellular fungal pathogen |
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Where in nature does Histoplasma like to grow?
|
moist soil that has high nitrogen content
most prevalent in eastern and central regions of US |
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What is the pathogenesis of Histoplasma?
|
inhalation of spores from disturbed soil
spores germinate to yeast in the lungs may stay localized or spread via lymphatics intensity of exposure and immune status are important- but it can infect healthy people |
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|
What is the name of the disease caused by Histoplasma capsulatum?
|
Histoplasmosis, aka Ohio Valley Fever
|
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|
What are the symptoms of Histoplasmosis?
|
70-90% of infections are asymptomatic
When symptomatic, most often an acute self-limited pulmonary infection with flu-like symptoms Rarely, progressive disease develops with marked tissue destruction Can sometimes cause chronic disease Can disseminate in severely immuno-compromised people |
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How is Histoplasma diagnosed in a lab?
|
microscopic identification of intracellular yeast
culture can take 2-3 weeks can detect polysaccharide antigen in urine- esp if disease is disseminated |
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|
How is Histoplasma treated?
|
Usually self-limited and not treated
For severe cases or immunocompromised individuals, use itraconazole and amphotericin followed by itraconazole |
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|
Where does Coccidiomycosis like to live in nature?
|
In dry soil, in SW US
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|
What is the structure of Coccidiodes?
|
block-like artoroconidia in nature, spherules containing endospores in lungs
|
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How do people become infected with Coccidiodes?
|
Arthrospores inhaled from dust, create spherules and nodules in lung. When spherules rupture, they release spores which spread and start the process again
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|
What is the name of the disease caused by Coccidiodes?
|
Coccidiomycosis, aka (San Joaquin) Valley Fever
|
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|
What are the symptoms of Coccidiomycosis?
|
60% of cases are asymptomatic
When causes symptoms: flu-like, usually self-resolves, can get a cough chest film shows infiltrates with nodules disseminated disease is rare, but can cause almost any organ, ESPECIALLY MENINGES- can be fatal if not treated |
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|
How is Coccidiodes diagnosed in a lab?
|
often misdiagnosed
Culture is slow Microscopic examination can be good b/c of distinct appearance |
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|
How is Coccidiomycosis treated?
|
self-limited infections do not require treatment
for disseminated disease or patients with risk factors: amphotericin B plus an azole, then treat with the azole for a year |
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|
What is the structure of Aspergillus?
|
mold, has acutely branching hyphae with septae
|
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|
What is the difference between aspergillus and mucor?
|
mucor lacks septae
|
|
|
What is the pathology of aspergillus?
|
infection usually occurs in lungs. spores germinate in lungs and form fungal balls- can colonize sinuses, ear canals, eyelids, conjunctiva
aspergillus can blast through blood cells, leading to hemorrhage and necrosis |
|
|
What is aspergilloma?
|
when aspergillus infection remains localized, it is called aspergilloma.
It forms a fungal ball which can be seen on chest films and scans. Sometimes need surgical resection to remove fungal balls |
|
|
What are the symptoms of Aspergilloma?
|
often asymptomatic
can cause blood in sputum, chest pain, shortness of breath |
|
|
What is invasive Aspergillosis?
|
Very bad news
Incredibly destructive Can get infarction, necrosis Lung infection is common and what patients typically die from |
|
|
How is invasive Aspergillosis treated?
|
early diagnosis is essential
amphotericin B and voriconazole |
|
|
How is Aspergillosis diagnosed in lab?
|
early diagnosis is essential --> culturing is ineffective
need tissue to visualize fungus |
|
|
What are the symptoms of cutaneous mycoses?
|
long infection period followed by localized inflammation and allergic reactions to fungal proteins
|
|
|
What are risk factors for cutaneous mycoses?
|
moist, chafed skin
|
|
|
How are cutaneous mycoses typically treated?
|
topical antifungals such as nystatin
|
|
|
What are some gender differences in terms of STD infection?
