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158 Cards in this Set

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  • Back
Describe the characteristics of clostridium difficile.
-the name dificile is in reference to its oxygen sensitivity and difficulty associated with culturing
-gram positive, rod,
-anaerobe
-spore former
What are some of the problems produced by C. dificile?
1)diarrhea with lower abdominal cramping
2)severe colitis w/o psuedomembrane-profuce diarrhea, pain, and systemic sx
3)classic pseudomembranous colitis-same sx as for severe colitis with elevated yellowish plaques 2-10 mm diameter over inflamed regions of mucosa
-pseudomembrane is a fibrin mesh of nectrotic cells, PMNs, monocytes, and RBCs
What are the virulence factors of C. dificile?
1)toxin A-enterotoxin that causes fluid secretion, mucosal damage and intestinal inflammation
2)toxin B-cytotoxin
How is the diagnosis of C. dificile made?
-gram stain of stool gram positive rods with subterminal spores (counts must be high)
-isolation and culture from feces (need substantial volume, swabs arent anough)
-biopsy sample of expelled pseudomembranes may work
-detection of toxin of specific proteins in pts. feces is best tool to ascertain disease etiology
-latex agglut. available
How is C. dificile infection tx?
-fluid and electrolyte tx
-discontinue original abx therapy and admin. new abx
-vancomycin, metronidazole
-recent studies suggest that C. dif is evolving and initial vancomycin tx is better than metronidazole in halting disease progression
What are the complications of C. dificile infections?
-spores are resistant to abx
-a large portion of pts will relapse
Describe the epidemiology of C. dificile.
-the major predisposing factor is disruption of normal gut flora in some pts., with subsequent colonization and overgrowth by C. dificile and release of toxins
-estimated that 10% of pop. carry this bacterium as normal flora w/o a problem
-age is a factor, many infants harbor organism with no ill effect
-nosocomial outbreaks known to occur, asx pts as reservoir
What measures will help to control C. dificile infection?
-prompt ID and tx of infected pts, proper cleaning of pt. restrooms, proper handwashing/cleanliness will aid control
Describe the characteristics of Clostridium perfringens.
common cause of acute food borne diarrheal disease in US
-gram pos, rod
-nonmotile
-anaerobe
-spore former
What are the clinical manifestations of C. perfringens?
-has a short incubation period
-rapid onset of moderately severe watery diarrhea, abdominal cramping
-pts will NOT have fever or vomiting
-complete recovery in a day
What are the virulence factors of C. perfringens?
-enterotoxin (most active in ileum)
-this acts on the intestinal mucosa and inhibits glucose and chloride uptake, denudes brush borders at villi tips, causes hypersecretion of water and electrolytes into lumen disrupting osmotic equilibrium
-this toxin is produced during sporulation
-toxin IS destroyed by heating food
-refrigeration of cooked food could prevent many cases
Describe the epidemiology of C. perfringens.
-common member of the gut flora of humans and animals
-consumption of contaminated meat, poultry, and gravy when cooking is not adequate to destroy spores
-if food is allowed to stand unrefrigerated for enough time, spores will germinate and cells will multiply
-this is a HIGH DOSE organism
-must get a large dose for infection
How is C. perfringens diagnosed?
-detection of large numbers of this microbe found in food and feces and diagnosis depends on quantitative testing
-a latex agglut. kit to detect the presence of the enterotoxin in feces is available
What is C. perfringens type C-Enteritis necroticans?
-a rare, but highly fatal disease
-caused by an atypical C. perfringens type C producing heat resistant spores and a beta-toxin
-more severe food poisoning sx than the type A bug
-acute onset 24 hr incubation period
-severe abdominal pain and BLOODY DIARRHEA
-may be fatal
-different form of the toxin than type A disease
Describe the general characteristics of Bacillus cereus.
gram positive rod
aerobic
spore former
motile
What are the 2 forms of B.cereus infection?
1)emetic form-preformed toxin is ingested, very fast onset of upper GI sx 1-5 hrs after eating bad food, vomiting, cramps, diarrhea
2)diarrheal form-ingestion of large numbers of vegetative cells that produce toxin in site
-abdominal pain, profuse watery diarrhea 1-17 hrs after eating bad food
What are the virulence factors of B. cereus?
-produces 2 enterotoxins
1)heat stable (emetic)
2)heat labile (diarrheal)
-stimulates AC and increases cAMP levels in intestinal epithelial cells
How is the diagnosis of B. cereus made?
