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629 Cards in this Set
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53-year-old male farmer has a 4.5cm circular skin lesion of black eschar surrounded by vesicles and edema. Gram stain on microscopy shows gram-positive bacilli in chains.
what organism is most likely causing this? |
Bacillus anthracis
(cutaneous infection) |
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what are the primary virulence factors of Bacillus anthracis?
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capsular polypeptide
anthrax toxin |
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what are the three methods by which bacillus anthracis infects humans?
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cutaneous penetration of spores (most common)
ingestion of spores inhalation of spores |
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why are patients infected with bacillus anthracis not quarantined?
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person-to-person transmission has not been described/witnessed
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what are the only two species of bacillus that are frequently associated with human disease?
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Bacillus anthracis
Bacillus cereus |
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how does cutaneous Bacillus anthracis infection present?
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within 2-3 days of exposure to an infected animal or animal product, a papule develops at the site of inoculation and then progresses to form a vesicle
a black eschar is formed after rupture of the vesicle and necrosis develops in the area rarely, this progresses to bacteremia, which is fatal if untreated |
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what is an eschar?
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skin lesion associated with cutaneous anthrax and resembling a black, necrotic sore
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what is wool-sorters' disease?
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disease associated with inhalation of anthrax spores from infected animal products, most often associated with sheep wool
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list the characteristics of Bacillus anthracis
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large
motile facultative anaerobic gram-positive rods central spore virulent forms are more likely surrounded by a capsule |
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how is Bacillus anthracis seen on a Gram stain?
on blood agar plates? |
in chains
large colonies within 24 hours, which resemble a Medusa head |
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what does the capsule of Bacillus anthracis consist of?
what is the advantage of the capsule? |
poly-D-glutamic acid
allows organism to resist phagocytosis |
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what are the three proteins which comprise anthrax toxin?
what functions are associated with each one? |
protective antigen - confers immunity in experimental situations
edema factor and lethal factor bind to protective antigen to become edema toxin and lethal toxin respectively |
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what happens to the anthrax toxins? how are they produced and released?
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edema factor and lethal factor bind to protective antigen to become edema toxin and lethal toxin respectively
toxins are transported across cell membranes and are released in the cytoplasm where they exert their effects |
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what happens to the spores of Bacillus anthracis once they enter the body?
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taken up by macrophages
because of the lethal and edema factors, the spores survive killing and subsequently germinate |
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what is the differential diagnosis for a patient with fever, adenopathy, and black eschar?
what makes Bacillus anthracis most likely? |
furuncles (staphylococci)
ecthyma gangrenosum (pseudomonas aeruginosa) spider bites cutaneous anthrax other etiologies are not known to cause eschar formation with surrounding edema |
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how is specific diagnosis of anthrax made?
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growth of Bacillus anthrax from blood (inhalation) or wound (cutaneous)
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how does Bacillus anthrancis grow on blood-containing agar?
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nonmotile
spore-forming nonhemolytic |
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what does bacillus antracis produce when grown on egg yolk agar?
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lecithinase
enzyme that degrades lecithin in egg yolk agar leaving a white precipitate |
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what bacteria produce lecithinase?
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bacillus anthracis
bacillus cereus |
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why is it important to carefully examine a gram stain from a primary specimen of a patient with suspected anthrax?
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they have the propensity to easily decolorize and appear gram-negative
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what is a key to the identification of bacillus anthracis as a gram-positive bacillus?
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presence of spores
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by what results can a presumptive identification of bacillus anthracis be made?
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large gram-positive bacilli, nonhemolytic, lecithinase positive
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what do confirmatory tests for bacillus anthracis involve?
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fluorescently labeled monoclonal antibodies as well as DNA amplification assays
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what is India Ink used for?
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determines the presence of a capsule around bacteria
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why is India Ink used for bacillus anthracis?
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its capsule is not stained by India ink, which is easily visualized against the dark background
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what is the drug of choice for anthrax?
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ciprofloxacin
was penicillin, but weaponized strains were identified which were resistant thanks to production of beta-lactamase |
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how is anthrax prevented?
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vaccination of animals as well as humans at high risk of exposure (military personnel)
prophylaxis is not recommended for asymptomatic persons when deemed necessary, prophylaxis with ciprofloxacin must be maintained for up to thirty days b/c of potential delay in germination of inhaled spores |
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60-year-old man has a ruptured diverticulitis leading to peritonitis.
what organism is most likely causing symptoms? |
bacteroides fragilis
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what are the characteristics of bacteroides fragilis on gram staining?
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encapsulated
irregular staining pleomorphism vacuolization |
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what are the primary mechanisms of bacteroides fragilis for resisting phagocytosis?
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capsular polysaccharide
succinic acid production |
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19-year-old male with bacterial gastroenteritis that mimics appendicitis
what is the most likely etiology of the infection? |
Campylobacter jejuni
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what is the preferred atmospheric environment of Campylobacter jejuni?
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microaerophilic (high concentration of carbon dioxide)
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how many serotypes are there of C. jejuni? by what are they determined?
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more than 50 based on heat labile (capsular and flagellar) antigens
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how is C. jejuni transmitted?
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eating poorly cooked chicken
(milk, water, and other meats have also been implicated) |
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what type of infection does C. jejuni most commonly cause?
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gastroenteritis
one of the most frequent causes of bacterial diarrhea occurring most often in the summer or early fall |
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what is the incubation period for C. jejuni?
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1-3 days
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what are the symptoms of C. jejuni infection?
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fever
malaise abdominal pain bloody diarrhea mucosal inflammation bacteremia |
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what is suggested by the symptoms of C. jejuni?
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that it is invasive to the lining of the intestine
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how long do most cases of C. jejuni last?
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usually self-limited, resolving within 7 days
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what are the potential complications from C. jejuni infection?
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pancreatitis
peritonitis arthritis osteomyelitis sepsis Guillain-Barre syndrome |
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why is C. jejuni associated with Guillain-Barre syndrome?
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Guillain-Barre syndrome is a serious post-infection sequelae of C. jejuni, because of the antigenic similarities between surface surface lipopolysaccharides and myelin proteins
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what are the Campylobacter species, and what infections are they known for?
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C. jejuni - gastroenteritis
C. coli - gastroenteritis (clinically indistinguishable from C. jejuni) C. fetus - bacteremia, septic arthritis, peritonitis, abscesses, meningitis, endocarditis in immunocompromised patients |
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what are fecal leukocytes?
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WBCs present in the stool, which correlate loosely with the presence of an invasive pathogen
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describe campylobacter species
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small
motile nonspore-forming comma-shaped gram-negative |
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what are the gram-staining properties of campylobacter species?
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gram-negative
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what accounts for the motility of campylobacter species?
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a single flagellum at one or both poles
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at what temp. does C. jejuni grow best?
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42degC
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why is isolation of C. jejuni difficult from stool samples? how is this overcome?
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it multiplies more slowly than other enteric bacteria
selective media are used |
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how do C. jejuni colonies appear on selective media?
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gray
mucoid wet |
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what are the virulence factors of C. jejuni?
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LPSs in outer membrane - endotoxic activity
extracellular toxins - cytopathic activity |
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what is the relevance of pH to C. jejuni?
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it is sensitive to decreased pH, so factors that neutralize gastric acid enhance its chances for survival
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what is included in the DDx of acute gastroenteritis?
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salmonella
shigella yersinia campylobacter |
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why is C. jejuni infection commonly misdiagnosed as appendicitis or irritable bowel syndrome?
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abdominal pain and cramps, sometimes in the absence of diarrhea
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what is suggested by bloody diarrhea?
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enterohemorrhagic E. coli
C. jejuni |
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how is definitive diagnosis of C. jejuni made?
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culture of the stool and growth of campylobacter
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what bacteria is more fastidious than most other causes of bacterial gastroenteritis and should be transported to the laboratory in media such as Cary-Blair?
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C. jejuni
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what is important about campy blood agar or Skirrow medium?
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includes antibiotics which inhibit normal stool flora, allowing for growth of campylobacter within 48-72 hours
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does C. jejuni produce oxidase?
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yes
oxidase positive |
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what are the treatment options for C. jejuni infections?
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mostly just supportive care (hydration)
erythromycin - b/c of increased resistance to fluoroquinolones |
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how are C. jejuni infections prevented?
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careful food preparation
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19-year-old female with probable pelvic inflammatory disease would probably have a positive DNA probe assay for what bacteria?
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chlamydia trachomatis
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how does chlamydia trachomatis enter a target cell?
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elementary body binds to receptors on the host and induces endocytosis
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what are the two stages of the life cycle of chlamydia trachomatis?
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elementary body
reticulate body |
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what is the causative agent of the most common STD in the united states?
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chlamydia trachomatis
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what is the most common cause of preventable blindness around the world?
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chlamydia trachomatis
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what other infection is very common for those infected with gonorrhea? why?
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chlamydia
both infect columnar epithelial cells of the mucous membrane |
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how are children a main reservoir for transmitting chlamydia trachomatis?
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transmit the disease by hand-to-hand transfer of infected eye fluids or by sharing contaminated towels or clothing
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what is an elementary body?
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nondividing 300-nm infectious particle of chlamydia trachomatis; has an outer membrane with disulfide linkages which allows it to survive extracellularly
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what is Chandelier sign?
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cervical motion tenderness during the bimanual exam, characteristic of pelvic inflammatory disease
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what is exudate?
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material, such as fluids, cells or debris, which has extravasated from vessels and has been deposited on tissue surfaces or in tissue
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what is a papule?
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small palpable elevated lesion that is less than 1cm
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describe chlamydia trachomatis
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gram negative
obligate intracellular parasite |
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why is chlamydia trachomatis unique among gram-negative bacteria?
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has no peptidoglycan layer
has no muramic acid |
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what stabilizes chlamydia trachomatis?
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disulfide linkages in outer membrane
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what is the name for the extracellular form of chlamydia trachomatis?
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elementary body
(has a small spore-like structure |
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to what types of cells does the elementary body of C. trachomatis attach?
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columnar
cuboidal transitional epithelial cells (in structures lined by mucous membranes) |
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what are the membrane-protected structures that contain endocytosed C. trachomatis bacteria?
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inclusions
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what is the larger, more metabolically active form of C. trachomatis?
how does C. trachomatis enter this form? |
reticulate body
elementary body undergoes reorganization |
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what part of the life cycle of C. trachomatis reproduces?
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reticulate bodies - grow and multiply by binary fission to create larger intracellular inclusions
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how long does the life cycle of C. trachomatis last?
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48-72 hours
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list, in sequential order, the stages of the life cycle of chlamydia trachomatis
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elementary body attaches to host cell
hos cell phagocytizes elementary body residing in a vacuole, inhibiting phagosome-lysome fusion elementary body reorganizes to form a reticulate body reticulate body divides by binary fission some reticulate bodies convert back into elementary bodies elementary bodies are released into host cell and then exocytized |
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what results from infection of the conjunctiva by C. trachomatis?
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scarring and inflammation, which pulls the eyelid inward, causing eyelashes to rub against cornea
because eyelid is rolled inward, individual is unable to completely close the eye and eye dessicates |
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what two features cause corneal scarring from conjunctival infection by C. trachomatis?
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inability to maintain moisture (because eyelids don't close fully)
constant abrasion by eyelashes (because eyelids are rolled inward by fibrosis) |
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what diseases are caused by C. trachomatis?
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ocular trachoma
pneumonia urethritis epididymitis lymphogranuloma venereum cervicitis pelvic inflammatory disease |
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how does lymphogranuloma venereum present?
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painless papule on the genitalia that heals spontaneously
infection is then localized to regional lymph nodes where it resides for approximately 2 months lymph nodes may then sweel and rupture, releasing exudate |
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how does epididymitis present?
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fever, unilateral scrotal swelling, pain
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how does cervicitis present?
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swollen, inflamed cervix
may also be a yellow purulent discharge |
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when does PID occur?
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PID occurs when an infection spreads to the uterus, fallopian tubes, and ovaries
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how does PID present?
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lower abdominal pain
dyspareunia vaginal discharge uterine bleeding nausea vomiting fever chandelier sign |
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how do infants present with congenital C. trachomatis?
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inflammation of the infant's conjunctiva, with a yellow discharge and swelling of the eyelids within 2 weeks after birth
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what bacteria is suggested by the presence of basophilic intracytoplasmic inclusion bodies in the conconjunctiva?
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C. trachomatis
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by what bacteria is atypical pneumonia caused?
how does it present? |
chlamydophila pneumonia
species related to chlamydia trachomatis presents with fever, headache, and a dry hacking cough |
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by what bacteria is psitacosis caused?
how is it acquired? |
chlamydophila psittaci
inhalation of feces from infected birds |
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how can C. trachomatis be rapidly diagnosed?