|
Women are biologically more susceptible to STD infection, often asymptomatic or minimally symptomatic, and more likely to suffer more frequent and serious health complications
|
|
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What leads to adolescent females being more susceptible to gonorrhea and chlamydia infection?
|
they do not have full cervical maturity
also, might not have same access to healthcare services, have experienced sexual trauma, don't discuss sex at routine physicals |
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What are the clinical symptoms of cervicitis in women?
|
Lower Reproductive Tract infection --> cervical neoplasia
|
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|
How do cervitis and vaginitis affect the upper reproductive tract?
|
Infections can ascend from lower to upper reproductive tract
In upper reproductive tract, can cause fetal wastage, low birth weight, congenital infection, infertility, ectopic pregnancy, chronic pain, recurrent infection |
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|
What are the two most common bacterial STDs?
|
gonorrhea
chlamydia |
|
|
What is the structure of Neisseria gonorrhoeae?
|
gram negative
diplococci, resembles coffee beans |
|
|
How is Neisseria gonorrhoeae diagnosed?
|
aerobic
in men, test by gram stain of urethral discharge requires special media and 5% CO2 for isolation in culture in men and women PCR and other nucleic acid amplification tests (NAATs) combination NAAT assays for gonorrhea and chlamydia urine or swab based diagnostics |
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What is the pathology of Neisseria gonorrhoeae?
|
Attaches to mucosal cells via pili and Opa protein
Infects subepithelial space Lipoogliosaaccharide stimulates inflammatory response Por protein allows it to evade destruction by phagolysosome Antigenic mutation makes immunity impossible |
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What is the epidemiology of Neisseria gonorrhoeae?
|
Spread by direct mucosal contact with infected membranes or fluids
6-7x higher prevalence in adolescents does not survive well outside the body |
|
|
What are the symptoms of Neisseria gonorrhoeae?
|
What isn't a symptom???
in men: urethritis and epididymitis in women: mucopurulent cervicitis, pelvic inflammatory disease, dysuria (pain with urination), pyuria (pus in urine), Fitz Hugh-Curtis syndrome (a complication of PID) in both: conjunctivitis, anorectal infection, pharyngitis, sequelae of disseminated gonococcal infection (joint lesions, arthritis), Reiter's syndrome (arthritic, conjunctivitis, urethritis, skin lesions) |
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|
What are the symptoms of chlamydia infection?
|
Very similar to gonorrhea- minus pharyngitis, disseminated gonococal infection, and plus neonatal syndrome
depending on the serotype, can cause eye disease, genitourinary disease, or lymphogranuloma venereum chronic infection is asymptomatic and causes tubal infertility, lymphogranuloma venereum (inguinal lymphadenopathy, proctitis [inflammation of rectum], fever, tenesmus [feeling of needing to poop], bleeding, rectal pain) same as gonorrhea: in men: urethritis and epididymitis in women: mucopurulent cervicitis, pelvic inflammatory disease, dysuria (pain with urination), pyuria (pus in urine), Fitz Hugh-Curtis syndrome (a complication of PID) in both: conjunctivitis, anorectal infection, Reiter's syndrome (arthritic, conjunctivitis, urethritis, skin lesions) |
|
|
What is the structure of Chlamydia trachomatis?
|
gram negative
bacilli |
|
|
How is Chlamydia trachomatis diagnosed in a lab?
|
grows on living cells/tissue only
test by nucleic acid amplification tests non-culture based diagnostics are preferred can do combined NAAT tests for both gonorrhea and chlamydia urine or swab based diagnostics |
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|
What is the pathology of Chlamydia trachomatis?
|
obligate intracellular pathogen
infectious elementary body enters cells, replicates as reticulate body receptors for elementary body are only found in mucous membranes of: urethra, endocervix, endometrium, Fallopiuan tubes, anorectum, respiratory tract, conjunctiva destroys host cells stimulates inflammatory response no lasting immunity inflammatory response with re-infection is strong, can lead to end organ damage (ex: blindness, sterility) |
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In what two forms does Chlamydia trachomatis exist?