-afebrile disease
-high index of suspicion if upper GI illness is evident 1-5 hrs after eating or lower GI illness 5-17 hrs after eating
-these are often confused with Staph or clostridial poisoning
-isolate more than 10^5 B. cereus/gram of food or feces
Describe the epidemiology of B. cereus.
spores are commonly found on grains and veggies
-vomiting disease-improperly cooked and refrig. rice
-diarrheal is associated with meats, stews, gravies
What causes Staphylococcal foodborned disease?
consumption of heat stable preformed toxin in foods
What are the clinical manifestations of Staphylococcal foodborne infection?
-acute emetic and diarrheal disease caused by the ingestion of preformed heat stable toxin
-this is a disease w/o colonization, the pt. may be ill while never having been colonized or invaded by S. aureus at any time
-short incubation period 1-6 hrs after food consumption
-N/V, cramps, diarrhea, acute salivation, self-limiting
-rapid course b/c toxin is NOT produced in pt.
-recovery in 1-4 days
-some strains produce enterocolitis with watery diarrhea, F, cramps and these pts. are typically on long-term broad spectrum abx where normal flora has been disrupted
What are the virulence factors of Staphylococcus?
-key factor for GI disease is the heat stable, protease resistant enterotoxin
-Type A is most often food poisoning associated in the US (there are 8 antigenic types)
-toxin is water soluble and heat stable, acts as a superantigen
-results in an emetic response-absorbed in gut stimulus reaches CNS and sends impulse to vomiting center
-diarrheal disease-enhanced fluid transmucosal movement into lumen coupled with decreased water absorption
Describe the epidemiology of Staph GI infection.
-humans are source of organisms
-toxin is undetectable in food
-toxin is produced quickly in warm conditions
How is diagnosis of Staph GI infection made?
-it is an afebrile disease
-there is high index of suspicion with short time btwn eating and sx eruption
-custard filled baked goods, canned foods, processed meats, potato salad are all ideal environments since it is adapted to high osmotic stress environments such as human skin
-just remember that many disease pts. are never colonized by the bacterium
-can sometimes have enterotoxin detection or demonstration of organism in suspect food/vehicle
How is Staph GI infection prevented?
-the human reservoir is the key to control of infection
-examination and education of food handlers
-many outbreaks are linked to a handler with a staph-infected wound who inoculates the food, about 50% cannot be traced this way though
-proper refrigeration of foods
What are the common general characteristics of the foodborne intoxication diseases (Staph, B cereus, C perfringens)?
-abx not useful
-these are intoxications and not directly transmissible person to person
-fever minimal or lacking
-common factors are inadequate cooking, re-heating, or refrig. of foods
What are the most prevalent species of bacteria that cause GI disease?
campylobacter
salmonella
shigella
When are stool cultures indicated?
immunocompromised
febrile
bloody diarrhea
severe abdominal pain
severe or persistent illness
many fecal leukocytes present
What do routine stool cultures in the lab test for?
salmonella/shigella
campylobacter jejuni/coli

-must inform the lab if you suspect something else
What are the parasite groups?
1)protozoan-unicellular and animal like
2)helminth-parasitic worm
3)arthropod-jointed appendages
What 3 parasitic infections are associated with meat contamination?
hydatidosis
cysticerosis
trichinosis
What are synanthropic animals?
-have contact with people and food
-most parasitoses are zoonotic and therefore are spread this way
-ex:pets, rodents, livestock
What are the mechanisms for pathogenesis or parasites?
1)obstruction-ascaris lumbricoides, intestinal blockage
2)tissue destruction-plasmodium spp destroys RBCs
3)competition for nutrients-diphyllobothrium latum-competes for B12 (pernicious anemia)
4)malabsorption-giardia lamblia causes mechanical interference with digestion
5)loss of blood and iron defic-whipworms and hookworms, attachment site oozing and microcytic anemia
6)pressure-echnococcus granulosus, cyst development in CNS
7)host immune responses-wuchereria bancrofti, inflammatory responses
What are the transmission models of parasites?
1)ingestion (egg and cysts)
2)skin penetration-larval stage penetrates skin
3)direct (person to person)-STD
4)arboborne via arthropod bite
What are the 3 types of hosts that can house parasites?
1)definitive-parasite reaches sexual maturity
2)paratenic-transport host
3)intermediate-parasite is not sex. mature
What are quinolones used to treat?
plasmodium infections
What are arsenic and antimonial compounds used to tx?
leishmania

-binds to sulfhydryl groups on proteins
What are folic acid inhibitors used to tx?