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detection of the bacterial nucleic acid in patient samples from the oropharynx, conjunctiva, urethra, or cervix
PCR, or direct DNA hybridization assays |
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what is the treatment for C. trachomatis?
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tetracycline
erythromycin azithromycin for cervicitis and urethritis PID with ceftriaxone and 2 weeks of doxycycline |
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how is C. trachomatis best prevented?
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education
proper sanitation ocular infection by topical tetracycline drops |
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52-year-old male who recently took antibiotics, now has diarrhea. Fecal leukocytes are present in the stool, and a toxin test is positive.
what is the most likely etiology? |
clostridium difficile
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what conditions predisposes humans to clostridium difficile infection?
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**recent antibiotic exposure/regimen**
trauma surgery immunosuppression |
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how many species of clostridium are there?
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approximately 90
about 20 are known to cause disease in humans |
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where are clostridium species found?
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soil
decaying vegetation intestinal tracts of humans and other vertebrates |
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what is the most common clostridium species isolated from human infections?
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clostridium perfringens
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what bacterium is associated with the toxin-mediated disease, tetanus?
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clostridium tetani
occurs in unvaccinated persons who come in contact with the organism |
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how is clostridium tetani introduced into a human host?
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spores of the organism survive long periods of time in the soil and are introduced into a person following deep puncture wounds
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how does tetanus present?
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tonic spasms usually involving the muscles of the neck, jaw (lockjaw), and trunk
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what is the causitive agent of botulism?
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clostridium botulinum
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how is botulism transmitted?
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spores are consumed, usually from improperly canned vegetables
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what are the symptoms of botulism?
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nausea
blurred vision weakness of upper extremities spreading downward occurs within 12-36 hours after ingestion of the toxin |
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with what is infant botulism associated?
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consumption of honey
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from the stool of how many how many healthy adults can clostridium difficile be isolated?
in infants? |
fewer than 5 % (about 3%)
in infants, up to 70% have it in their stool |
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what are the further complications of pseudomembranous colitis?
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toxic megacolon
bowel perforation |
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what is antibiotic-associated diarrhea?
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gastroenteritis caused by C. difficile
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what is pseudomembranous colitis?
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presence of nodules or plaques on erythematous (red) colonic mucosa seen by sigmoidoscopy
associated with C. difficile colitis |
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describe Clostridium difficile
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anaerobic
spore-forming toxigenic gram-positive bacillus (rod) |
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from what does clostridium difficile acquire its name?
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initial difficulty in isolating and culturing the organism
requires a selective medium for growth which also inhibits normal stool flora |
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what are the virulence factors for C. difficile?
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toxin production
hyaluronidase production |
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what are the two toxins released by clostridium difficile?
what are their functions? which is more biologically active in humans? |
toxin A - enterotoxin - chemotactic and initiates the release of cytokines, hypersecretion of fluids in GI tract, and hemorrhagic necrosis
toxin B - more active - cytotoxin |
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why is the new strain of C. difficile so much more virulent than the previous strains?
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produces larger quantities of Toxins A and B
produces binary toxin |
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what is the importance of spore formation?
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allows the organism to survive under stressful situations in the environment for extended periods of time
allows organisms to survive in hospital environment allows organism to be transferred from person to person on fomites |
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what is the most common cause of diarrhea that develops in patients who have been hospitalized for 3 or more days?
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antibiotic-associated diarrhea
gastroenteritis caused by C. difficile |
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how can antibiotic-associated diarrhea be diagnosed?
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visualization of the pseudomembrane (fibrin, bacteria,cell debris, WBCs)
gold standard = detection of toxin production in the stool using a tissue culture assay |
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how can C. difficile be cultured?
how does it appear? |
selective media, cycloserine, cefoxitin, and fructose agar in an egg yolk agar base (CCFA medium) in an anaerobic environment for 24-48 hours
colonies fluoresce chartreuse on CCFA and have a barnyard odor |
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what are the treatments for C. difficile?
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first-line: oral metronidazole
failure of first-line: oral vancomycin |
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in how many patients, properly treated for C. difficile, does relapse occur?
why? |
20-30 percent
resistance of spores to treatment |
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how is C. difficile prevented in hospitalized patients?
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good infection control procedures, including isolation of infected patient
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6-year-old female with 4 day history of sore throat and fever; immigrated from Russia about 6 months prior; child is anxious, tachypneic, and ill appearing, with a hoarse voice
gray membrane coats tonsil, extends over uvula and soft palate; prominent cervical adenopathy, clear lungs what is the presumptive diagnosis? |
corynebacterium diphtheriae
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what gram stain characteristics does Corynebacterium diphtheriae have on microscopy?
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club-shaped appearance of the gram-positive bacillus, often characterized as "chinese letters" because of adherence of cells following division
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what factor is required for the expression of diphtheria toxin?
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lysogenic bacteriophage
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with what is Corynebacterium jeikeium associated?
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bacteremia
line-related infection in immunocompromised patients one of the few Corynebacteria that tends to be multidrug resistant |
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what is one of the most pathogenic Corynebacterium?
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Corynebacterium diphtheriae
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what is the only known reservoir for C. diphtheriae?
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humans
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how is C. diphtheriae transmitted?
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aerosolized droplets, respiratory secretions, infected skin lesions
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how does respiratory C. diphtheriae progress?
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2-6 days after inhalation, patients develop nonspecific signs and symptoms of upper respiratory infection (organisms reproduce locally within epithelial cells)
toxin is produced eliciting systemic symptoms (fever and cervical lymphadenopathy) exudate, containing organisms, fibrin, WBCs, and RBCs is formed (pseudomembrane) over tonsils, uvula, and palate |
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what are the complications of membrane formation in C. diphtheriae infection?
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respiratory compromise by aspiration of the pseudomembrane (common cause of death in this disease)
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what is bull neck?
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cervical lymphadenopathy
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what is cutaneous diphtheria?
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invasion of C. diphtheriae from a patient's skin into the subcutaneous tissue
papule develops at the site of contact that later becomes covered by a grayish membrane toxin produced elicits systemic response |
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at what sites are the effects of diphtheria toxin found?
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heart (myocarditis)
nervous system (dysphagia, paralysis, fever) |
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what is lysogenic bacteriophage?
|
virus that infects bacteria
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what is an Elek test?
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an immunodiffusion test to detect the production of diphtheria toxin in a strain of C. diphtheria
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what is a pseudomembrane in diphtheria?
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membrane formed, which consists of dead cells, leukocytes, and fibrin
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describe Corynebacterium diphtheriae
|
nonencapsulated
gram-positive bacillus (rod-shaped) non-motile non-spore-forming club shaped |
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why do Corynebacterium diphtheriae have a characteristic "Chinese letter" appearance on microscopy?
|
cells often remain attached after division and form sharp angles
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what are the three subtypes of Corynebacterium diphtheriae?
based on what are they divided? |
gravis
intermedius mitis based on colony morphology and biochemical testing |
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what is the major virulence factor of C. diphtheriae?
what is necessary for it to be produced? |
exotoxin
lysogenic beta-phage |
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what are the two components of the potent exotoxin, produced by C. diphtheriae in the presence of a lysogenic beta-phage?
what are their functions? |
B segment - binds to specific receptors on susceptible cells
A segment - released into the host cell, following a proteolytic cleavage, where it can inhibit protein synthesis |
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how can the potent exotoxin, produced by C. diphtheriae in the presence of lysogenic beta-phage, cause host tissue damage without affecting bacterial replication?
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targets a factor present in mammalian cells but not in bacterial cells
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what causes the characteristic pseudomembrane seen in clinical diphtheria?
|
toxin-related tissue necrosis
caused by the potent exotoxin produced by C. diphtheriae in the presence of lysogenic beta-phage |
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what is included in the differential diagnosis of sore throat, fever, and cervical lymphadenopathy?
|
streptococcal pharyngitis
infectious mononucleosis respiratory diphtheria |
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how is clinical diagnosis of diphtheria made?
|
visualization of the characteristic pseudomembrane formation
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should the pseudomembrane from corynebacterium diphtheriae be removed? why or why not?
|
no - because of the tight adherence to the epithelial surface and the chance for subsequent bleeding
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how do Corynebacterium species grow on nonselective media?
|
well within 24 hours, with the exception of a few lipophilic species
colonies are usually nonpigmented and small, without hemolysis on blood agar |
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on what type of media should corynebacterium diphtheriae be cultured?
|
selective medium such as Tellurite (where colonies will appear black) and nonselective media (C. diphtheriae are more fastidious than other species of corynebacterium)
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what is the significance of Loeffler media for corynebacterium diphtheriae?
|
colonies of C. diphtheriae can be stained with methylene blue to observe the characteristic metachromatic granules
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how is Corynebacterium diphtheriae treated?
|
antimicrobial therapy (erythromycin) with antitoxin
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why must antitoxin for diphtheria be administered quickly?
|
must not be able to bind to epithelial cells
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how is Corynebacterium diphtheriae infection prevented?
|
vaccination with diphtheria toxoid (DPT)
infected patients are isolated from other susceptible persons to prevent secondary spread of the disease prophylaxis with erythromycin can be given to close contacts who are at risk |
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72-year-old woman with an indwelling urinary catheter has a UTI and bacteremia. Gram-positive cocci are isolated from the urine and blood cultures.
what is the most likely etiology of this infection? |
Enterococcus faecalis
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how does Enterococcus faecalis acquire antibiotic resistance?
|
DNA mutation
plasmid or transposon transfer |
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what is the source of Enterococci?
|
normal flora of the GI tract
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what is the most common predisposing factor for infection with Enterococci?
|
history of preceding abdominal or genital tract procedures
commonly associated with nosocomial UTI, especially in patients with urinary catheters |
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what patients are at higher risk for enterococcal endocarditis?
|
elderly patients
patients with underlying heart disease (esp. the presence of artificial heart valves) |
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what types of endocarditis are typically associated with Enterococci?
|
subacute left-sided endocarditis
mitral valve endocarditis |
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what is tachycardia?
|
increased heart rate above 100 bpm
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what are transposons?
|
small pieces of DNA that can replicate and insert randomly in the chromosome
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what is leukocyte esterase?
|
an enzyme present in leukocytes, therefore used as an indirect marker of their presence
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describe Enterococcus faecalis
|
aerobic
gram-positive coccus (spherical-shaped) |
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in what extreme conditions is Enterococcus faecalis able to grow?
|
wide range of temperatures
high pH presence of high concentrations of bile salts saline concentrations up to 6.5 percent |
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why were Enterococci considered a member of the Streptococcus family for years?
|
they are difficult to distinguish morphologically from Streptococci
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what carbohydrate antigen is present on the cell surface of Enterococci?
|
group D streptococcal carbohydrate antigen
|
|
|
in what arrangements are enterococci often seen in microscopy?
|
single
pairs short chains |
|
|
what is a major virulence factor of enterococcus species?
|
intrinsic resistance to multiple antibiotics (ampicillin, penicillin, and aminoglycosides)
|
|
|
what have enterococci species been shown to transfer to Staphylococcus aureus?
|
gene for vancomycin resistance
|
|
|
how is clinical diagnosis of UTI made?
|
urgency and/or dysuria
urinalysis bacterial culture |
|
|
what is indicated by the presence of WBCs (positive leukocyte esterase) and bacteria in the urine?
|
cystitis (urinary bladder inflamation)
|
|
|
what is considered significant for a UTI?
|
>10^5 CFUs per mL of clean catch urine
>10^4 CFUs per mL of catheterized urine |
|
|
what is a CFU?
|
colony forming unit
|
|
|
how do species of Enterococcus appear on blood agar?
|
nonhemolytic usually
alpha-hemolytic in rare cases |
|
|
what is alpha hemolysis?
|
agar under the colonies is dark and greenish on a blood agar plate
aka incomplete or partial hemolysis |
|
|
what is beta hemolysis?
|
complete lysis of red cells in the media around and under the colonies: the area appears lightened (yellow) and transparent
aka complete hemolysis |
|
|
what is gamma hemolysis?
|
organism does not lyse red blood cells in blood agar: area appears unchanged (red)
aka non-hemolytic |
|
|
how can Enterococcus be specifically identified?
|
rapid PYR test
|
|
|
what is included in conventional, overnight identification of Enterococcus species?
|
growth in 6.5 percent sodium chloride and esculin hydrolysis in the presence of bile
|
|
|
what are the most clinically significant species of Enterococci?
|
E. faecalis
E. faecium |
|
|
what is significant about E. faecium?