|
Elementary body: infectious form
Reticulate body: noninfectious intracellular form that promotes replication |
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What is the epidemiology of Chlamydia trachomatis?
|
Humans are only natural hosts
Disease spread by: - direct mucosal contact with infected membranes of fluids - congenital Most commonly reported infectious disease in US 75% of women, up to 50% of men are asymptomatic --> can cause infertility, spread of disease screening is essential! |
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|
What is the treatment for Chlamydia trachomatis?
|
single-dose azithromycin or 7-day regimen of doxycycline
screening is essential |
|
|
What is the treatment for Neisseria gonorrhoeae?
|
single dose ceftriaxone, other cephalosporins
spectinomycin for those allergic fluoroquinolone resistance increasingly common treat for chlamydia too if not ruled out |
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|
What is silent pelvic inflammatory disease?
|
Chlamydia can last for as long as 2 years in female genital tract. Asymptomatic infection is thought to be the leading cause of rising rates of tubal infertility
|
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|
What is urethritis? What are its symptoms? What are some common causes? (yes, this is a lot of questions for one card)
|
In males
signs/symptoms: dysuria (painful urination), discharge, burning usually (but not always) gonococcal or chlamydia- can distinguish by gram stain since have different shapes |
|
|
How is the cause of urethritis diagnosed?
|
gram stain can tell you if it's gonorrhea (diplococci- coffee bean shape)
use culture or nucleic acid amplification to confirm diagnosis |
|
|
What is epididymitis? What are its symptoms?
|
an upper genital tract infection in men
symptoms: subacute onset of swelling, pain, erythema (reddening) of scrotal sac, usually unilateral |
|
|
What are common causes of epididimytis?
|
in young sexually active males, it is almost always caused by gonorrhea or chlamydia. Can be caused by E. coli with insertive anal sex
|
|
|
How is the cause of epididymitis diagnosed?
|
diagnosis usually made clinically.
should do gram stain, culture and nucleic acid amplification test for confirmation |
|
|
What is mucopurulent cervicitis?
|
Often asymptomatic.
Symptoms can include: discharge, dyspareunia (painful sexual intercourse), bleeding, dysuria, and/or lower abdominal pain On exam, can see swelling, discharge, redness |
|
|
What are the major causes of mucopurulent cervicitis?
|
gonorrhea, chlamydia, or both
|
|
|
How is the cause of mucopurulent cervicitis diagnosed?
|
Can swab endocervix.
Gram stain not very helpful. Do culture/testing to confirm diagnosis |
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|
What is pelvic inflammatory disease? (include symptoms and sequelae)
|
includes inflammation of upper genital tract
may manifest as salpingitis (inflammation of fallopian tubes), tubo-ovarian abscess, endometritis (inflammation of lining of uterus), peritonitis 1/4 of women with PID develop chronic sequelae, including ectopic pregnancy, infertility, chronic pelvic pain (gonorrhea and chladmydia are two organisms that cause this) |
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|
What is Fitz-Hugh Curtis Syndrome?
|
inflammation of adhesions b/w liver and stomach wall
(can be a symptom of gonorrhea and/or chlamydia) |
|
|
Describe the symptoms of pharyngeal gonorrhea
|
often asymptomatic
non-exudative difficult to eradicate |
|
|
Describe the symptoms of conjunctivitis from gonorrhea
|
pain, erythema (reddening), discharge
can gram stain the discharge for diagnosis |
|
|
Describe the symptoms of perirectal gonorrhea
|
tenesmus (the feeling of needing to poop), pain, discharge
exam shows friable mucosa with discharge |
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|
How is disseminated gonoccocal infection treated?
|
culture all exposed sites
treat with IV ceftriazone initially change to oral therapy after see improvement for 7-10 days |
|
|
What is disseminated gonococcal infection?