-trimethoprim and sulfonamides
-used for cyclospora
What are nitroimidazoles used to tx?
giardia, trichomonads, amoebas
What are benzimidazoles used to tx?
for ascarids, hookworms

-they inhibit tubulin polymerization and formation of microtubules
What are paralytic agents used to tx?
they stimulate NM paralysis which results in expulsion of the worm

-tx ascarids, other roundworms
What are pyrazinoisoquinolines used to tx?
tapeworms

-target Ca balance which results in mm. spasms and causes alteration of parasite tegument (allows for increased killing by host immunity)
What are tetracyclines used to tx?
plasmodium, balantidium
What are the basic parasite types?
obligate:compulsory
facultative:free living and obligatory
accidental:spurious
What is a temporary parasite?
only has parasitic existence for part of its life cycle
What is a hyperparasite?
parasite of a parasite

-ex: larval tapeworm infects a flea
What is a biological vector?
the microbe lives and develops in this animal
What does heteroxenous mean?
living within more than one host during the life cycle
What does metacyclic mean?
infective to the definitive host

-ex: trypanosomes
What is the infective stage of parasites that will infect humans?
cyst
NOT troph
What is xenodiagnosis?
diagnosis of a disease by infecting a test animal
Define monoecious vs. dioecious.
mono=individual with both sexes
di=separate sexes
What is the definition of a protozoa?
-microscopic, eukaryotic, single celled organism
Describe the trophozoite stage of giardia.
-this is the feeding or vegetative state
-teardrop shaped
-dorsoventrally flattened
-2 nuclei
-adhesive disc
-the troph resides (swims) in duodenum and feeds on epithelial mucous secretions
-does not invade tissue or feed on RBCs but is considered the pathogenic stage
Describe the cyst stage of giardia.
-this is the environmental resistance stage
-infective stage, it is ingested
-oval
-chitin cyst wall
-2-4 nuclei (4 in older cyst)
-1 cyst produces 2 trophs
Describe the typical presentation of giardia.
-children are commonly infected
-intestinal pain, diarrhea, steatorrhea, malabsorption (B12 defic), flatulence
-abdomen can be slightly distended, intermittent episodes of watery nonbloody diarrhea
-colonization may promote inflammation and villous atrophy=decrease absorption
-usually a 2 week incubation
What is the infective dose of giardia?
100 cysts
What are our innate/acquired defenses against giardia?
1)human milk-giardiacidil (secretory IgA), lack of IgA leads to recurring and chronic infections
2)killing of trophs linked to abs, complement, and ox. microbicidal activity (macrophages)
-mediated by T cell dependent ab
-protective immunity develops (self-limiting infections)
Who are the high risk people for contracting giardia?
-day care kids and close contacts
-men have sex with other men
-backpackers and campers
-travelers to disease endemic areas
-persons who drink from shallow wells or surface waters
Describe the epidemiology of giardia.
-worldwide
-traveler's disease
-highly contagious (poor hygiene practices)
-fecal contamination
-waterborne-most likely
-zoonotic-beavers (endemic in USA), used to be called beaver fever
-prevalence highest among kids
-most common intestinal parasite pathogen diagnosed in USA
How is ID of giardia made?
-stool sample is negative for ova and protozoa
-but the GSA is positive (GSA is detectable even when cysts are not, has 100% sens. and spec.)
-for identification, multiple stool samples are often necessary, the diagnostic stage is the troph and cyst (in the feces)
What are the therapies for giardia?
albendazole is as effective as metronidazole with fewer side effects, DOC is metronidazole 5-7 days, tinidazole

-kids are given furazolidone
What is amoebiasis and what causes it?
-a protozoan illness that results in colitis and liver abscess and is a common disease throughout the world (including US)
-caused by entamoeba histolytica
Describe the 2 stages of entamoeba histolytica.
1)troph-1 nucleus, central endosome, feeding virulence, found in cecum, colon, extraintestinal
2)cyst-round to oval, 4 nuclei, blunt chromatoidal bar, infective, protection
What are the extraintestinal effects of entamoeba histolytica.?
hepatic (liver abscess through hematogenous spread, will lead to R. upper quadrant pain),
pleuropulmonary
cerebral
GU

-pts. often die of peritonitis (gut perforation) and cardiac failure and exhaustion
What are the intestinal effects of entamoeba histolytica.?
-can be asx
-acute colitis
-fulminant colitis
-ameboma
-intestinal ulcers
What are the virulence factors of entamoeba histolytica?
1)lectin-adhesion
2)cysteine proteinases-degrade mucus, antibody, complement, digest cell. matrix
3)phospholipases-disrupt membranes
4)amebapore-cytolytic activity
Describe the epidemiology of entamoeba histolytica.
-worldwide distribution
-transmitted through fecal contamination, water and foodborne, flies can be mechanical vectors
-it is a public health reportable disease
How is ID of entamoeba histolytica made?
-trophs or cysts in stool sample
-can see evidence of extraintestinal disease on radiologic tests
What is entamoeba dispar?