|
it tends to be more resistant to antibiotics, particularly ampicillin and vancomycin, than E. faecalis
|
|
|
what is the first choice treatment for uncomplicated enterococcal urinary tract infections?
why is this counterintuitive? |
beta-lactam antibiotics, such as ampicillin
enterococci are intrinsically resistant to low concentrations of beta-lactam antibiotics |
|
|
what are the treatments for Enterococcal infections?
|
beta-lactam antibiotics (ampicillin) for uncomplicated enterococcal UTIs w/o resistance
ampicillin/vancomycin plus aminoglycoside for complicated UTI or endocarditis |
|
|
21-year-old female with urinary frequency and dysuria; urinalysis shows numerous white blood cells.
what is the most common etiologic agent? |
E. coli
|
|
|
how does E. coli appear on gram stain?
|
gram-negative rod
|
|
|
what is the most likely source of E. coli infection?
|
patient's own GI tract
|
|
|
what is the most likely mechanism of introduction of E. coli into the urinary tract?
|
urethral contamination by colonic bacteria followed by ascension of the infection into the bladder
|
|
|
what is the most commonly found aerobic, gram-negative bacilli in human GI tracts?
|
Escherichia coli
|
|
|
what bacteria is responsible for over 80% of all UTIs, along with other clinical diseases including gastroenteritis, sepsis, and neonatal meningitis?
|
Escherichia coli
|
|
|
for the different types of E. coli infections, from where is the bacteria most likely acquired?
|
E. coli causing diarrhea is usually acquired from the environment, whereas most other infections cause by E. coli are acquired endogenously from patient's own GI tract
|
|
|
what is E. coli serotype O157:H7?
|
serotype of enterohemorrhagic E. coli which causes a bloody diarrhea, and is usually acquired from eating poorly cooked meat from an infected cow
|
|
|
what are the complications of infection with E. coli serotype O157:H7?
|
hemolytic uremic syndrome (HUS)
triad of hemolytic anemia, thrombocytopenia and renal failure significant cause of acute renal failure in children |
|
|
what is pyelonephritis?
|
an ascending urinary tract infection that has reached the pyelum (pelvis) of the kidney
|
|
|
what is hemolytic uremic syndrome (HUS)?
|
syndrome characterized by hemolytic anemia, thrombocytopenia (low platelets) and acute renal failure
|
|
|
to what family does Escherichia coli belong?
|
Enterobacteriaceae
|
|
|
what do all members of the Enterobacteriaciae have in common?
|
ferment glucose
oxidase negative reduce nitrates to nitrites many are normal flora of the GI tract |
|
|
what is the abbreviated list of Enterobacteriaciae?
|
Shigella
Salmonella Escherichia Enterobacter Klebsiela Serratia Proteus (SSSEEKP) |
|
|
what does Escherichia coli produce which allows it to attach to cells in the urinary and GI tracts?
what is the advantage of this adaptation? |
adhesins
prevents bacteria from being flushed from the organs by normal passage of urine or intestinal motility |
|
|
what are the exotoxins involved in the E. coli mediated pathogenesis of diarrhea?
|
shiga toxins
heat-stable toxins heat-labile toxins hemolysins |
|
|
what exotoxin from E. coli is particularly important in producing an inflammatory response in the urinary tract?
where are the rest of the exotoxins important? |
Hemolysin HlyA
the other exotoxins are more pathogenic in the GI tract |
|
|
where is the O antigen of E. coli found?
|
on lipopolysaccharide (LPS) of the cell membrane
|
|
|
where is the H antigen of E. coli found?
|
on the flagella
|
|
|
where is the K antigen of E. coli found?
|
on the capsule
|
|
|
how would pyelonephritis be indicated?
|
fever and flank pain, with appropriate urinalysis and urine culture
|
|
|
how well does E. coli grow on culture plates?
|
easily grown on most culture media
|
|
|
how does E. coli appear on MacConkey agar?
what does this indicate? |
pink colonies
indicates fermentation of lactose |
|
|
what would a rapid spot indole test give a preliminary identification for?
how would this be confirmed? |
E. coli
biochemical analysis |
|
|
how are UTIs treated?
|
based on affecting organism and its susceptibility to antibiotics
common antimicrobials chosen are trimethoprim sulfamethoxazole or a fluoroquinolone |
|
|
to what antibiotics are most E. coli resistant?
|
ampicillin and penicillin
|
|
|
how are UTIs prevented?
|
consumption of large amounts of liquid
totally emptying the bladder during urination |
|
|
how should patients with E. coli diarrhea be treated?
prevented? |
treated: fluid and electrolyte replacement
prevention: improved hygiene |
|
|
in response to what cytokines are acute phase proteins released from the liver?
|
IL-1
IL-6 TNF-alpha |
|
|
what are the acute phase response proteins that increase in response to certain cytokines?
|
C-reactive protein
mannose-binding lectin |
|
|
what part of a gram-negative bacteria has a specific ability to activate macrophages?
|
endotoxin (LPS)
|
|
|
what is secreted by activated macrophages?
what is its effect? |
TNF-alpha
causes fever and hemorrhagic tissue necrosis |
|
|
what is the easy way to ID E. coli?
|
growth of a flat lactose fermenter on MacConkey agar that is indole positive
|
|
|
48-year-old male with diffuse gastritis and a gastric ulcer on endoscopic examination. what organism will likely be seen in a histologic evaluation of a gastric biopsy?
|
Helicobacter pylori
|
|
|
what clinical test is useful for rapid detection of Helicobacter pylori?
|
urease test
|
|
|
what two factors facilitate Helicobacter pylori's ability to colonize the stomach?
|
blockage of acid production by a bacterial acid-inhibitory protein
neutralization of acid by ammonia produced by urease activity |
|
|
with what GI diseases has Helicobacter pylori been implicated?
|
gastritis
ulcers gastric cancers |
|
|
what is the primary reservoir for H. pylori?
|
humans
|
|
|
how is H. pylori transmitted?
|
fecal-oral route
|
|
|
describe Helicobacter pylori
|
curved
gram-negative microaerophilic bacillus (rod-shaped) oxidase positive catalase positive mucinase positive phospholipase positive motility facilitated by corkscrew motion and polar flagella produces vacuolating cytotoxin |
|
|
by the presence of what is urease activity enhanced?
|
heat shock protein (HspB) which exists on the surface of H. pylori
|
|
|
the identification of urease activity in a gastric biopsy sample is highly specific for the presence of what?
|
an active H. pylori infection
|
|
|
what is urease?
|
enzyme utilized by H. pylori to convert urea into ammonia and CO2; increased urea produced by this reaction neutralizes gastric acid, which allows H. pylori to survive normally harsh gastric environment; also damages gastric mucosa
|
|
|
what is Type B gastritis?
|
gastritis of the antrum caused by H. pylori infection
|
|
|
what is Type A gastritis?
|
gastritis of the fundus caused by autoimmune disorders
|
|
|
what two organisms are microaerophilic? what does this entail?
|
H. pylori
C. jejuni require reduced oxygen concentration (5%) and elevated CO2 concentration to grow optimally |
|
|
what is an upper endoscopy?
|
visual examination of the mucosa of the esophagus, stomach, and duodenum using a flexible fiberoptic system introduced through the mouth
|
|
|
under what genus was H. pylori originally classified?
|
Campylobacter
|
|
|
what is the most important enzyme that distinguishes H. pylori from Campylobacter species and other various Helicobacter species?
|
Urease
|
|
|
what is speculated to be a reservoir for H. pylori?
|
contaminated water or food sources
no data to support this currently |
|
|
with what disorders is H. pylori clearly associated?
|
Type B gastritis
gastric ulcers gastric adenocarcinoma of the body and antrum gastric mucosa-associated lymphoid tissue (MALT) B-cell lymphomas |
|
|
when using what stains is microscopy of a gastric biopsy both sensitive and specific for H. pylori?
|
Warthin-Starry silver stain
hematoxylin-eosin (H&E) stain Gram stain |
|
|
what test is sensitive and specific for H. pylori, while also inexpensive and easy to perform?
|
antigen detection in stool samples via a commercial polyclonal enzyme immunoassay
|
|
|
why is culturing more challenging and time-consuming for H. pylori?
|
must be grown in a microaerophilic atmosphere on an enriched medium containing charcoal, blood, and hemin
|
|
|
why is serology a preferred diagnostic test?
what is its drawback? |
H. pylori stimulates a humoral immune response (IgM early in infection; IgG and IgA later in infection and persisting)
drawback: can't distinguish between past and present infections |
|
|
how can H. pylori be prevented?
|
frequent hand washing, esp. before meals
|
|
|
how is H. pylori treated?
|
combination therapy with:
(1) acid suppression by proton pump inhibitor (2) one or more antibiotics (3) occasional additive therapy with bismuth |
|
|
19-month-old male has not received many immunizations presents with meningitis; lumbar puncture shows multiple small gram-negative coccobacilli
what organism is most likely causing this infection? |
type B Haemophilus influenzae
|
|
|
what component of type B Haemophilus influenzae is the target of vaccine-induced immunity?
|
purified polyribitol phosphate, a component of the polysaccharide capsule
|
|
|
what is the source for Haemophilus species?
|
normal flora of upper respiratory tract (esp. H. parainfluenzae and H. influenzae non-type B)
|
|
|
why is Haemophilus influenzae no longer the leading cause of pediatric meningitis (ages 2 months to 2 years)?
|
routine childhood immunization against a component of its polysaccharide capsule
|
|
|
how is H. influenzae transmitted?
|
close contact with respiratory tract secretions from a patient colonized or infected with the organism
|
|
|
how does prior viral infection affect the colonization of H. influenzae in the respiratory tract?
|
promotes colonization
|
|
|
how does meningitis occur from a respiratory infection with H. influenzae?
|
organism invades the bloodstream and subsequently the meninges
|
|
|
what virulence factor for H. influenzae aids in adherence of the organism and evasion of phagocytosis?
|
capsule
|
|
|
in how many cases of meningitis do neurological sequelae occur?
|
20 percent of cases
|
|
|
other than meningitis, what can Haemophilus influenzae type B cause in young children?
|
epitlottitis
can result in respiratory obstruction requiring intubation |
|
|
for what are Haemophilus aphrophilus and Haemophilus paraphrophilus responsible for causing?
|
culture negative endocarditis, so named because of the fastidious nature and difficulty in recovering the organisms from the blood of infected patients
|
|
|
for what is Haemophilus ducreyi responsible for causing?
|
chancroid - an uncommon STD characterized by genital skin lesions and lymphdenopathy, leading to abscess formation if it remains untreated
|
|
|
what is epiglottitis?
|
inflammation of the epiglottis, usually caused by H. influenzae, which presents as sore throat, fever, and difficulty breathing
|
|
|
what is meningitis?
|
inflammation of the meninges leading to headache, stiff neck, and fever with increase in cells in the CSF
|
|
|
what is a Grand-mal seizure?
|
seizure that results in loss of consciousness and generalized muscle contractions
|
|
|
describe Haemophilus species
|
small
pleomorphic facultative anaerobes gram-negative bacilli or coccobacilli |
|
|
what factors are necessary to grow Haemophilus species?
what types of agars contain these factors? |
X factor (hematin)
V factor (NAD) Heated sheep blood agar, aka chocolate agar |
|
|
what are used to identify strains of H. influenzae?
how many types are there? |
specific antigens on the polysaccharide capsule
six types (A-F) |
|
|
what is the major virulence antiphagocytic factor of Type B H. influenzae?
|
polysaccharide capsule, which contains ribose, ribitol, and phosphate, known collectively as polyribitol phosphate (PRP)
|
|
|
what are the symptoms of acute meningitis?
|
rapid onset (over several days) of headache, fever, and stiff neck, although in young children only fever and irritability may be evident
sometimes presents with a rash w/o treatment, progresses to loss of consciousness and/or seizures and coma |
|
|
how is specific diagnosis of acute meningitis made?
how is a rapid presumptive diagnosis of bacterial meningitis made? |
culture of the etiologic organism from CSF
increased number of polymorphonuclear leukocytes in the CSF, elevated protein, and decreased glucose |
|
|
what are polymorphonuclear leukocytes?
|
broadly, granulocytes (neutrophils, eosinophils, basophils)
in practice, usually refers specifically to neutrophils |
|
|
when will gram stain of CSF of a patient with meningitis reveal the presence of bacteria?
what is seen in the case of H. influenzae meningitis? |
when the number of organisms is high enough/very high
tiny gram-negative coccobacilli |
|
|
what is the implication of H. influenzae requiring both X and V factors for growth?