|
organism disseminates from GU tract into bloodstream.
patients may present with dermatitis-arthritis syndrome or septic monoarticular arthritis |
|
|
What is Dermatitis-Arthritis syndrome?
|
one presentation of disseminated gonococcal infection
patients may have between 10-20 pustular, hemhorragic lesions around small joints |
|
|
What is septic, monoarticular artritis?
|
one presentation of disseminated gonococcal infection
often get it in the knee |
|
|
What are some common chlamydial infections aside from genital?
|
perirectal- in those practicing receptive anal sex
conjunctivitis - less symptomatic than gonorrheal dysuria-pyuria syndrome- consider this for young sexually active women who present with urinary tract symptoms but have WBCs in urine and sterile urine cultures Lymphogranuloma Venerum |
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|
What are the symptoms of Lymphogranuloma Venereum?
|
inguinal lymphadenopathy (swollen lymph nodes in inguinal canal)
proctitis: - fever, tenesmus, bleeding, rectal pain, LGV in colon |
|
|
What is Reiter's Syndrome? (and what are its symptoms)
|
a post-inflammatory syndrome more commonly seen after chlamydia than after gonorrhea
classic triad of symptoms: - arthritis, conjunctivitis, urethritis also see skin lesions |
|
|
What is the species that causes syphilis?
|
Treponema pallidum
|
|
|
What is the structure of Treponema pallidum?
|
corkscrew-shaped (spirochete), helical, motile, as long as a WBC (10-20 micrometers)
|
|
|
How is syphilis diagnosed?
|
Cannot be cultured or seen under light microscope
Most diagnoses are based on serologic tests - this is done in two steps - if screening test of antibody against nontreponemal antigen is positive, do confirmatory test - confirmatory test is for antibody against Treponema pallidum Can also scrape at site of 1st or 2nd degree lesion and look for under Darkfield microscope |
|
|
What is the treatment for syphilis?
|
penecillin G
if patient is allergic, use doxycycline in non-pregnant, non-HIV patients use RPR card to test if patient is responding to therapy- patients usually test positive for syphilis for life |
|
|
What is the pathology of syphilis?
|
enters mucosa and proliferates
activates macrophages travels to lymph nodes and bloodstream, sometimes invading CNS immunity is present with chronic infection but lost after treatment |
|
|
What is the epidemiology of syphilis?
|
Can be contracted by:
direct contact with active lesions or infected membranes (usually sexually) Patients are most infectious/most capable of transmitting disease in first year of infection congenitally bloodborne (rarely) MSMs at high risk |
|
|
What are the symptoms of primary syphilis?
|
get a single painless ulcer (called chancre) within 1-6 weeks- heals spontaneously, usually without a scar. Often not seen, especially in females
Painless regional adenopathy (enlargement of lymph node) Patient may not be serologically positive at this point |
|
|
What are the symptoms of secondary syphilis?
|
"the great immitator"- can look like a lot of things- but don't get vesicular (blister) symptoms
manifestations occur 2-8 weeks after chancre, range for 30-180 days many skin manifestations rash, condylomata lata (grey-white or pink moist plaques where skin might chafe), alopecia (absence of hair where it usually grows) 70% of patients get: fever, malaise, anorexia, weight loss, pharyngitis, myalgias (muscle pain) Other symptoms: CNS disease, arthritis, hepatitis, ostelitis (bone inflammation) |
|
|
What happens to patients with latent syphilis?
|
Has no clinical manifestations
Only evidence is positive serology 25% of untreated early latent (<1 year asymptomatic infection) cases may relapse into secondary syphilis After 4 years, generally considered to be non-infectious except mom to child Individuals with untreated latent syphilis are resistant to re-infection |
|
|
What are the 3 types of tertiary syphilis?
|
Gummatous
Cardiovascular Neurosyphilis (most common of the 3) |
|
|
What are the symptoms of gummatous syphilis and how is it characterized?