-has morphology similar to entamoeba histolytica but it is a noninvasive commensal parasite
-lack of cysteine proteinases
What is the tx for entamoeba histolytica?
albendazole or metronidazole (also w/iodoquinol), tinidazole another option

-tx intestinal with iodoquinol + tini +metro
-tx hepatic cyst only with metro and tini
-liver abscess resolves in time with chemo
What is cryptosporidiosis?
usually a self-limited (no tx) diarrheal illness that mostly affects children but has the potential to be serious in immunosuppressed ppl
-caused by Cryptosporidium parvum and c. hominis
-infects GI microvilli (parasitophorous vacuoles)
-causes diarrhea, fever, and malaise
-person to person transmission (fecal)
-zoonotic (manure contaminated drinking water)
-associated with AIDS in which therapy would be nitazoxanide (DOC) or paromomycin
How is diagnosis of Cryptosporidium parvum and c. hominis made?
-acid fast stain allows for rapid ID -ELISA ID (highly reliable)
What is cyclosporiasis?
-caused by cyclospora cayetanensis
-a diarrheagenic protozoan disease that has a Latin american connection
-this is an autofluorescent oocyst large than that produced by cryptosporidium
-causes diarrhea, cramps, and low grade fever
-acid-fast and autofluoresces
-therapy is TMPSMX
-berries are implicated?
What is blastocytosis?
-caused by blastocytosis hominis
-polymorphic protozoan
-sometimes characterized with large central vacuole and multiple nuclei distributed around rim of cytoplasm
-associated with diarrhea and IBS
-if tx needed, most often metronidazole
What is balantidiasis?
-caused by balantidium coli
-has a troph and cyst stage -macronucleus (often kidney shaped, metabolic function), micronucleus often not visible and has repro. function
-cilia evident on troph
-large intestine resident
-diarrheagenic microbe
-zoonotic in pigs
-tx is tetracylince or metronidazole
-parasite of rural areas, fecalborne transmission
Describe the general characteristics of nematodes.
-size is variable
-long, cylindrical, tapered
-non-segmented
-tube within a tube (outer tube, inner tube-complete digestive and repro system, and the in-btwn space-filled with non-compressible fluid-->hydrostatic skeleton)
-usually male and female
-NO LEGS
What is the transmission cycle of trichuris trichuria or the whipworm?
-fecal oral transmission
-no intermediate host or vector
-the eggs are ingested and then passed in feces, which then embryonate in the soil and are ingested again
Describe the life cycle of the whipworm.
1)infective stage: embryonated egg, development in soil takes about 3 wks
2)diagnostic stage: unembryonated egg in feces, ingestion to egg production takes about 3 months
-no migration out of intestine
What are the clinical manifestations of whipworm infection?
-asx with low worm burdens (<100 worms), unless they get in the appendix
-sx occur with moderate to heavy worm burdens which depends on # of eggs ingested
-tissue damage due to ant. end of worm embedded in mucosa
-will cause abdominal pain, loss of appetite, vomiting, blood diarrhea, anemia, rectal prolapse, secondary bacterial infections possible, worms can accumulate, effects on growth
Describe the epidemiology of the whipworm.
-third most common human roundworm
-has a worldwide distribution, most common in tropical areas, found in southern US
-associated with inadequate sanitation
-found where human feces is used as a fertilizer
-eggs can remain viable in soil for years
How is diagnosis is whipworms made?
-microscopy, eggs in feces are diagnostic
-have characteristic bipolar plugs (champagne corks)
-observation of adult worms in rectal mucosa by protoscopy (or direct observation in case of prolapse)
How are whipworms tx?
DOC usually mebendazole with albendazole as alternative
How is ascaris lumbricoides transmitted?
fecal oral transmission route
-no intermediate host or vector
-transmitted exactly like whipworms
-these are the large intestinal roundworms
Describe the ascaris lumbricoides life cycle.
1)infective stage:embryonated egg with 2nd stage larvae, development in soil takes 2-4 wks
2)diagnostic stage:fertilized and unfertilized eggs, ingestion to egg production takes about 3 months
-worms may be passed or emerge from mouth or nose
-intestine-->liver-->lung-->intestine
-worms usually live about a year
What are the clinical manifestations of ascaris lumbricoides?
-often asx, esp. w/low worm burdens
-high worm burdens cause intestinal and lung sx
-burden depends on # of eggs ingested
-intestinal sx include abdominal pain, Loss of appetite, effects on nutrition and cognition, intestinal obstruction, more common in kids, pain, vomiting, constipation, complications include volvulus, intususseption, gangrene, perforation
-lung sx include cough, pneumonitis, Loeffler's syndrome (eosinophilic pneumonia), ascaris is allergenic
Describe the problems that can arise with migrating worms in ascaris infection.
