Phase A Flashcards
Vibrio sp. general Physiology and Structure
Gram negative, facultatively anaerobic, fermentative curved rods with both a polar flagella and pilli. They have a positive oxidase reaction.
- Vibrio* require salt for growth, and are susceptible to low pH (stomach acid)
- V. cholerae* is subdivided based on O polysaccharide (lipid A is endotoxin). O1 and O139 are associated with epidemics (O1 divided into El Tor and Classical biotypes)
- Vibrio* organisms survive poorly in an acidic or dry environment, and therefore specimens must be collected early in the disease and inoculated promptly onto culture media.
Vibrio cholerae
Agent of cholera, a disease that begins with an abrupt onset of watery diarrhea (“rice water stools”) and vomitting and can progress to severe dehydration, metabolic acidosis and hypokalemia, and hypovolemic shock
Found in salt water environments; shellfish
Spread through contaminated water, has a relatively high inoculation dose due to susceptibility to stomach acid.
The cholera toxin is an A-B toxin that is carried by a bacteriophage which binds to V. cholerae’s toxin co-regulated pilus. The toxin binds to GM1, and causes an excretion of water and salt (through cAMP mediated activation of CFTR)
Also produces zonula occludens toxin (loosens zonula occludens leading to increased intestinal permeability) and an accessory cholera enterotoxin, which increases fluid secretion.
Treat with azithromycin and fluid/electrolyte replacement
Vibrio parahaemolyticus
Can cause a self-limiting gastroenteritis similar to mild cholera with explosive watery diarrhea. Wound infections can occur on exposure to contaminated seawater.
Most strains produces a thermostable direct hemolysin (TDH, Kanagawa hemolysin). This is important for marking virulent strains
Most common gastroenteritis associated with contaminated seafood (especially in Japan/Asia)
Vibrio vulnificus
Causes a life-threatening bacteremia that must be treated promptly with minocycline combined with a fluroquinolone or cefotaxime.
Associated with infection after exposure to seawater or eating improperly cooked shellfish
High mortality rate, particularly in patients with underlying hepatic disease.
Capsule production is important for widespread bacteremia
Clostridium sp. General Physiology and Structure
Originally defined by four properties: 1) endospore formation, 2) strict anaerobic metabolism, 3) inability to reduce sulfate to sulfite, and 4) gram-positive cell wall. There are exceptions to all of these.
Organisms are ubiquitous in soil, water, and sewage as well as the normal GI flora of animals and humans.
Clostridium perfringens
Naturally inhabits skin, often contaminates samples collected
Causes soft-tissue infections (gas gangrene):
Treat with surgical debridement and high-dose penicillin therapy
Cellulitis is localied edema and erythema with gas formation in the soft tissue, generally nonpainful
Suppurative myositis is accumulation of pus in the muscle plains without muscle necrosis or systemic symptoms
Myonecrosis is a painful, rapid destruction of muscle tissue; systemic spread with high mortality. Assisted by Alpha toxin, a lecithinase (phospholipase C). This is often (40%-100%) fatal.
Can also cause gastroenteritis:
Food poisoning: rapid onset of abdominal cramps and watery diarrhea with no fever, nausea, or vomitting. Short duration and self-limited. Follows eating of poorly prepared meat products. Usually caused by enterotoxin-containing type A C. perfringens. Cooking food at 74*C can destroy toxin.
Necrotizing enteritis: acute, necrotizing destruction of jejunum with abdominal pain, vomiting, bloody diarrhea, and peritonitis. Usually caused by type C C. perfringens containing Beta toxin (which is inactivated by trypsin)
Clostridium septicum
Cause of nontraumatic myonecrosis and often exists in patients with occult colon cancer, acute leukemia, or diabetes.
If the bowel mucosa is compromised, the organism can spread into tissue and rapidly proliferate, producing gas and tissue destruction.
Most patietns die withing 1 to 2 days after initial presentation.
Tinea Versicolor
A superficial mycosis caused by Malassezia furfur, a lipophilic yeast that requires olive oil for growth in culture.
Occurs worldwide, but more prevalent in tropical regions in young adults. Thought to be person to person spread.
Lesions are small hypo- or hyperpigmented macules along the upper body. Color change is due to interference with melanin production
Diagnosed upon microscopy
Treated with topical azoles or selenium sulfide shampoos
Tinea Nigra
A superficial phaeohyphomycosis caused by the black dematiaceous fungus Hortaea werneckii.
A tropical or subtropical condition initiated by inoculation into the superficial layers of the epidermis.
Appears as a solitary brown macule (often on palms), confused with melanoma. Can be diagnosed via skin scrapings
Treat with topical azole creams, terbinafine
White Piedra
A superficial infection of hair caused by yeast-like fungui of the genus Trichosporon.
Tropical and subtropical conditions w/ poor hygiene
Affects hairs of groin and axillae, but does not damage hair shaft
Shave the hair to get rid of fungus, start using better hygiene
Black Piedra
Also affects the hair, particularly the scalp, caused by Piedraia hortae
Uncommon, found in South America. A condition of poor hygiene.
Treat with a haircut
Herpes Viruses
Large, enveloped, spherical, double-stranded linear DNA viruses that replicate in the nucleus and are capable of establishing a latent infection in the host.
Replicate by “rolling circle replication” using many of its own proteins (drug targets)
HSV-1 and HSV-2
Cause oropharyngeal disease, keratoconjunctivitis (HSV-1), genital herpes (HSV-2), skin infections (herpetic whitlow and herpes gladiatorum), encephalitis (HSV-1), and neonatal herpes.
Histopathology: causes formation of syncytia as well as type A Cowdry inclusion bodies (seen on a Tzanc smear)
Most common human virus; majority of population has antibodies to HSV-1
Treat with acyclovir, valacyclovir, or vidarabine