|
Gummas are granuloma-like lesions
these lesions are present in skeletal, spinal, mucosal areas eye and viscera may also be affected average time of onset is 10-15 years |
|
|
What is cardiovascular syphilis?
|
characterized by presence of thoracic aortic aneurysm (thinning of arterial wall)
aneurysms rarely rupture, but often lead to aortic insufficiency average time of onset is 20-30 years |
|
|
What are the symptoms of the different forms of neurosyphilis?
|
many forms- these are most common:
- meningovascular- earliest to occur, within 5-10 years after infection, usually presents as stroke in younger person - parenchymatous - personality changes, dementia, delusions of grandeur, paraonoia- around 20 years after infection - tabes dorsalis- occurs between 25-25 years after infection, get lightning pains down the legs, neuropathy, characteristic gait, incontinence |
|
|
Clinically speaking, what kinds of organisms are we referring to when we talk about parasites?
|
Protozoa (single-celled organisms like amoeba, flagellates)
Helmiths (worms) |
|
|
What is the definition of a parasite?
|
An organism that lives on or within another organism AND obtains nourishment from it
(TECHNICALLY, this includes all viruses, some bactiera, some fungi, and others) |
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|
What are some general features of protozoa?
|
Uni-cellular
Eukaryotic Multiply in host Short life cycles Acute or chronic infections |
|
|
What are some general features of helmiths?
|
Multi-cellular
Do not multiply- lay A LOT of eggs that spread to new hosts Long life cycles Chronic infections |
|
|
What are the portals of entry for parasites?
|
Ingestion (most common)
- often via contaminated water Direct penetration - directly into skin - across placenta - organism-directed (get bitten by something) |
|
|
What are some structural features common to protozoa?
|
No cell wall
Single-celled Eukaryotic Do not photosynthesize Motile (usually) |
|
|
How do motile protozoa get around?
|
Pseudopods (foot-like)- ameobas
Cilia- ciliates Flagella - flagellates |
|
|
How do protozoa live and reproduce?
|
Usually reproduce by binary fission
Obtain nutrients by diffusion or pinocytosis Often produce cysts to survive under harsh conditions Transmitted through cysts and transmitted by vectors |
|
|
What are three GI protozoa?
|
Entamoeba histolytica - only medically important amoeba in US
Giardia Lamblia Cryptosporidium |
|
|
What is a genitourinary protozoa?
|
Trichomonas vaginalis
|
|
|
What are two blood and tissue protozoa?
|
Toxoplasma gondii
Falciparum (malaria) |
|
|
How is Enamoeba histolytica infection spread?
|
Fecal-oral route
When it is growing it is termed a trophozoite and makes a cyst Infection begins when cyst is ingested Low pH in stomach activates the cyst and trophozites emerge |
|
|
What do Enamoeba histolytica trophozoites do once inside the stomach?
|
Attach to and invade colonic epithelium
Lysis of cells provides nutrients for parasite Make characteristic flask-shaped ulcers Both cysts and trophozoites are excreted- the trophozoites then die but the cysts spread the infection |
|
|
What is the epidemiology of Enamoeba histolytica?
|
Found all over world
Associated with poor sanitation Many patients are asymptomatic Infected patients shed millions of cysts per day |
|
|
What are the three possible clinical outcomes of Enamoeba histolyca infection and what are their symptoms?
|
asymptomatic (most common)
- lasts 1-2 years on average intestinal amebiasis - cramping, diarrhea, pain, bloody stools extraintestinal amebiasis - fever, rigors (chills) - liver is primary target, can lead to abscess formation in liver |
|
|
How is Enamoeba histolyca infection diagnosed?
|
Detection of trophozoites and cysts in stool (should test multiple stool samples)
Serology can be useful outside of endemic areas (where the protozoa is usually found) |
|
|
How is entamoeba histolytica treated?
|
Metronidazole followed by iodoquinol
|
|
|
What type of organism is Entamoeba histoclytica?
|
amoeba
|
|
|
What type of organism is Giardia lamblia?
|
flagellate
|
|
|
What does Giardia lamblia look like?
|
has characteristic smiley face
|
|
|
How is Giardia lamblia transmitted?
|
Lives in streams, lakes- often get it from camping and using water that is not purified properly.