-adult worms can migrate and emerge from the nose or mouth
-hepatobiliary and pancreatic ascariasis
-larvae deposited in other organs-->inflammation-->granulomas
-larvae can die during migration and cause inflammation, necrosis and abscess
Describe ascaris infection and the subsequent immune response.
-Th2 and Treg cells (typical for a helminth infection)
-response can vary with level of exposure to antigen and tends to be directed toward larval stages
-IgE response both specific and non-specific
-reinfection is common
-ascaris is allergenic, experimental inhalation of worm proteins can cause asthma attacks
Describe the epidemiology of ascaris.
-most common helminthic infection in humans
-most common in tropical and subtropical areas
-associated with inadequate sanitation
-found where human feces is used as fertilizer
-eggs can remain viable for several years
How is ascaris lumbricoides diagnosed?
-microscopy-eggs in feces are diagnostic
-peripheral eosinophilia
-serology-can cross react with ags from other helminths
-radiographic imaging-mass of worms can produce a whirlpool image
-ultrasound-hepatobiliary/pancreatic, movement of worms
How is ascaris infection tx?
albendazole or mebendazole-single dose
What is ascaris suum?
-pig large intestinal roundworm
-very similar to A. lumbricoides, but probably a diff. spp.
-humans can be infected-accidental host
-can be distinguished by diff. denticles, morphology of sex chrom., diff. in internal transcribed sequences of ribosomal DNA, diff. in 2D gel electrophoresis are reproducible
What is anisakiasis?
-anisakis simplex AKA herring worm
-also P. decipiens AKA cod worm
-normally infects large marine mammals
-humans are accidental hosts-ingestion of larvae in infected raw/undercooked fish or squid
-found in areas where raw, undercooked fish are eaten such as Japan, netherlands, pacific coast of S. america
Describe the life cycle is anisakis.
-humans are not part of the natural life cycle which is very complex with crustacean and fish/squid intermediate hosts
1)infective stage: larvae in fish/squid
2)diagnostic stage:larvae in stomach or intestine
What are the clinical manifestations of anisakis infection?
-sx seen w/in hours of ingestion
-abdominal pain
-nausea, vomiting
-larvae may be coughed up
-if larvae get to the intestine, there may be eosinophilic granulomatous response 1-2 wks after infection that may present similarly to Crohn's disease
How is anisakis diagnosed and tx?
-by gastroscopic examination-visualization and removal of larvae
-exam. of tissue removed during biopsy or surgery
-there is also an ELISA
What is the EAT mnemonic?
Enterobius (pinworm)
ascaris (ascarid)
trichuris (whipworm)
the infective stage is an embryonated egg, we eat or ingest the infective stage
Describe strongyloidiasis.
-caused by strongyloides stercoralis
-infective stage is the filariform larva
-adult lives in the sm. intestine
-facultative parasite
-transmammary transmission
-zoonotic from dogs and cats
-common in immunosuppressed ppl
-pathogenicity:creeping eruptions, pneumonitis, and enteritis
-autoinfections
How does strongyloides stercoralis infect?
-infective stage is the filariform larva
-penetrates intact skin
-migrates via lymph/blood to lungs
-migrates to trachea
-coughed up and swallowed
-adult resides in small intestinal mucosa
-the rabditiform larva are passed in feces
Describe hookworms.
-necator americanus and ancylostoma duodenale
-stout worm w/buccal capsule
-infective stage-filariform larva
-skin/lung/intestine route
-adult is in sm. intestine
-pathogenicity:creeping eruption, pneumonitis, and hypochromic anemia
-transmission-geohelminth
-DOC is mebendazole
Describe cutaneous larva migrans.
-ancylostoma brasiliense and ancylostoma caninum
-skin migration-dog is definitive host
Describe enterobiasis.
-caused by enterobius vermicularis
-the adults congregate in the ileocecal area
-infective stage is the embryonated egg
-pruritis ani or no sx
-not zoonotic!
-diagnosed via cellophane tape technique
-tx is mebendazole
What is the pinworm life cycle?
adult worm lives in human-->egg passes from intestine-->embryonates-->human ingests the egg and the cycle continues
Describe the general characteristics of trematodes (flukes).
-they are endoparasites
-larval infects invertebrate hosts
-adults infect vertebrate hosts
-B/L symmetry, dorsoventrally flattened
-oval or leaf shaped
-has a cuticle
-oral and ventral suckers
-incomplete digestive system
-has ganglia near pharynx
-usually monoecious
Describe fasciolopsis buski.