|
no growth of H. influenzae will be seen on blood agar unless growth of S. aureus on the agar allowed for lysis of the blood and release of the required factors into the media
(could also be accomplished by heating the agar) |
|
|
when would good growth of H. influenzae be evident on chocolate agar?
|
after 24 hours of incubation at 35degC (95degF) and 5% CO2
|
|
|
how can ID of haemophilus to the species level be made?
|
requirement of X or V for growth
commercially available identification system, based on the presence of preformed enzymes |
|
|
why does it only take 4 hours to distinguish H. influenzae from other Haemophilus species?
|
H. influenzae grows much more quickly than other Haemophilus species, particularly H. ducreyi (5-7 days of incubation)
|
|
|
how is Haemophilus influenzae treated?
|
meningitis - third-generation cephalosporin (cefotaxime, ceftriaxone)
respiratory - amoxicillin-clavulanate or a macrolide (azithromycin) |
|
|
how is Haemophilus ducreyi treated?
|
erythromycin or a newer macrolide antibiotic
or fluoroquinolone |
|
|
how many generations of cephalosporins are there?
what is the difference between the generations of cephalosporins? |
4 generations
First-generation cephalosporins are predominantly active against Gram-positive bacteria, and successive generations have increased activity against Gram-negative bacteria (albeit often with reduced activity against Gram-positive organisms) fourth generation have true broad-spectrum activity |
|
|
45-year-old homeless, alcoholic male presents to ED with 4 day history of fever and cough (thick, bloody, productive cough); complains of pain in right side of chest with coughing or taking a deep breath; has developed a bacterial cavitary pneumonia with evidence of pulmonary abscess
what organism will most likely be isolated in the sputum and blood cultures? |
Klebsiella pneumoniae
|
|
|
by what mechanism does Klebsiella commonly develop antibiotic resistance?
|
plasmid acquisition from other organisms
|
|
|
with what types of infections is Klebsiella associated?
|
lower respiratory infections
wound soft tissue infections hospital-acquired UTIs Klebsiella pneumoniae is also associated with lobar pneumonia in a person w/ an underlying debilitating condition such as alcoholism or diabetes |
|
|
what are the tendencies for pneumonia caused by Klebsiella pneumoniae?
|
causes necrosis
inflammatory hemorrhagic high propensity for cavitation or abscess formation patients often produce thick, bloody sputum carries a high mortality (b/c of destructive nature and underlying debility of patient) |
|
|
what is an abscess?
|
a collection of pus in any part of the body that, in most cases, causes swelling and inflammation around it
|
|
|
why is Klebsiella pneumoniae pneumonia considered an opportunistic infection?
|
it has few virulence factors to fight host response in lower respiratory tract, so it does not commonly cause pneumonia in normally healthy patients
|
|
|
what are the symptoms of bacterial pneumonia?
|
usually nonspecific
malaise anorexia headache myalgia arthralgia fever |
|
|
what are the symptoms of Klebsiella pneumoniae?
|
severe acute, necrotic, and hemorrhagic pneumonia, evidenced by cavitary lung lesions on chest x-ray, pleural effusions, and possible abscess formation or empyema
patients tend to have blood-tinged sputum b/c of hemorrhagic nature of pneumonia |
|
|
with what is Klebsiella rhinoscleroma associated?
|
chronic granulomatous disease of the upper respiratory mucosa
(uncommon species and found predominantly outside the US) |
|
|
with what is Klebsiella ozaenae associated?
|
chronic atrophic rhinitis
(uncommon species) |
|
|
what is chronic obstructive pulmonary disease?
|
aka COPD
a progressive lung disease that commonly results from heavy smoking and is evident by difficulty breathing, wheezing , and a chronic cough |
|
|
what is an empyema?
|
accumulation of pus in the pleural space around the lung
|
|
|
to what family does the genus Klebsiella belong?
|
Enterobacteriaceae
|
|
|
how many species are in the genus Klebsiella? what is the most important?
|
5 species
most important is Klebsiella pneumoniae |
|
|
describe Klebsiella pneumoniae
|
large
nonmotile gram-negative bacillus (rod-shaped) prominent polysaccharide capsule |
|
|
how does the prominent polysaccharide capsule of Klebsiella pneumonia act as a virulence factor?
|
antiphagocytic
retards leukocyte migration into an infected area |
|
|
what are the virulence factors of Klebsiella?
|
prominent polysaccharide capsule
propensity to develop resistance to multiple antibiotics (via transfer of plasmids) recently some strains of nosocomial-acquired K. pneumoniae have been isolated that produce extended spectrum beta-lactamase |
|
|
what is the function of extended spectrum beta-lactamase?
how is it different from regular lactamase? |
removes beta-lactam antibiotics from the bacterial cells, prohibiting their effects (killing the bacteria)
while other beta-lactamases remove only early generations of beta-lactam antibiotics, extended spectrum removes ALL beta-lactam antibiotics |
|
|
what does the term "nosocomial infection" mean?
|
infections that are a result of treatment in a hospital or a healthcare service unit
|
|
|
how is community-acquired pneumonia diagnosed clinically?
|
based on symptoms of cough, esp. with blood, and chest x-ray indicating infiltrates, cavitary lesions, or pleural effusions
|
|
|
how is specific diagnosis of pneumonia made?
|
culture of expectorated sputum
sputum samples must be of good quality (many white blood cells and rare squamous epithelial cells) and represent the flora of the lower respiratory tract rather than oral flora |
|
|
what is special about culturing Klebsiella pneumoniae?
|
grows rapidly producing large mucoid colonies on routine laboratory media; the colonies are often extremely mucoid and will tend to drip into the lid of the plate while incubating in an inverted position
|
|
|
how does Klebsiella appear on MacConkey agar?
what does this indicate? |
pink colonies
indicates fermentation of lactose |
|
|
why is it so difficult to differentiate Klebsiella species with commercial identification systems?
|
all species are closely related with nearly identical biochemical reactions, except for the fact that K. pneumoniae is indole negative and K. oxytoca is indole positive
|
|
|
what is the response of Klebsiella pneumoniae to an indole test?
|
indole negative
|
|
|
what are the three important process by which DNA is transferred between bacteria?
|
transformation - uptake of soluble DNA by a recipient cell
transduction - transfer of DNA by a virus from one cell to another conjugation - direct transfer of soluble DNA (plasmids) between cells |
|
|
what are the three antigens that differentiate between members of the Enterobacteriaceae family?
|
O-antigen: cell wall antigen on outer polysaccharide portion of the LPS/endotoxin
H antigen: on flagellar proteins (escherichia and salmonella) K antigen: on capsule (particularly prominent in heavily encapsulated organisms such as Klebsiella) |
|
|
18 day old female presents with meningitis and Gram stain of CSF reveals gram-positive coccobacilli
what organism is responsible for this infection? |
Listeria monocytogenes
|
|
|
by what mechanism does Listeria monocytogenes avoid antibody-mediated defenses?
|
intracellular replication and spread from cell to cell by phagocytosis
|
|
|
how is Listeria transmitted?
|
ingestion of organism from infected foods (milk, soft cheese, undercooked meat, unwashed vegetables)
|
|
|
what types of infections are caused by Listeria monocytogenes?
|
PERSONS WITH INTACT IMMUNE SYSTEM:
asymptomatic infections mild gastrointestinal infections PREGNANT WOMEN, NEONATES, AIDS PATIENTS, AND MEDICALLY IMMUNOSUPPRESSED PATIENTS: most commonly meningitis |
|
|
what are the two types of neonatal Listeria monocytogenes?
|
Early-onset disease (occurring in the first two days of life) is the result of transplacental infection
Late-onset disease (occurring 2- weeks aftr birth) is thought to result from exposure to Listeria during delivery or shortly thereafter |
|
|
what is early-onset neonatal Listeria monocytogenes?
|
occurs in the first two days of life
result of transplacental infection initial signs and symptoms include difficulty breathing and pneumonia also called granulomatosis infantiseptica b/c severe disease can be associated with a granulomatous rash with abscesses |
|
|
what is late-onset neonatal Listeria monocytogenes?
|
occurs 2-3 weeks after birth
thought to result from exposure to Listeria either during delivery or shortly thereafter most commonly presents as meningitis |
|
|
with what syndromes are Listeria monocytogenes infections easy to mistake clinically?
|
group B streptococci
|
|
|
what is cold enrichment?
|
food is enriched in a selective broth media at room temperature or lower
used to enhance growth of Listeria, especially from food |
|
|
what is granulomatosis infantiseptica?
|
severe form of Listeria infection of neonates in which granulomatous skin lesions are evident
|
|
|
what is Gravida?
|
total number of pregnancies
|
|
|
what is Para?
|
number of deliveries (usually after 20-week gestation); a pregnancy that ends prior to 20-week gestation is an abortus
|
|
|
describe Listeria monocytogenes
|
small
facultative anaerobic catalase positive gram-positive bacillus or coccobacillus appears in pairs or chains intracellular pathogen |
|
|
how is being an intracellular pathogen a virulence factor?
|
allows it to avoid antibody-mediated defenses of the host
|
|
|
what protein induces the phagocytosis of Listeria monocytogenes?
|
internalin
induces phagocytosis of of the bacteria |
|
|
describe the life cycle of Listeria monocytogenes
|
internalin induces phagocytosis of the bacteria
Listeria produces a toxin which lyses the phagosome bacteria replicates in the host cytoplasm and moves to the host membrane bacteria pushes against the membrane, making a protrusion adjacent cells phagocytize protrusion cycle begins again |
|
|
what is a filopod?
|
a protrusion of the cellular membrane, caused by a bacteria pushing against the cell membrane, which enables adjacent cells to phagocytize the bacteria
|
|
|
why do host cellular immunity factors protect against Listeria infection?
|
since Listeria is spread from cell to cell by being phagocytized by adjacent cells, so it is never exposed to antibodies or other humoral immunity factors, and the only way to inhibit it is to kill the host cells in which it grows
|
|
|
how is being an intracellular pathogen a virulence factor?
|
allows it to avoid antibody-mediated defenses of the host
|
|
|
what protein induces the phagocytosis of Listeria monocytogenes?
|
internalin
induces phagocytosis of of the bacteria |
|
|
describe the life cycle of Listeria monocytogenes
|
internalin induces phagocytosis of the bacteria
Listeria produces a toxin which lyses the phagosome bacteria replicates in the host cytoplasm and moves to the host membrane bacteria pushes against the membrane, making a protrusion adjacent cells phagocytize protrusion cycle begins again |
|
|
what is a filopod?
|
a protrusion of the cellular membrane, caused by a bacteria pushing against the cell membrane, which enables adjacent cells to phagocytize the bacteria
|
|
|
why do host cellular immunity factors protect against Listeria infection?
|
since Listeria is spread from cell to cell by being phagocytized by adjacent cells, so it is never exposed to antibodies or other humoral immunity factors, and the only way to inhibit it is to kill the host cells in which it grows
|
|
|
how is a definitive diagnosis of Listeria made?
|
culture of the CSF and/or blood
gram stain of CSF and/or blood demonstrate small gram-positive bacilli, appearing similar to corynebacteria or S. pneumoniae |
|
|
how does Listeria monocytogenes grow on routine agar media?
|
grow within 24-48 hours
demonstrate beta-hemolysis on blood agar |
|
|
how is specific identification of Listeria monocytogenes made from a wet preparation?
|
after room temperature incubation, characteristic tumbling motility
|
|
|
how is Listeria monocytogenes treated?
|
septicemia or meningitis is with ampicillin plus or minus gentamycin
|
|
|
to what class of antibiotics is Listeria resistant to?
why is this important? |
cephalosporins
these are commonly chosen as empiric therapy for meningitis in adults and would be appropriate for treatment of streptococcal meningitis in children |
|
|
how is Listeria monocytogenes infection prevented?
|
avoidance of consumption of under-cooked foods, especially in high-risk patients
|
|
|
50-year-old vietnamese man presents with chronic bloody sputum, weight loss, and a cavitary lesion on left upper lobe of chest radiograph
what is the most likely etiology? |
mycobacterium tuberculosis
|
|
|
how does mycobacterium tuberculosis appear on gram staining?
|
colorless ("ghost") cells
|
|
|
what is the most commonly used staining technique for mycobacterium tuberculosis?
|
acid-fast staining
|
|
|
what are the histologic characteristics of Langhans cells?
|
multinucleated cells of fused macrophages
|
|
|
how is mycobacterium tuberculosis spread?
|
aerosolized respiratory droplets that travel to the terminal airways
|
|
|
what happens to mycobacterium tuberculosis after it has reached the terminal airways?