Once ingested, acid in stomach releases trophozites from cysts |
|
|
What is the pathology of Giardia lamblia?
|
chronic inflammation leads to villus blunting --> mild diarrhea and severe malabsorption
|
|
|
What are the symptoms of Giardia lamblia?
|
50% of those infected are symptomatic
sudden onset, foul-smelling, watery diarrhea, cramps, lots of gas, steatorrhea (fatty stool) incubation is about 10 days |
|
|
How is Giardia lamblia diagnosed?
|
Detection of trophozites, cysts in stool
Should test multiple stool samples Rapid antigen test available |
|
|
How is Giardia lamblia treated?
|
Metronidazole
(takes weeks-to-months to go away on its own) |
|
|
What type of organism is Cryptosporidium?
|
Coccidia- a non-motile protozoa
|
|
|
How is Cryptosporidium transmitted?
|
fecal-oral transmission
carried by many farm animals can get really big outbreaks due to contaminated drinking water |
|
|
What are the symptoms of infection with Cryptosporidium parvum?
|
can be asymptomatic
usually mild, self-limiting enterocolitis (inflammation of small intestine and colon) Remission after 10 days Life threatening if immunocompromised |
|
|
What is the treatment for Cryptosporidum parvum?
|
No specific treatment
|
|
|
What type of organism is Trichomonas vaginalis?
|
Flagellate (kind of protozoa)
- has four flagella and undulating membrane |
|
|
How is Trichomonas vaginalis transmitted?
|
Sexually. It is the most common STD in the world.
|
|
|
What are the symptoms of Trichomonas vaginalis?
|
men almost always asymptomatic
women often asymptomatic when women have symptoms: - watery discharge, vaginitis |
|
|
Where in human body is Trichomonas vaginalis found?
|
urethras and vaginas of women
urethras and prostate glands of men |
|
|
How is Trichomonas vaginalis diagnosed?
|
microscopic diagnosis
serologic test available |
|
|
How is Trichomonas vaginalis treated?
|
Metroindazole
|
|
|
What type of organism is Toxoplasma gondii?
|
Coccidia- nonmotile protozoa
An intracellular organism |
|
|
What is the epidemiology of Toxoplasma gondii?
|
Cats are an important source of infection for humans
- cats excrete cysts into their stool and almost any warm-blooded animal can become infected by ingestion or inhalation Can be infected by uncooked meat, and transplacentally By adulthood, 50% of US population is infected with this organism |
|
|
What is the pathology of Toxoplasma gondii in humans?
|
After released from ingested cyst, engulfed by macrophages and transported to all organ sytems in body, ESPECIALLY CNS
Parasite grows and replicates, causing macrophages to rupture and leading to spread Can cause acute disease in normal host if parasite moves to tissues, associated with tissue destruction Immune system destroys the parasites but ALSO causes them to encyst- these cysts can persist for life and be reactivated if become immunodeficient |
|
|
What are the symptoms of Toxoplasma gondii?
|
Most infections are asymptomatic
Symptoms include: fever, headaches, chills, fatigue Sometimes mimics mono If the disease is reactivated, usually presents as encephalitis- common in HIV/AIDs |
|
|
What happens when a pregnant woman gets Toxoplasma gondii?
|
Can transmit to child. In 1st trimester --> abortion or very severe disease
If after 1st trimester, can get: epilepsy, microcephaly, blindness, mental retardation, anemia, jaundice Infant may be born asymptomatic and develop problems later |
|
|
How is Toxoplasma gondii diagnosed?