-largest intestinal fluke in humans
-lives in sm. intestine and attaches to intestinal wall
-development from ingested metacercariae (on water chestnut) to adult takes about 3 mos
-diagnostic stage is eggs in feces
-snail is intermediate host
-epidemiology depends on the snail, central and SE asia, china, vietnam, etc
-reservoir hosts are pigs, dogs, rabbits
What are the clinical manifestations of Fasciolopsis buski (giant intestinal fluke)?
-depend on worm burden
-light infections are often asx
-heavy infections cause diarrhea, enteritis, intestinal obstruction may occur, eosinophilia, fever
How is diagnosis is Fasciolopsis buski (giant intestinal fluke) made?
-microscopy-eggs in feces are definitive, but indistinguishable from Fasciola
-clinical sx in endemic areas
What is the tx, prevention, and control of Fasciolopsis buski?
tx:praziquantel
-improved sanitation to prevent contamination of food and water
-molluscacides to control snail pop.
-education regarding the safe consumption of vegetation
Describe fasciola hepatica.
-adult is leaf-shaped, relatively small
-lives in the bile duct
-development from metacercariae (which encyst on watercress) to adult takes 3-4 mos.
-snail in int. host
-catte and sheep are definitive/reservoir hosts and humans are definitive hosts
-
What are the clinical manifestations of Fasciola hepatica infection?
-acute phase while fluke is migration will see abdominal pain, fever, diarrhea, eosinophilia, hepatomegaly, vomiting, urticaria
-there is a chronic phase as well
Describe the epidemiology of fasciola hepatica.
-worldwide
-found in areas that raise sheep/cattle and consume raw watercress
-reservoir hosts are sheep and cattle
How is diagnosis of fasciola hepatica made?
-microscopy-eggs in feces are diagnostic
-may see pseudofascioliasis if pt has recently ingested infected liver
-some ab tests available
How is fasciola hepatica tx, prevented, and controlled?
tx:triclabendazole or bithionol
-improved sanitation to prevent contamination of food and water
-education regarding safe consumption of vegetation
-molluscacides to control snail population
What is clonorchis sinensis?
-adult is small
-live in small-medium biliary ducts
-development from metacercariae to adult takes about 1 month
-metacercariae encyst in freshwater fish
-infective stage is metacercariae encysted in fish
-carnivorous mammals are the reservoir hosts
-diagnostic stage is eggs in feces
-snail is the 1st int. host (ingests eggs), freshwater fish is 2nd int. host
What are the clinical manifestations of clonorchis sinensis infection?
-severe infections present with fever, epigastric pain, hepatomegaly, jaundice
-invasion of gall bladder presents with cholecystitis, cholelithiasis, impaired liver function
-associated with cholangiocarcinoma
Describe the epidemiology of clonorchis sinensis.
-endemic areas in Asia include korea, china, taiwan, and vietnam
-reports in non-endemic areas are usually in asian immigrants
-reservoir hosts-dogs, cats, and fish eating mammals in endemic areas
How is diagnosis of clonorchis sinensis made?
-microscopy-eggs in feces are diagnostic
-adults may be recovered during surgery
How is clonorchis sinensis tx, prevented, and controlled?
tx:praziquantel with albendazole as alternative
-improved sanitation to prevent contamination of food and water
-education regarding safety consuming raw/undercooked fish
What is heterophyes heterophyes?
-adult is small
-live in sm. intestine and attach to wall
-it is a fluke
-development from metacercariae (encyst in fresh/brackish water fish) to adult takes about 1 month
-human is definitive host
-carnivorous mammals/birds are reservoir hosts
-snail is the 1st int. host (ingests eggs), fresh/brackish water fish are 2nd int. host
What are the clinical manifestations of heterophyes infection?
-intestinal sx such as abdominal pain and diarrhea
-myocarditis can occur if eggs reach the heart
-eggs sometimes migrate to other areas
What is the epidemiology of heterophyes?
-found in egypt, middle east, far east
-reservoir hosts are carnivorous mammals and birds
How is the diagnosis if heterophyes made?
microscopy-eggs in feces are diagnostic
-eggs are indistinguishable from metagonimus, and clonorchis and opisthorchis
What is the tx for heterophyes?
praziquantel
What is the epidemiology of metagonimus yokogawai?
it is a fluke that acts much like the others
-far east, siberia, manchuria, balkans, israel, spain
-reservoir hosts are carnivorous mammals and birds
-tx:praziquantel
What is paragonimus wetermani?
-the lung fluke
-infective stage:metacercariae encrusted in crustaceans
-human is definitive host
-snail is 1st int host, crustaceans are 2nd int host
-reservoir hosts are pigs, dogs, cats
-diagnosis is eggs in feces or sputum
Describe the use of the O and H antigens to classify E. coli.