|
they are phagocytized by alveolar macrophages, but inhibit destruction by the phagosome and proceed to replicate
circulating macrophages are attracted to the area and form Langhans cells extrapulmonary sites are infected through the spread of infected macrophages |
|
|
what populations are at high risk for infection with mycobacterium tuberculosis?
|
AIDS patients
alcoholics drug abusers persons living in crowded, close quarters (i.e. prisoners) |
|
|
what is important about the granulomas formed by mycobacterium tuberculosis?
|
the organism can remain dormant in the granulomas for many years and reactivate following immunosuppression at a later date
|
|
|
what is mycobacterium avium-intracellulare?
|
a pathogen found in the environment which is an opportunistic pathogen that causes disease in AIDS patients
disease ranges from pneumonia to gastroenteritis to disseminated disease |
|
|
what is mycobacterium kansasii?
|
a pathogen which mimics pulmonary tuberculosis but is most often seen in middle-aged men with prior lung damage (silicosis or asbesosis)
|
|
|
what is mycobacterium leprae?
|
a pathogen acquired by contact with the nine-banded armadillo
most infections are seen in the souther US, including Texas and Louisiana |
|
|
why were patients with mycobacterium leprae contained in sanitariums and left to die?
|
they were thought to be lepers because of their skin lesions and facial deformaties
|
|
|
what is a granuloma?
|
chronic inflammatory response to either mycobacterium or funi, composed of macrophages and multinucleated giant cells
|
|
|
what is PPD?
|
purified protein derivative, prepared from M. tuberculosis antigens, inoculated intradermally and a positive reaction is indicative of exposure to M. tuberculosis
|
|
|
describe mycobacteria
|
small
bacillus (rod-shaped) stains as ghost cells with Gram stain stain with an acid-fast stain b/c of mycolic acids in cell wall |
|
|
why does mycobacterium tuberculosis stain with acid-fast stain?
what are two examples of acid-fast stains? |
it has mycolic acid in its cell wall
Kinyon Ziehl-Neelsen |
|
|
what are the effects of the complex, lipid-rich cell wall of mycobacteria?
|
makes the organisms resistant to many commonly used laboratory stains
responsible for resistance of organisms to many common detergents and antibiotics |
|
|
what is the generation time of mycobacterium species?
|
15-20 hours (most bacteria are about 1 hour)
|
|
|
how are mycobacteria characterized?
|
pigment production
|
|
|
what are photochromogens?
|
mycobacteria that only are pigmented in the presence of light
M. kansasii and other saprophytic mycobacteria |
|
|
what are scotochromogens?
|
mycobacteria that are pigmented even in the absence of light
M. szulgai M. gordonae (nonpathogenic - orange pigment) |
|
|
what are nonchromogens?
|
mycobacteria that are not pigmented in the light or in the dark
M. avium-intracellulare M. haemophilum |
|
|
what is the fourth runyon group?
|
rapidly growing Mycobacteria
M. fortuitum M. chelonae M. abscessus |
|
|
what is included in the M. tuberculosis complex?
|
M. tuberculosis
M. africanum M. ulcerans M. bovis rarely identified mycobacteria |
|
|
what is special about the M. tuberculosis complex?
|
these colonies appear buff or tan color and are dry when growing on Lowenstein-Jensen agar
|
|
|
why is mycobacterium leprae difficult to classify?
|
it cannot be cultured in the laboratory
|
|
|
what is cord factor?
|
a virulence factor of M. tuberculosis
organisms grown in broth culture will demonstrate a ropelike pattern indicating cording |
|
|
how is tuberculosis made initially?
|
based on history (exposure to patient with tuberculosis, immigration, a stay in jail or homeless shelter) and physical exam in patients with a productive cough, night sweats, and fever
|
|
|
what is indicated by a positive PPD test?
|
exposure to M. tuberculosis
warrants further testing with chest x-ray |
|
|
what are classic chest radiograph findings for tuberculosis?
|
lower lobe consolidation in active infection
apical lobe scarring with reactivation |
|
|
what are the current prophylactic measures for tuberculosis?
|
oral isoniazid for 6-9 months
given to all patients with a recent conversion of PPD to positive and a negative chest x-ray |
|
|
how is tuberculosis treated?
|
based on culture of M. tuberculosis from any patient specimen
initially with a multiagent regimen based on likely resistance patterns (isoniazid, rifampin, ethambutol, pyrazinamide) for two months when results indicate susceptibility to the four drugs, can back off to two (usually isoniazid and rifampin) for 4-6 months |
|
|
why is it important to individualize the tuberculosis treatment regimen?
|
rifampin interacts with several other drugs, particularly HIV drugs and antifungals
|
|
|
how is the spread of tuberculosis prevented?
|
prophylactic isoniazid
isolation of patients in hospital vaccination with BCG (uncommon in US) |
|
|
what is in the BCG vaccine for tuberculosis?
|
attenuated strain of M. bovis
|
|
|
why are people in the U.S. not routinely vaccinated for tuberculosis?
|
comparatively low incidence of tuberculosis in US
protection is not 100 percent with the vaccine can confuse the results of the PPD for screening of recent converters |
|
|
how is mycobacterium avium-intracellulare treated?
|
clarithromycin or azithromycin and ethambutol plus or minus amikacin
|
|
|
what is the current treatment for mycobacterium leprae?
|
dapsone and rifampin for at least 6 months
|
|
|
15-year-old adolescent presents with a persistent cough, patchy infiltrate on chest x-ray, and exposure to a friend with "walking pneumonia"
what is the most likely infectious agent? |
mycoplasma pneumoniae
|
|
|
why are no organisms seen on gram stain in a patient infected with mycoplasma pneumoniae?
|
it does not stain because it does not have a cell wall
|
|
|
what is the rapid blood test for presumptive evidence of M. pneumoniae?
|
cold agglutinins
|
|
|
how is mycoplasma pneumoniae transmitted?
|
aerosolized respiratory droplets
|
|
|
in what populations is mycoplasma pneumoniae most common?
|
children
adolescents |
|
|
what is the progression of mycoplasma pneumoniae?
|
insidious onset
progresses to tracheobronchitis or pneumonia, which is often patchy or diffuse (as opposed to lobar) |
|
|
what is the most common method to test for mycoplasma pneumoniae?
why? |
serologic testing
inability to diagnose on microscopy difficulty and length of time required to culture |
|
|
what is tracheobronchitis?
|
inflammation of the trachea in addition to the bronchi; causes swelling and narrowing of the airways
|
|
|
what are rhonchi?
|
coarse rattling sounds heard on auscultation of the lungs of a patient with partially obstructed airways
|
|
|
what is pruritus?
|
itching; can have many causes: food allergy, drug reaction, kidney/liver disease, aging or dry skin, cancers, infectious agents or other unknown causes
|
|
|
describe mycoplasma pneumoniae
|
short
strictly aerobic bacillus smallest free-living bacterium/prokaryote trilamellar, sterol-containing cell membrane, but no cell wall |
|
|
what are the effects of having no cell wall (mycoplasma pneumoniae)?
|
not identifiable with Gram or other stains
resistance against beta-lactams and other antibiotics that act on the cell walls |
|
|
what is the doubling time of mycoplasma pneumoniae?
|
about 6 hours
|
|
|
how does mycoplasma pneumoniae replicate?
|
entirely extracellular, even during infection
divides by binary fission |
|
|
what is responsible for the attachment of mycoplasma pneumoniae to a protein on target cells and may confer its preference for respiratory epithelium?
|
adherence protein PI at one end
|
|
|
what happens after mycoplasma pneumoniae attaches to ciliated, respiratory epithelial cells?
|
it destroys the cilia and then the cell, interfering with normal mucociliary clearance and allowing the lower airways to be irritated and contaminated with infectious agents
|
|
|
how long is the incubation period before the onset of clinical disease in patients with mycoplasma pneumoniae?
|
1-3 weeks
|
|
|
what percentage of community acquired pneumonias are caused by mycoplasma pneumoniae?
|
15-20%
|
|
|
what is the clinical presentation of mycoplasma pneumoniae infection?
|
low-grade fever
headache malaise nonproductive cough later slow resolution |
|
|
how is diagnosis of mycoplasma pneumoniae typically made?
|
clinical presentation
serologic testing to confirm antibody-directed enzyme immunoassays and immunofluorescence tests or complement fixation tests titer of cold agglutinins |
|
|
what autoimmune phenomenon often results from mycoplasma pneumoniae infection?
what is the importance of this? |
stimulation of an IgM antibody against the I-antigen on erythrocytes
antigen-antibody complex binds at 4degC, causing the clumping of erythrocytes at low temperatures |
|
|
what is the pitfall to cold agglutinin diagnosis of mycoplasma pneumoniae?
what are the limits of the test to assume a presumptive diagnosis of mycoplasma pneumoniae? |
this response can be triggered by other organisms
titers of these antibodies of 1:128 or greater, or fourfold increase with the presence of appropriate clinical presentation |
|
|
what infections are associated with mycoplasma hominis?
|
pelvic inflammatory disease
nongonococcal urethritis pyelonephritis postpartum fever |
|
|
what is ureaplasma urealyticum?
|
a facultative anaerobic bacillus which is is a cause of nongonococcal urethritis
can be commensal or STD (leads to infertility) |
|
|
what are the symptoms of nongonococcal urethritis?
|
urethral discharge
pruritus dysuria typically no systemic symptoms onset of symptoms is usually subacute |
|
|
how many new cases of NGU are there each year? how many women suffer PID as a result?
|
3 million new cases (including M. hominis, U. urealyticum, C. trachomatis, and trichomonas vaginalis)
10-40percent of women (only 1-2% of males) |
|
|
how is mycoplasma pneumoniae associated pneumonia treated?
|
tetracycline and macrolides
tetracycline treats most mycoplasmas and chlamydia macrolides treat Ureaplasma |
|
|
why are mycoplasma pneumoniae infections difficult to prevent?
|
patients are infectious for extended periods of time, even during treatment
no vaccines have been developed |
|
|
19-year-old female with septic arthritis; has had infection previously with Chlamydia
what is the most likely finding on gram stain of the joint fluid aspirate? |
multiple polymorphonuclear leukocytes with intracellular gram-negative diplococci (neisseria gonorrhoeae)
|
|
|
what cell surface factor facilitate the attachment and penetration of Neisseria into host cells?
|
pili - attach to epithelial cells
Opa protein - promotes firm attachment and cell penetration |
|
|
what is the only known reservoir for Neisseria species?
|
humans
|
|
|
how is neisseria gonorrhoeae transmitted?
|
sexual contact
|
|
|
how many men and women have an asymptomatic carrier state of Neisseria gonorrhoeae?
|
about half of women
much fewer men |
|
|
what are the symptoms of gonorrhoea in men and women?
|
men - urethritis
women - cervicitis |
|
|
what are the complications of Neisseria gonorrhoeae?
|
pelvic inflammatory disease
rectal infection oropharynx infection |
|
|
what is ophthalmia neonatorum?
|
conjunctivitis in a newborn (first month of life) caused by passing through a birth canal infected with usually Neisseria gonorrhoeae or Chlamydia trachomatis
|
|
|
in what patients is disseminated disease from Neisseria gonorrhoeae a common sequelae?
what does disseminated disease include? |
patients with complement deficiencies
joint and/or skin infections septic arthritis (two forms: systemic disease with fever, chills and polyarticular syndrome; monoarticular suppurative infection of a single joint without skin lesions or systemic symptoms) most disseminated cases occur in persons with an asymptomatic genital infection |
|
|
what percentage of the population carries Neisseria meningitidis as normal upper respiratory flora?
|
10 percent of the population
|
|
|
what are the functions of the polysaccharide capsule of Neisseria meningitidis?
|
allow organism to avoid phagocytosis
under unknown circumstances, allows organism to enter blood and central nervous system |
|
|
what is caused by inflammatory response induced by Neisseria meningitidis?
|
causes shock and disseminated intravascular coagulation
evidenced by skin lesions, which can mimic those in disseminated gonococcal infection bacteremia with or without meningitis usually occurs in teenage children if untreated, has a high mortality rate |
|
|
describe Neisseria species
|
aerobic
nonmotile nonspore-forming gram-negative oxidase positive cocci (sphere-shaped) usually arranged in pairs (diplococci) with adjacent sides flattened |
|
|
what are the virulence factors of Neisseria gonorrheae?
|
pili - attach to host epithelial cells and provides resistance to killing by neutrophils
Opa (opacity) proteins - promote tight attachment and migration of bacteria into host Por proteins (porin) - forms channels in the outer membrane, prevents phagolysosome fusion, aloowing intracellular survival Rmp proteins (reduction modifiable proteins) - stimulate antibodies, which inhibit host bactericidal antibodies (protects other surface antigens from host attack) |
|
|
what are the two methods that appear to play significant roles in the development of antibiotic resistance by N. gonorrhoeae?