|
Serologically- need to look for CHANGES in serology, not just positive serology
Demonstrate trophozite (not cyst) in tissue |
|
|
How is Toxoplasma gondii treated?
|
Normally, don't need to treat
If chronic or CNS infection: use pyrimethamine plus sulfadiazine |
|
|
What type of organism is Plasmodium?
|
Coccidia - nonmotile protozoa
|
|
|
What disease does Plasmodium cause in humans?
|
malaria
|
|
|
Where does Plasmodium like to live and reproduce?
|
Need two hosts:
- mosquito for sexual reproduction - humans/other animals for asexual reproduction sexual reproduction: trophozite grows and replicates in RBCs. When RBCs lyse, releasing schizonts which enter new RBCs asexual reproduction: occurs in hepatocytes. When cells rupture, merozoites released, they invade RBCs Anapholes mosquito delivers sporozites via its saliva |
|
|
What is the epidemiology of malaria?
|
Half of world's population at risk
About 1 million deaths per year Many strains can develop dormant liver stages- left untreated they can reactivate Plasmodium falciparum does not cause latent infections, but is most likely to cause death |
|
|
What are the symptoms of malaria?
|
Lysis of RBCs --> anemia
Deformed RBCs can stick to endothelium --> cause clots Other symptoms: after 2 week incubation period, get flu-like symptoms. As infection proceeds, get pattern of chills, fever, malarial rigors cycle every 48 hours |
|
|
How is malaria diagnosed?
|
RBC smear
|
|
|
How is malaria treated?
|
Quinine- has too much resistance
Chloroquine - quite a bit of resistance Several other drugs available |
|
|
What do helminths look like?
|
elongated, bilateral symmetry, eukaryotic, multicellular, typically macroscopic
|
|
|
What are the three major types of helminths?
|
Nematodes- round worms; have a digestive system, male and female
Trematodes- flukes- leaf shaped, no digestive system, hermaphrodites Cestodes- tapeworms, segmented, no digestive system, hermaphrodites |
|
|
What kind of organism is Enterobius vermicularis?
|
nematode- kind of helminth
|
|
|
How big is Enterobius vermicularis?
|
Small (for a worm)- 10 mm in length
|
|
|
How do people become infected with Enterobius vermicularis?
|
ingest or inhale ova
female will crawl out and deposit eggs in perianal area |
|
|
What are symptoms of Enterobius vermicularis?
|
Usually not serious
Anal itching, especially at night, may get bacterial infection secondary to itching |
|
|
How is Enterobius vermicularis diagnosed?
|
Scotch tape or swab to anal region
|
|
|
How is Enterobius vermicularis treated?
|
Treat entire family with albendazole or mebendazole
|
|
|
What type of organism is Schistosoma mansoni?
|
Trematode- aka a fluke- a kind of helminth
|
|
|
How do people become infected with Schistosoma mansoni?
|
By swimming in the Schuykill!
Bind to and penetrate skin |
|
|
What is the pathology of Schistosoma mansoni do in people?
|
this is an obligate intravascular parasite in people
inhabits mesenteric vessels --> their blockade can lead to hepatosplenomegaly can get thickening of bowel wall due to granulomatous inflammation portal vein can become fibrotic due to rxn in eggs |
|
|
What are symptoms of Schistosoma mansoni?
|
fever, malaise, abdominal pain
dermatitis at site of skin penetration (Swimmer's itch) |
|
|
How is Schistosoma mansoni treated?
|
Praziquantel
|
|
|
What type of organism is Taenia solium?
|
cestode- aka, a tapeworm, kind of helminth
|
|
|
How do people get infected with Taenia solium?
|
associated with eating under-cooked prok
we ingest the larval worm |
|
|
What does Taenia solium do once it infects people?
|
the larval worm's "hooks" (scolex) attach to our intestines
there, the cestode lays eggs and disseminates. Can have eggs in any solid organ, leading to abscess formation. can grow to be a very long worm and is gross! |