O antigen=serogroup
H antigen (flagella)=serotype

-at least 160 serogroups exist and there is some correlation btwn the serogroup and virulence
What are the 5 currently recognized GI virotypes of E. coli?
1)enterotoxigenic
2)enteroaggregative
3)enteropathogenic
4)enterohemorrhagic
5)enteroinvasive
Describe the characteristics of enterotoxigenic E. coli.
-resemble V. cholerae in disease process
-adhere to mucosa of small intestine with colonization factor antigens and produce sx by elaboration of plasmid-mediated toxins that induce diarrhea
-disease is like cholera, but much less severe
-may be fatal in infants
-partial immunity in adults in endemic/epidemic areas
-travelers are particularly susceptible
-ETEC is not being recognized much more frequently as cause of GI disease outbreaks in non-travelers as well tho
What are the 2 types of toxins that are produced by ETEC (enterotoxigenic E. coli)?
1)heat labile toxins-cholera-like toxins whose structure and action are like those of choleragen
2)heat stable-short peptide that does not readily denature with heat, increases cGMP in cell
How can we prevent traveler's diarrhea caused by ETEC?
the dukoral vaccine
Describe the characteristics of enteroaggregative E. coli.
-found principally in kids with chronic diarrhea
-cells bind to small intestine mucosal cells in discrete clumps
-NOT invasive, cause no obvious changes in bound intestinal cells
-may produce an ST like toxin
-special attachment and aggregation fimbriae (known as the GVVQP fimbriae)
Describe the characteristics of the enteropathogenic E. coli.
-bind to small intestine mucosal cells in a patchy pattern
-mucous production is prominent, no blood
-causes disease primarily in infants in the developing world
-substantially alters bound cells by creating attaching effacement or A/E lesions (pedestal like structures)
-much more invasive than the other forms of E. coli
-it harbors an adherence factor plasmid that encodes a bundle forming protein and other virulence factors
-they express an adhesin molecule from a pathogenicity island intimin and produces and inserts the receptor for intimin into the host cell membrane
-mechanism similar to that used by EHEC
Describe the characteristics of Enterohemorrhagic E. coli.
-an emerging infection only recently recognized as a cause of disease
-can be fatal due to hemolytic uremic syndrome development
-one form predominates at present O157H7
-production of disease is similar to that of shigella dysentery through toxins that are virtually identical to shiga toxin (toxins encoded by a bacteriophage)
-HUS may be ppt by abx like norfloxacin
How is diagnosis of EHEC made and in whom?
-most common in kids under 4 yrs old
-diarrhea that becomes grossly bloody and may go on to HUS
-fever is not a general feature!
-do a stool culture
-special medium:MacConkey's sorbitol agar (colonies are white b/c cannot ferment sorbitol), this is not a routine test inform lab of suspicions.
What is the tx for EHEC?
oral rehydration
-abx may be harmful
-do not use antimotility agents in kids and infants
What are the complications of EHEC?
HUS, acute renal failure with poor prognosis is greatest worry
-more common in elderly and young pts. especially
-want to monitor urine production as best you can
Describe the epidemiology of EHEC.
-classic source is undercooked hamburger but the pathogen is found in cattle and infections have been associated with beef and raw milk, cattle linked products or food items tainted with cow manure
-emerging pathogen, incidence increasing
-feeding cattle on grain acidifies the rumen and promotes the colonization and retention of E. coli O157H7 (grass fed animals do not have this same tendency)
-other known sources are contaminated water, unpasteurized juice, raw fruits, veggies, salami, apple cider (downer apples)
-2006 spinach and 2008 pepper outbreak
-person to person transmission is documented, very LOW DOSE organism
What does "the big 6" refer to?
shiga toxin producing strains of E. coli
-after March 2012 the sale of ground beef with these agents will be banned!
What was the strain of E.coli that emerged in europe in 2011?
O104:H4
-rate of kidney failure induction was extraordinary
Describe the characteristics of enteroinvasive E. coli.
-invade intestinal epithelium and cause disease clinically indistinguishable from shigella (dysentery with bloody diarrhea)
-however, there is either NO or very little shiga toxin production and HUS is rare
-not as virulent as shigella
-cells are non-motile, late or non lactose fermenters (different than typical E. coli)
Describe the characteristics of Campylobacter jejuni.
-widely found in poultry products
-gram neg. curved rod, motile microaerophilic
-grows well at 42 C
-
Describe the clinical manifestations of campylobacter.
-incubation 1-7 days
-very commonly pt. has prodrome with fever, HA, malaise, myalgia 12-24 hrs before diarrhea
-enteritis with diarrhea, loose stools to frank dysentery, fever, abdominal pain
-self-limiting
-convalescent carriage and excretion for 2-3 wks after disease
-pseudoappendicitis
-invasion of mesenteric LNs with inflammation
What are the virulence factors of campylobacter?