|
plasmid acquisition and transfer
|
|
|
what is in the cell wall of N. gonorrhoeae is responsible for the inflammatory response which causes most of the symptoms?
|
lipooligosaccharide (LOS)
causes release of TNFalpha |
|
|
how is definitive diagnosis of septic arthritis made?
|
analysis of cells and gram stain from an aspirate of the joint
|
|
|
what selective media are usually used to isolate N. gonorrhoeae from nosterile sites such as the cervix or urethra?
|
thayer martin
martin lewis |
|
|
why might special transport media (like Jembec) be necessary for N. gonorrhoeae?
|
very sensitive to drying, so plates must be placed in a warm environment quickly to maintain viability
special transport media are necessary if a delay in transit to the laboratory is expected to be longer than several hours |
|
|
how can N. gonorrhoeae be differentiated from N. meningitidis?
|
N. gonorrhoeae ferments only glucose
N. meningitidis ferments both glucose and maltose |
|
|
what is the treatment of choice for meningococcemia?
|
penicillin
|
|
|
what are the treatments for N. gonorrhoeae?
|
ceftriaxone or quinolones
|
|
|
how in meningococcal disease prevented?
|
vaccination of adolescents at the age of 11-12 years, of military personnel, of college students, and of asplenic patients
prophylaxis of close contacts |
|
|
how is N. gonorrhoeae prevented?
|
safe sex and use of a condom
screening of pregnant women for congenitally transmitted infections with appropriate treatment |
|
|
35-year-old woman with UTI and nephrolithiasis (kidney stones); her urine has a high pH
what organism is most likely responsible for this infection? |
proteus mirabilis
|
|
|
what is the mechanism by which proteus creates a high pH in the urine?
|
produces urease, which splits urea into carbon dioxide and ammonia, rasing the urinary pH
|
|
|
what is the source of proteus species?
|
normal flora of the GI tract
predominantly associated with hospital-acquired UTIs as well as bacteremia, osteomyelitis, empyema, and neonatal encephalitis |
|
|
how do proteus infections result in significant renal damage?
|
produce large amounts of urease, which results in high urinary pH (direct renal toxicity and increased urinary stone formation)
urinary stones obstruct urine flow and serve as a focus for ongoing infection |
|
|
what is nephrolithiasis?
|
presence of calculi (solid, crystalline) that develop in the kidney and pass through the genitourinary tract
|
|
|
what is hydronephrosis?
|
enlargement of the kidney because of an abnormality such as the presence of stones
|
|
|
how many species are in the genus proteus?
what are the two most common? |
five
Proteus mirabilis Proteus vulgaris |
|
|
describe proteus species
|
nonspore-forming
facultative anaerobic gram-negative bacillus has hemolysin - damages cells by forming pores has fimbriae - facilitate attachment to uroepithelium has flagellae - motility required for ascending infection transforms from single cell form to multicell elongated (swarmer) form |
|
|
what is a swarmer cell?
how is it important? |
multicell elongated form of proteus species, which is more likely to be associated with cellular adherence in the kidney
|
|
|
how is Proteus identified on a MacConkey agar plate?
|
clear colony (nonlactose fermenter)
|
|
|
what is a quick test to differentiate between proteus mirabilis and proteus vulgaris?
|
P. vulgaris is indole positive, while P. mirabilis is indole negative
|
|
|
what is the treatment for Proteus species?
|
most susceptible to penicillin, among all of the enterobacteriaceae
(not uncommon that they're resistant to tetracyclines |
|
|
which common Proteus specie is more resistant to more antimicrobials?
|
P. vulgaris is more resistant than P. P. mirabilis
|
|
|
what is swarming?
what type of bacteria commonly do this? |
thin film of bacteria over the entire agar plate
Proteus species do this b/c of rapid motility |
|
|
73-year-old male with malignant otitis externa
what organism most likely causes this infection? |
Pseudomonas aeruginosa
|
|
|
what two toxins contribute to most of the systemic signs of infection with Pseudomonas aeruginosa?
|
LPS endotoxin
exotoxin A |
|
|
what is the common factor among the numerous types of infections caused by Pseudomonas?
|
usually in a debilitated host
|
|
|
what types of infections are associated with Pseudomonas aeruginosa?
|
skin infections - burn or trauma patients
respiratory infections - cystic fibrosis or chronic lung/heart disease UTIs - catheterized patients chronic otitis/malignant otitis externa - elderly and diabetics |
|
|
what is an erythrocyte sedimentation rate?
|
(ESR)
measure of the time it takes for red blood cells to settle, which is a nonspecific measure of inflammation |
|
|
what is ecthyma gangrenosum?
|
pustular skin lesions that later become necrotic ulcers and can lead to gangrene
|
|
|
describe Pseudomonas species
|
ubiquitous
aerobic gram-negative bacillus (rod-shaped) opportunistic pathogens |
|
|
describe Pseudomonas aeruginosa
|
ubiquitous
aerobic gram-negative bacillus (rod-shaped) opportunistic pathogen polar flagellae intrinsic resistance to many antibiotics and disinfectants |
|
|
what are common reservoirs for Pseudomonas aeruginosa?
|
nature - soil, vegetation, water
hospitals - sinks, toilets, mops, respiratory therapy, dialysis equipment |
|
|
what are the virulence factors for Pseudomonas aeruginosa?
|
pili and nonpili adhesins - adheres to host cells
polysaccharide capsule - adhere to epithelial cells, inhibits phagocytosis, protects against antibiotic activity LPS endotoxin - contribute to fever, leukocytosis, and hypotension (sepsis) Exotoxin A - blocks protein synthesis in host cells - direct cytotoxicity |
|
|
what are the mechanisms for antibiotic resistance in Pseudomonas aeruginosa?
|
polysaccharide capsule prevents penetration of many antibiotics
mutation of porin proteins (which allow antibiotics into capsule) so that antibiotics aren't allowed in beta-lactamase production multidrug efflux pumps |
|
|
what pigments are produced by different strains of P. aeruginosa?
|
pyocyanin - blue color
fluorescein - yellow color pyorubin - red-brown color |
|
|
what is pyocyanin?
|
blue colored pigment produced by some strains of Pseudomonas aeruginosa
aids virulence of organism by stimulating an inflammatory response and by producing toxic oxygen radicals |
|
|
how is malignant otitis externa diagnosed?
|
common clinical features of otorrhea, painful edematous ear canal with a purulent discharge
culture grows P. aeruginosa in most cases (grows readily on routine lab media) preliminary - colony morphology, particularly if typical green pigment is produced |
|
|
how does Pseudomona aeruginosa appear on MacConkey agar?
|
clear to dark colony
indicates that it doesn't ferment lactose |
|
|
how does P. aeruginosa appear on blood agar?
|
beta-hemolytic and dark color
|
|
|
does P. aeruginosa ferment glucose?
|
no
|
|
|
is P. aeruginosa oxidase negative or positive?
|
positive
|
|
|
what is the distinct odor of P. aeruginosa colonies?
|
grape-like
|
|
|
how is malignant otitis externa treated?
|
surgery - remove necrotic tissue and pus
appropriate antibiotics (treatment with two to which the organism is susceptible is optimal u |
|
|
48-year-old male with acute gastroenteritis has a fever, a positive tilt test, abdominal pain, and diarrhea after eating eggs a day before
what is the most likely etiology of this infection? |
Salmonella
|
|
|
what are the most common sources of Salmonella infection?
|
undercooked poultry
eggs dairy products foods prepared on contaminated work surfaces |
|
|
what is indicated by a positive tilt test?
what constitutes a positive tilt test? |
significant volume depletion
rise in HR of 10bpm, with drop in BP of 10mmHg |
|
|
what mode of Salmonella transmission is common among children?
|
fecal-oral spread
|
|
|
what is the body's first/primary defense mechanism against salmonella?
what does this imply? |
gastric acidity
conditions/medications that reduce gastric acidity may predispose the person to infection |
|
|
what is the primary site of invasion of Salmonella?
|
M (microfold) cells in the Peyer's patches of the distal ileum
infection then spreads to adjacent cells and GALT host defenses usually limit infection to GI tract, but bacteremia is possible |
|
|
what is the function of M (microfold) cells?
|
internalize and transfer foreign antigens from intestinal lumen to macrophages and leukocytes
|
|
|
in what populations is salmonella bacteremia more common?
|
children
elderly patients those with immune deficiencies (AIDS) |
|
|
what is the most common clinical manifestation of salmonella infection?
|
gastroenteritis
nausea, vomiting, nonbloody diarrhea, fever, and abdominal cramps starting 8-48 hours after ingestion of contaminated food (lasts 2-7 days, self-limited) |
|
|
which species of Salmonella are associated with Enteric fever or typhoid fever?
what is enteric fever? |
Salmonella typhi
Salmonella paratyphi enteric fever (typhoid fever) is a more severe form of gastroenteritis with systemic symptoms |
|
|
what are the symptoms of enteric fever (typhoid fever)?
|
chills, headache, anorexia, weakness, muscle aches
later: fever, lymphadenopathy, hepatosplenomegaly, maculopapular rash (rose spots in 1/3 of patients) symptoms persist longer than in nontyphoidal gastroenteritis |
|
|
what other infection is mimiced (signs and symptoms) by Salmonella gastroenteritis?
|
Shigella
|
|
|
what are the symptoms of Shigella?
|
predominantly diarrhea, sometimes grossly bloody as a result of invasion of mucosa
usually self-limited, however dehydration can occur if diarrhea is severe |
|
|
what are rose spots?
|
papular rash usually on the lower trunk leaving a darkening of the skin, characteristic of typhoid fever
|
|
|
what are fecal leukocytes?
|
WBCs found in the stool, a nonspecific finding of an invasive process
|
|
|
describe Salmonella
|
motile
facultative anaerobic nonspore-forming gram-negative bacilli acid tolerance response gene Salmonella-secreted invasion proteins (Sips or Ssps) |
|
|
what is the acid tolerance response gene?
|
a gene in Salmonella species which protects them from gastric acid and from the acidic pH of the phagosome
|
|
|
what is Salmonella-secreted invasion protein?
|
aka Sips or Ssps
proteins that rearrange M-cell actin, resulting in membranes that surround and engulf the Salmonella and enable intracellular replication of the pathogen with subsequent host cell death |
|
|
what 2 of the 2400 serotypes of Salmonella only colonize humans?
|
S. typhi
S. paratyphi all others are capable of infecting almost all animal species |
|
|
to what family of bacteria does Salmonella belong?
|
Enterobacteriaceae
|
|
|
to what family does Shigella belong?
|
Enterobactericeae
|
|
|
what mechanisms protect salmonella from phagocytic destruction?
|
acid tolerance response gene - protects from acidic pH of phagosome
Salmonella-secreted invasion proteins - rearrange M-cell actin resulting in membrane that surrounds and engulfs Salmonella |
|
|
describe Shigella
|
nonmotile
gram-negative bacilli lactase negative doesn't produce H2S |
|
|
what are the four groups or species of Shigella?
how many serotypes of Shigella are there? |
group A - Shigella dysenteriae
group B - Shigella flexneri group C - Shigella boydii group D - Shigella sonnei 40 serotypes of Shigella, which fall into these four groups |
|
|
what are the virulence mechanisms of Shigella?
|
ability to invade intestinal mucosa
production of shiga toxin |
|
|
what is the function of shiga toxin?
from what bacteria is it released? |
destroy intestinal mucosa once the organism has invaded the tissue
exotoxin released from Shigella and some strains of E. coli (enterohemorrhagic) |
|
|
on what is a diagnosis of gastroenteritis made?
|
patient's age, risk factors, exposures, and symptoms
|
|
|
what is necessary for a definitive diagnosis of gastroenteritis if fever and other systemic symptoms are present?
|
collection of stool and blood cultures
|
|
|
how does a direct exam for fecal leukocytes and occult blood narrow down the DDx?
|
blood in stools usually indicates invasive bacterial infection
in cases of bacterial gastroenteritis, final diagnosis is made by culture of stool for enteric pathogens (Campylobacter, Shigella, Salmonella) |
|
|
does Shigella ferment lactose?
|
no
appear as clear colonies on MacConkey agar |
|
|
does Salmonella ferment lactose?
|
no
appear as clear colonies on MacConkey agar |
|
|
what is a good way to differentiate between Shigella and Salmonella?
|
use a medium that contains an indicator for production of H2S (i.e. Hektoen enteric agar)
Shigella - negative - clear or green colonies Salmonella - positive - black colonies |
|
|
to what is a DDx narrowed down in the case of gastroenteritis, with a positive test for shiga toxin in the stool?
|
Shigella
enterohemorrhagic E. coli |
|
|
with what disorder is enterohemorrhagic E. coli associated?
|
hemolytic uremic syndrome (HUS)
|
|
|
what are the treatments for Salmonella?
|
nontyphoid gastroenteritis - supportive (fluid replacement)
bacteremia, long-term carriers, typhoid fever - amoxicillin, sulfamethoxazole and trimethoprim (SMX-TMP), or quinolones (for resistant strains |
|
|
what is the treatment for Shigella infection?
|
antibiotic therapy - useful for preventing person-to-person spread
quinolones |
|
|
how is salmonella prevented?
|
control of contaminated source in environment
good personal hygiene thoroughly cook poultry and eggs vaccine for typhoid fever (50-80% effective) |
|
|
what does halophilic mean?
|
organisms requiring high salt concentration
(vibrios are well known for this ability) |
|
|
59-year-old male with emphysema secondary to 50-pack-year history presents with fever and cough, and rust colored sputum; chest x-ray shows a dense infiltration of the left lower lobe and a left pleural effusion
what are the most likely findings in gram stain? |
multiple polymorphonuclear leukocytes
encapsulated gram-positive cocci in pairs and short chains (streptococcus) |
|
|
what is the most likely reservoir of streptococcal infection?
|
colonization of the upper airway (naso- or oropharynx) and aspiration into the lower airways
|
|
|
what is the range of Streptococcus infections?
|
localized skin and soft tissue infections
to systemic infections (necrotizing fasciitis, endocarditis, and arthritis) |
|
|
with what is streptococcus pyogenes commonly associated?
|
pharyngitis & its sequelae (rheumatic fever and glomerulonephritis)
skin and soft-tissue infections |
|
|
with what is Streptococcus agalactiae associated?
|
neonatal meningitis following vaginal colonization of pregnant women
|
|
|
what is caused by streptococcus pneumoniae?
|
otitis media
sinusitus bronchitis pneumonia meningitis |
|
|
what is the most common cause of bacterial pneumonia, otitis, and meningitis?
|
Streptococcus pneumoniae
(aka pneumococcus) |
|
|
how does pneumococcal pneumonia occur?
|
streptococcus pneumoniae is aspirated into the distal airways from its site of colonization (naso- or oropharynx) into the distal airways and multiplies in the alveoli
usually follows upper respiratory infection |
|
|
what are the symptoms of pneumococcal pneumonia?
|
cough
fever chills shortness of breath increased WBCs anemia |
|
|
what are the common complications of Streptococcus pneumoniae infections?
|
pneumococcal pneumonia - pleural effusion
sinusitis or otitis - meningitis (result of bacteremic spread of organism) |
|
|
what populations are at higher risk than normal for developing serious disease with S. pneumoniae?
|
immunocompromised patients
elderly patients patients with underlying heart/lung disease asplenic patients |
|
|
what are rhonchi?
|
vibration of the chest wall that can be felt with the hand and sounds like a dull roar or murmuring
|
|
|
what are cytokines?
|
proteins produced by leukocytes that act as mediators of a further inflammatory response
|
|
|
by what are the multiple species in the genus streptococcus differentiated?
|
cell wall carbohydrate group antigen (not all streptococci have cell wall antigen)
hemolysis on blood agar biochemical reactivity |
|
|
describe streptococci
|
facultative anaerobes (require CO2 for growth)
gram-positive cocci (form pairs or chains) polysaccharide capsule |
|
|
describe streptococcus pneumoniae
|
elongated
lancet-shaped gram-positive cocci (sphere shaped) pairs or short chains |
|
|
why must virulent strains of pneumococcus be encapsulated?
|
without the polysaccharide capsule, the bacteria would be easily cleared by host defenses
|
|
|
what are the virulence factors for pneumococcus?
|
polysaccharide capsule - antiphagocytic
surface protein adhesins - facilitate colonization by binding pneumococcus to epithelial cells secretory IgA protease - prevents host IgA from binding to it pneumolysin - destroys phagocytic and ciliated epithelial cells by creating pores in cell membrane |
|
|
what is the mechanism by which pneumolysin works?
in what bacteria is this found? |
pneumolysin creates pores in the cell membrane of phagocytic and ciliated epithelial cells; in the phagocytic cells, this inhibits the oxidative burst required for intracellular killing
found in streptococcus pneumoniae (aka pneumococcus) |
|
|
what is the pathogen that causes pneumococcal pneumonia?
|
streptococcus pneumoniae
|
|
|
what cause much of the tissue damage from pneumococcal infections?
|
host inflammatory response
teichoic acid, peptidoglycan fragments, and pneumolysin activate complement system, stimulating cytokine production HOOH produced by pneumococcus, which causes tissue damage via ROS |
|
|
why is antibiotic resistance an increasingly important problem with pneumococcus?
|
penicillin resistance has developed, mainly b/c of penicillin-binding proteins in cell wall
efflux pumps confer some degree of resistance to antibiotics |
|
|
by what means has antibiotic resistance increased in pneumococcus?
|
mutations in cellular DNA
acquisition of DNA from other pneumococci and from other bacteria |
|
|
how is pneumococcal pneumonia diagnosed?
|
clinical signs and symptoms
chest x-ray demonstrating infiltration of a single lobe sputum gram stain with many PMNs and gram-positive cocci in pairs and chains |
|
|
how is pneumococcal pneumonia diagnosis confirmed?
|
culturing organism from sputum and/or blood (grows rapidly on routine lab media including blood and chocolate agar)
urinary antigen test |
|
|
how does streptococcus pneumoniae (pneumococcus) appear on blood agar?
|
demonstrate beta-hemolysis
colonies are green may be slighlty to extremely mucoid b/c of the polysaccharide capsule |
|
|
how are colonies of streptococcus pneumoniae (pneumococcus) distinguished from viridans streptococci?
|
sensitivity to optochin and bile solubility
optochin is definitive addition of bile will ID organism as S. pneumoniae if the colony lyses and dies in a few minutes |
|
|
how is pneumococcus treated?
|
uncomplicated - quinolone or macrolide
complicated (disseminated) - penicillin or cefotaxime |
|
|
how are non-pneumococcal strep species treated?
|
usually penicillin
but dependent on individual isolate susceptibility in serious infections |
|
|
to whom is it recommended a pneumococcal vaccine is administered?
|
children
persons over 65 yo people at high risk for pneumonia (diabetics or COPD/fibrosis patients) |
|
|
what is targeted by the pneumococcal vaccine?
|
pneumococcal capsular antigens
|
|
|
where are group B streptococci normal flora?
|
aka streptococcus agalactiae
female genital tract (important causes of neonatal sepsis and meningitis) |
|
|
what is the rule of thumb for penicillin therapy?
|
concentration of penicillin in CSF should be 10x the MIC
|
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|
15-year-old male with gastroenteritis after eating food at an outdoor picnic; several other participants developed similar symptoms
what organism is most likely causing the infection? |
Staphylococcus aureus
|
|
|
should S. aureus gastroenteritis be treated with antibiotics? why or why not?
|
no - S. aureus gastroenteritis is caused by a preformed toxin, not by ingestion of the bacteria itself, so antibiotic therapy would be no help
|
|
|
how does infection with S. aureus occur?
|
S. aureus commonly colonizes the nasopharynx and the skin
when normal skin barrier is disrupted by either surgery or trauma, S. aureus penetrates |
|
|
what infections, caused by S. aureus, are toxin mediated?
|
toxic shock syndrome
scalded skin syndrome gastroenteritis |
|
|
what is Panton-ValentineLeukocidin?
|
aka PVL
toxin produced by a majority of ca-MRSA strains that is associated with more severe disease, including skin and soft tissue infections and necrotizing pneumonia |
|
|
what is the second most reported cause of food poisoning in the US?
what causes it? |
staphylococcal food poisoning
caused by enterotoxin that rapidly produces nausea, vomiting, and diarrhea, usually within 2-6 hours of ingestion disease usually rapidly resolves within 12-24 hours |
|
|
what are the common vectors of staphylococcal food poisoning?
|
processed meats
custard-filled baked goods potato salad ice-cream introduced to the vectors by a human carrier |
|
|
what are the majority of the species of staphylococcus isolated from the skin?
|
staphylococcus epidermidis
|
|
|
what is the common predisposing factor for disease with staphylococci (not S. aureus)?
|
presence of artificial devices (i.e. catheters and replacement joints) in patient
|
|
|
what is the effect of the slime produced by staphylococcus epidermidis?
|
allows it to adhere to plastics and form a biofilm that makes it difficult for antibiotics to penetrate
|
|
|
what is a biofilm?
|
a conglomerate with secreted polysaccharides and glycopeptides formed by bacteria growing on an artificial surface
|
|
|
what are superantigens?
|
antigens, most often bacterial toxins, that recruit large numbers of T lymphocytes to an area
|
|
|
what are enterotoxins?
|
substances produced by bacteria that are toxic to the GI tract, that cause diarrhea and/or vomiting
|
|
|
to what family do staphylococci belong?
what is the other genus in this family? |
micrococcaceae
cicrococcus |
|
|
describe staphylococcus aureus
|
large
nonmotile nonspore forming facultative anaerobic gram-positive coccus (spherical-shaped) grows in clusters or clumps |
|
|
why does S. aureus grow in clusters or clumps?
|
bound coagulase (aka clumping factor)
binds fibrinogen, converts it to insoluble fibrin, and results in aggregation |
|
|
what is the only Staphylococcus found in humans which produces coagulase?
what is the designation for other Staphylococci? |
S. aureus
coagulase-negative staphylococci |
|
|
what are the toxins produced by S. aureus?
|
at least five cytolytic toxins
two exfoliative toxins eight enterotoxins toxic shock syndrome toxin |
|
|
why does cooking not inactivate the enterotoxins produced by S. aureus?
|
they are stable to heating at 100degC (112degF) for 30 minutes
resistant to gastric acids |
|
|
what are the factors which are giving S. aureus antibiotic resistance?
|
almost all produce penicillinase - beta-lactamase specific for penicillin
altered penicillin binding protein (PBP2) - resistance to semisynthetic penicillins and cephalosporins (methicillin and nafcillin) |
|
|
how are antibiotic resistance genes transferred to S. aureus?
|
plasmid transfer
transduction cell-to-cell contact |
|
|
what other infections are mimiced by staphylococcal infections?
|
streptococcal infections
|
|
|
how is a definitive diagnosis of staphylococcal infection made?
|
gram stain, culture of infected site, and culture of blood
|
|
|
describe staphylococci
|
large
gram-positive cocci (spherical shaped) arranged in clusters catalase-positive |
|
|
do staphylococci react with HOOH?
|
yes (catalase positive)
|
|
|
do streptococci react with HOOH?
|
no (catalase negative)
|
|
|
describe differences between streptococci and staphylococci
|
strep - smaller colonies, grey, negative catalase test
staph - larger colonies, white or yellow, positive catalase test |
|
|
how does S. aureus appear on blood agar?
|
beta-hemolytic
|
|
|
how is S. aureus differentiated from other staphylococci?
|
production of coagulase
positive latex agglutination for Staphylococcus protein A |
|
|
with what is Staphylococcus saprophyticus associated?
how is it differentiated from other coagulase-negative staphylococci? |
UTIs in young women
it is susceptible to novobiocin (tested by disk diffusion) |
|
|
with what is Staphylococcus lugdunensis associated?
|
significant cause of bacteremia and endocarditis
|
|
|
what is important about Staphylococcus saprophyticus and Staphylococcus lugdunensis?
|
look morphologically like Staphylococcus epidermidis
clinically resemble Staphylococcus aureus distinguishing feature is that they are PYR positive |
|
|
what is indicated by a positive PYR test?
|
group A streptococci
enterococci |
|
|
how are local wound Staphylococcus infections without systemic symptoms treated?
|
antimicrobial therapy is usually not warranted
|
|
|
what is the drug of choice for staphylococcal infections?
what is more commonly the initial treatment? why? |
nafcillin
vancomycin - b/c high percentage of strains that are resistant to methicillin and nafcillin |
|
|
how are Staphylococcus non-aureus infections treated?
|
with vancomycin - b/c majority of isolates are resistant to nafcillin
|
|
|
how is transmission of S. aureus prevented?