-it is an invasive agent with multiple but poorly understood virulence factors
-invasion factor (carb on surface, pathogen directed phagocytosis)
-cytolethal distending toxin (CDT), operates in host cell nucleus and directly damages DNA, locks host cell in permanent G2 phase, probably inhibits immune system reaction to infection
-heat labile enterotoxin similar to ETEC
Describe the epidemiology of Campylobacter.
-reservoir is the intestinal tract of animals, birds especially, includes pets
-transmission by food source primarily
-undercooked chicken is classic source of infection
-contaminated water and unpast. milk/dairy may also sometimes harbor it
-sporadic cases more common that large scale outbreak
-peaks in summer
-low dose organism!
-highest infection observed for young adults (around age 20)
What are the complications of Campylobacter?
1)Reiter's syndrome-esp. HLAB27
2)Guillan Barre syndrome-it is the chief precipitant of GB with the risk of developing GBS in the 2 mos following symptomatic Campylobacter infection 100 x's greater than the risk in the general pop.
How is diagnosis of Campylobacter made?
-fever and prodrome are notable features
-micro. exam of feces may allow for presumptive diagnosis
-highly motile curved rods
-stool culture-42C under microaerophilic conditions with enriched CO2 on special selective media such as Campy-BAP
-catalase, ox. pos. colonies
How is campylobacter prevented?
through cooking and careful handling of poultry
Describe the characteristics of Yersinia enterocolitica.
-gram neg. coccobacillus, motile, lactose nonfermenter, optimal temp range 22-29 C
-facultative IC organism
Describe the clinical manifestations of Yersinia enterocolitica.
-incubation period 4-7 days
-fever, abdominal pain, vomiting, diarrhea,
-the organism becomes established in the terminal ileum and penetrates
-enterocolitis in kids under 5 years
-often confused with acute appendicitis
-plays a role in transfusion rxns-has been found present in donated blood of asx individuals, can grow and produce endotoxin while refrigerated
What are the virulence factors of Yersinia?
-invasion of host is via the M cells of Peyer's patches
-invasin-binds the B integrin and induces endocytosis
-enterotoxin-ST like toxin GC (increases cGMP levels)
-yops (plasmid encoded proteins that are excreted they inhibit phagocyt. and macrophage resp. burst, cause contact dependent cytotoxic activity, synthesized when Ca levels are low)
How is diagnosis of Yersinia made?
special request culture medium with cold temp enrichment (room temp.) but process is too slow to help clinically
Describe the epidemiology of Yersinia.
-ubiquitous in the environment, lakes, reservoirs, many antigenic types often region specific
-infects a variety of wild an domestic animals with epizootic outbreaks recognizable
-infection more common in winter
-recently outbreaks have been more common in kids
-once thought to be solely a high dose organism, fecal oral transmission now recognized to occur
-transmission to infants from caregivers who prepared food harboring this bacterium have been documented
-contaminated food, milk, especially PORK are sources
Describe the characteristics of Helicobacter pylori.
gram neg, curved rods, highly motile
-stain best in tissue biopsy with giemsa
-copious production of urease
What are the clinical manifestations of Helicobacter infection?
-mucus secreting epithelial cells of pylorus are the only colonized site
-new evidence suggests that gastric mucin acts as a natural abx against this bacterium
-severe gastritis with cramps, halitosis, N/V
-eradication of bacteria not associated with relief of sx
What are the virulence factors of Helicobacter?
-not all strains equally virulent
-about 1/2 of strains carry the virulence plasmid "cag" which carries numerous virulence factors
-type IV secretion system-injects antagonistic factors directly into host cells
1)urease-raises pH
2)heat shock protein B-enhances urease expression
3)acid inhibitory protein-dampens acid production by host
4)flagella
5)peptidoglycan
Describe the epidemiology of Helicobacter pylori.
-the source is obscure
-about 1/2 the world pop. is thought to be colonized
-more common in developing countries, rates are declining in the developed nations
-oral carriage may be common, spread by fingers
-smoking is a risk factor
-association with stomach adenocarcinoma
How is Helicobacter diagnosed?
-histologic detection in fresh biopsy samples plus culture is considered optimal
-CLO test reveals urease activity via pH indicator in biopsy speciment in 2 hrs
-culture in special conditions (takes 7 days to grow)
-noninvasive detection of urease activity with C14 labeled substrates by breath test or urine ammonia assay
-screen for H. pylori ags in stool
-serology (abs to h. pylori)
What is the tx for helicobacter?
-optimal therapy not yet evolved
-re-infection possible
-combo of abx plus bismuth containing drugs as needed