|
strict adherence to hand washing policies, particularly in the hospital setting
in some situations attempts to decolonize nares with intranasal mupirocin and/or skin with oral anti-staphylococcal antibiotics in combination with topical agents |
|
|
20-year-old male has adenopathy and a macular papular rash affecting his soles and palms; had a painless penile "sore" that spontaneously resolved
what is the most likely causative organism? |
Treponema pallidium
|
|
|
what microscopic examination can confirm a diagnosis of Treponema pallidum?
|
examination by darkfield microscopy of exudates from skin lesions could confirm T. pallidum and secondary syphilis
|
|
|
what serologic tests could assist in diagnosis of syphilis?
|
INITIAL SCREENING:
Venereal Disease Research Laboratory (VDRL) Rapid Plasmin Reagin (RPR) SPECIFIC DIAGNOSTIC TESTS: fluorescent treponemal antibody absorption test (FTA-ABS) microhemagglutination test for T. pallidum (MHA-TP) |
|
|
what is the third most common bacterial sexually transmitted disease in the US?
|
venereal syphilis
|
|
|
describe Treponema pallidum
|
thin
gram-negative microaerophilic labile (susceptible to dessication) spirochete no capsule six axial filaments between outer membrane and PG layer |
|
|
how is Treponema pallidum transmitted? what disease does it cause?
|
contact with fluid from an ulcer containing the infectious agent either through sexual contact by penetrating intact mucous membranes or through nonsexual contact with the agent with skin that is broken or abraded
causes venereal syphilis |
|
|
what is a macule?
|
flat lesion that is not palpable, of a different color from surrounding skin and smaller than 1cm
|
|
|
what is microaerophilic?
|
organism that can tolerate small amounts of oxygen because they contain superoxide dismutase; they use fermentation in the absence of oxygen
|
|
|
what is tabes dorsalis?
|
a condition characterized by diminished vibratory, proprioceptive, pain, and temperature senses, as well as the loss of reflexes
associated with untreated syphilis |
|
|
what is Argyll Robertson pupil?
|
constricts during accomodation, but does not react to light
sometimes called a syphilitic pupil |
|
|
what type of pathogen is Treponema pallidum?
|
obligate human pathogen
|
|
|
how many subspecies of Treponema pallidum are there?
of these, how many cause disease in humans? |
three
all three cause disease in humans |
|
|
what toxins are produced by Treponema pallidum?
|
no known toxins have been currently identified
|
|
|
why can Treponema pallidum not be visualized with standard microscopy?
how can this be overcome? |
it is too thin to be seen with standard microscopy with Gram stain
darkfield microscopy staining antitreponemal antibodies labeled with fluorescent dyes |
|
|
what are the modes of transmission of Treponema pallidum?
|
direct contact with an infectious lesion
transfusion of infected blood congenital transfer |
|
|
is Treponema pallidum an intracellular pathogen?
|
no - though it attaches by one or both ends to host cells, is rarely penetrates the cell
|
|
|
what is the primary cause of the resultant disease of Treponema pallidus?
|
resultant disease = syphilis
primary cause = host immune response to treponemal infection, with both humoral and cell-mediated immune systems playing a role |
|
|
what are the stages of syphilis?
|
primary - formation of a painless ulcer at the site of entry (a chancre)
secondary - 2-12 weeks later - flu-like illness, followed by a rash that typically starts on trunk but can spread to any skin or mucous membrane surface latency - 3-12 weeks later - relatively asymptomatic (in some ppl never leaves this stage) tertiary - diffuse disease w/ many dermatologic, musculoskeletal, cardiovascularr, and CNS effects |
|
|
what population is most at risk for syphilis?
|
heterosexual African Americans living in urban areas
|
|
|
with how many stages does syphilis present?
|
three
(primary, secondary, tertiary) (latency is not considered a stage) |
|
|
describe primary syphilis
|
hard, painless, broad-based chancre, with a punched-out base and rolled-up edges, sometimes expelling serous exudate
presents 3-6 weeks following initial contact w/ infectious agent typically resolves in 4-6 weeks and does not leave scar tissue |
|
|
describe secondary syphilis
|
symmetrical widely distributed macular rash, which can infect mucous membranes (cervix, throat, mouth) and may appear on the palms and soles
patchy hair loss , typically causing eyebrows to fall out low-grade fever, weight loss, and general malaise condyloma latum - painless, wart-like lesion on the scrotum or vulva occurs several weeks after lesion of primary syphilis has healed this is when syphilis is considered most infectious |
|
|
how long does the latent period of syphilis last?
|
2 years-several decades
|
|
|
describe tertiary syphilis
|
personality changes, blindness, paresis, gummas, Argyll Robertson pupils, and Tabes dorsalis
|
|
|
what are Gummas?
|
granulomatous lesions of the skin and bone which are necrotic and fibrotic
associated with tertiary syphilis |
|
|
what causes loss of reflexes, pain, and temperature sense in Tabes dorsalis?
|
damage caused by Treponema pallidum to the dorsal roots and ganglia
|
|
|
what causes loss of proprioception and vibratory sense in Tabes dorsalis?
|
damage to cells of the posterior column by Treponema pallidum in tertiary syphilis
|
|
|
how is syphilis diagnosed?
|
ID of spirochetes by darkfield microscopy of a chancre or skin lesion sample of primary and secondary stages, respectively, however most syphilis is diagnosed by serologic studies
|
|
|
what are the serologic laboratory tests for syphilis?
|
VDRL and RPR are nonspecific tests of host production of anti-cardiolipin antibody (positive in about 80% of primary syphilis cases, and in 100% of secondary syphilis)
FTA-ABS and TP-PA are more specific treponemal tests used for confirmation of infection, detecting presence of antibodies specific to T. pallidum |
|
|
in patients with what conditions, would you expect a possible false-positive on the nonspecific syphilis tests (VDRL and RPR)?
when might you expect a false negative? |
false positives: lupus patients, infectious mononucleosis patients, hepatitis A patients, antiphospholipid antibody syndrome, leprosy, malaria, and occasionally pregnancy
false negatives: early in the disease |
|
|
what is the drug of choice for syphilis?
|
benzathine penicillin
one injection is given before 1 year injections each week for 3 weeks for infection lasting longer than 1 year |
|
|
how are patients treated if they are allergic to penicillin?
|
treated with erythromycin and doxycycline
(doxycycline is contraindicated in pregnant patients, b/c it crosses the placenta & is toxic to fetus) |
|
|
how is syphilis prevented?
|
universal precautions in clinical setting
safe sex out of clinical setting currently no vaccine |
|
|
what is Giemsa stain used to detect?
|
Borrelia
Plasmodium Trypanosomes Chlamydia species |
|
|
what is Ziehl-Neelsen stain used to detect?
|
acid-fast bacteria (mycobacteria)
|
|
|
35-year-old woman recently traveled to Africa and developed diarrhea causing hypovolemic shock and metabolic acidosis; she remembers eating undercooked shrimp
what is the most likely etiologic agent? |
Vibrio cholerae
|
|
|
what is the cause of diarrhea in patients with Vibrio cholerae?
|
hypersecretion of water and electrolytes into the intestinal lumen caused by the cholera toxin
|
|
|
where are vibrio species found?
when do infections usually occur? |
saltwater
spring and summer |
|
|
how is Vibrio transmitted?
|
consumption of contaminated shellfish
traumatic injury associated with infected water |
|
|
what serotypes of V. cholerae are the toxigenic cause cholera?
|
01 and 0139
|
|
|
how is V. cholerae transmitted?
|
ingestion of contaminated water or food
|
|
|
why is it necessary to have a large dose of V. cholerae to cause cholera?
|
the organism is sensitive to gastric acid
also, conditions that reduce gastric acid, such as antacid medications or achlorhydria, increase the risk of infection |
|
|
what is achlorhydria?
|
production of gastric acid in the stomach is absent
|
|
|
what is the hallmark of cholera?
|
severe watery diarrhea with mild to severe dehydration because of production of toxin by the organism
|
|
|
with what is vibrio parahaemolyticus associated?
|
self-limiting gastroenteritis even though patients present with explosive watery diarrhea, with abdominal pain and fever
|
|
|
with what is Vibrio vulnificus associated?
|
wound infections
(cellulitis rather than gastroenteritis) in alcoholic patients or those with underlying liver disease, the organism can become disseminated and be associated with a high mortality rate |
|
|
what is azotemia?
|
buildup in the blood of nitrogenous end-products of protein metabolism
|
|
|
what does it mean to become obtunded?
|
to experience a loss or dulling of sensations
|
|
|
describe Vibrio species
|
motile
curved gram-negative bacilli (rod-shaped) single polar flagellum facultative anaerobes |
|
|
what is the natural environment for Vibrio species?
|
salt water, where they can multiply freely
|
|
|
in what invertebrates have Vibrio species been found?
|
shellfish
plankton |
|
|
what are the major human pathogens from the genus Vibrio?
|
V. parahaemolyticus
V. vulnificus V. cholerae |
|
|
how many serotypes of V. cholerae have been identified?
based on what? |
over 200
based on O antigen |
|
|
what serotypes of V. cholerae are responsible for major cholera disease?
|
O1 - responsible for major cholera pandemics of last 200 years
O139 - contributing to the disease since 1992 |
|
|
what is the major virulence factor of V. cholerae?
|
enterotoxin
|
|
|
what are the subunits of the V. cholerae enterotoxin? what is their function?
|
5 B subunits - bind to mucosal cell receptors and allow for release of the single A subunit into the cell
1 A subunit - activates adenylate cyclase, resulting in the hypersecretion of water, sodium, potassium, chloride, and bicarb into the intestinal lumen |
|
|
what virulence factor is useful to Vibrio bacteria that survive transit through the stomach to attach to the intestinal mucosa?
|
pili facilitate the attachment of the bacteria to intestinal mucosa so that they can colonize the upper small intestine
|
|
|
what is caused by the loss of an isotonic, bicarb-containing fluid from Vibrio cholerae?
|
dehydration
hypovolemia metabolic acidosis hemoconcentration hypokalemia |
|
|
how is presumptive diagnosis of Vibrio disease made?
|
history of association with saltwater, either involving trauma or consumption of raw shellfish
watery diarrhea from V. parahaemolyticus can't be easily distinguished from other bacterial gastroenteritis cellulitis from V. vulnificus should be diagnosed rapidly to avoid mortality |
|
|
in what patients should cholera be expected?
|
those with severe diarrheal illness who live in or have traveled to an endemic area
|
|
|
how is cholera diagnosis confirmed?
|
culturing stool or wound samples
gram stain should demonstrate a characteristic curved appearance to the gram-negative bacilli |
|
|
describe growth of Vibrio species on different agars (blood, MacConkey, and specialized)
|
blood - appear beta-hemolytic
MacConkey - poor growth TCBS agar - V. cholerae appear as yellow colonies; V. parahaemolyticus and V. vulnificus appear as green colonies |
|
|
what is TCBS agar?
|
thisulfate citrate bile salts sucrose agar
a specialized media for Vibrio species, which has high salt concentration V. cholerae appears as yellow colonies V. parahaemolyticus appears as green colonies V. vulnificus appears as green colonies |
|
|
what is the significance of MacConkey agar?
|
designed to grow gram-negative bacteria and stain them for lactose fermentation
By utilizing the lactose available in the medium, Lac+ bacteria such as Escherichia coli, Enterobacter and Klebsiella will produce acid, which lowers the pH of the agar below 6.8 and results in the appearance of red/pink colonies Non-Lactose fermenting bacteria such as Salmonella, Proteus species, Pseudomonas aeruginosa and Shigella cannot utilize lactose, and will use peptone instead. This forms ammonia, which raises the pH of the agar, and leads to the formation of white/colorless colonies formed in the plate. But they can also look golden to brown with dark centers |
|
|
what is the treatment for cholera?
|
volume replacement with isotonic bicarb-containing fluids (ORS or IV fluids)
oral antibiotics kill bacteria and decrease duration of illness (doxycycline) |
|
|
how is V. parahamolyticus gastroenteritis treated?
|
antimicrobials not usually necessary
|
|
|
how are wound infections or bacteremia from V. vulnificus treated?
|
rapid administration of tetracycline or quinolones
|
|
|
how can cholera be prevented?
|
improve hygienic practices
treat potable water supply with either heat or chlorine ensure thorough cooking of seafood research is ongoing for a vaccine |
|
|
what does the lipopolysaccharide of gram-negative cell walls consist of?
|
complex lipid, lipid A, attached to a polysaccharide made up of a core and a terminal series of repeat units
attached to the outer membrane by hydrophobic bonds and is required for the function of many outer membrane proteins all toxicity of LPS resides in the lipid A component (activates complement resulting in inflammation) |
