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207 Cards in this Set

  • Front
  • Back
What "bug" can be involved in the stomach, in GI infections?
Helicobacter pylori
What "bugs" can be involved in the duodenum/jejunum, in GI infections? (8)
Vibrio cholerae
Enterotoxigenic E coli
Enteropathogenic E coli
Giardia lamblia
Cryptosporidium parvu
Rotavirus
Calicivirus
Adenovirus
What "bugs" can be involved in the illeum, in GI infections? 3
Salmonella spp
Camyplobacter jejuni
Yersinia spp
What "bugs" can be involved in the colon, in GI infections? 7
Shigella spp
Enterohemorrhagic E coli
Enteroinvasive e coli
Entamoeba histolytica
Clostridium difficile
Clostridium perfringens
Bacillus cereus
What is the "gold standard" for examining stool?
What are gram stains used for?
Bacterial culture is the gold standard.
Gram stains are used to look for leukocytes, not for bacteria, since there is so much bacteria.
What 6 GI bugs are not included in a bacterial stool culture?
Vibrio species
non O157 STEC's
Enterotoxigenic E coli
Enteroinvasive E coli
Clostridium difficile
Anything Else
What is STEC?
Shiga toxin producing E coli
General considerations for treatment of GI infections. (4)
Oral rehydration
Bismuth Sulfate (pepto)
Antimotility (possibly contraindicated)
Antibiotics
Is cultivation of helicobacter pylori difficult or easy?
Difficult
Tuft of sheathed polar flagella?
Helicobacter pylori
Single unsheathed flagella?
Camyplobacter
What are some virulence factors found in helicobacter pylori?
cagA and vacA
urease
What is the method of transmission for helicobacter pylori?
Currently unknown
human to human occurs/unconfirmed
Animal reservoir??
Typical method for diagnosing helicobacter pylori?
Though it is usually asymptomatic, what are the signs if it is symptomatic?
Hx of burning, gnawing epigastric pain
Urease breath test, endoscopy.

Vomiting, burping and fever.
What are the different clinical signs between gastric and duodenal helicobacter pylori infection?
Gastric - similar to hunger pangs, nausea, appetite loss, inconsistent ulcer pain.
Duodenal - heartburn, stomach pain, wt gain, burning @ back of throat 2-4 hours after meal
What is the most important serotype of vibrio cholera?
What are its two biotypes?
O1
Tor and Classical
In vibrio cholera there are two biotypes, Tor and Classical. Which one is more effective at colonizing the intestinal tract? Which one produces the most endotoxin?
Classical produces the most endotoxin.

Tor is more effective at colonizing the intestinal tract.
Rice water stools are caused by what GI bug? Why?
Due to vibrio cholera, but more specifically due to cAMP stimulating chloride leading to an isoosmotic loss of water.
Is vibrio cholera invasive/does it cause damage to the intestinal mucosa?
No
In the case of vibrio cholera, are leukocytes or blood present in the stool?
Who does vibrio cholera mainly effect, and why?
No

Children because adults have high vibriocidal titers.
Why is glucose necessary in oral rehydration solutions (ors)?
to facilitate the salt absorption
Definitive diagnosis, of vibrio cholera requires:
Culture with alkaline media (thiosulfate citrate bile salt)
What is most important in treatment of vibrio cholera? Are antibiotics recommended, and if so, which ones?
Fluid/electrolyte replacement.
Secondary measure, tetracycline, doxycycline
5 characteristics of:
Facultative GNR
Ferment Glucose
Oxidase Negative
Reduce nitrate to nitrite
Grow on macConkey Agar
Enterobacteriacea
5 characteristics of Enterobacteriacea
Facultative GNR
Ferment Glucose
Oxidase Negative
Reduce nitrate to nitrite
Grow on macConkey Agar
How does enterotoxigenic e coli attach to the small intestine epi?
Fimbriae
Is enterotoxigenic e coli cytotoxic? How many organisms are typically required to cause disease?
Non cytotoxic
10^9
What are the two types of toxins produced by enterotoxigenic e coli?
LT toxin - heat labile and shares immunological cross-reacts & DNA homology with choleragen and shares similar mode of action elevating intracellular levels of cAMP

ST toxin - heat stable, elevates intracellular levels of cGMP
How should you treat enterotoxigenic e coli? Are antibiotics recommended, and if so, which ones?
Supportive fluids and electrolytes.
No antibiotics
What is the diarrhea like in enterotoxigenic e coli?
Where is it most often in infants? When in adults?
Watery, but less profuse than cholera.
In infants in endemic areas, in adults (travellers)
ETEC, EPEC, vibrio cholera, vibrio parahemolyticus all cause secretory or osmotic diarrhea?
Secretory
Enteropathogenic Escherichia coli (EPEC), rank its severity in regards to ETEC and cholera.
It is less severe
EPEC is particularly confined to infants and young kids, espcially in ________ settings.
Why?
When might it be severe?
Institutional
Because kids have yet to acquire normal intestinal flora.
In premature infants
Does EPEC have fimbriae?
Does it produce LT, ST or cytotoxin?
Are antibiotics suggested, if so, what kind?
No
Possibly produces cytotoxin
No antibiotics
How can you test for H. pylori? (3)
Endoscopy
c14 urea ingestion/breath test
PCR
(serology doesn't work well)
What types of drugs should be used for H. pylori? How many should be used?
Use 2-4.
Antibiotics
H2 blocker
Proton pump inhibitors
Cytoprotective Agents
Combination Product
What type of vaccine is the H pylori vaccine?
Non-existent
Enterobacteriacea or cholera:
Non-enteric
Fermentative
Oxidase positive
Vibrio cholera
What is critical in epidemilogic studies of Vibrio cholera?
Serotyping, biotyping, and Phage typing.
Free living organism in fresh water causing human disease when ingested.
Attaches to algae, shells, and copepods. Survives for years in free living cycle.
Can switch to dormant state when conditions are unfavorable, and is then undetectable.
Vibrio cholera
When do epidemics of cholera tend to occur?
In the hot seasons
EPIDEMIC ASSOCIATED V CHOLERA
Serovars:
Biotypes:
Serotypes:
Toxin:
Serovars: 01, 0139
Biotypes: classic, el tor
Serotypes: Ianba, Ogawa, Hikpjima
Toxin: Cholera toxin
What must occur in order to contract Vibrio cholera?
Ingestion of contaminated water of at least 10^9 or more organisms, and organisms must survive the gastric acidity.
Incubation time for V cholera?
What can effect incubation time?
Initial and later symptoms?
How short may the clinical course be?
12-72 hours
Gastric acidity
Vomiting, abd distension and diarrhea. Later: profuse diarrhea, dehydration, hypovolemic shock, renal failure, death.
4 hours
Profound dehydration is seen in cholera unlike other GI diseases. ORS can be used. When is "tenting" seen?
When someone has lost more than 5% of their body water.
Definative cholera diagnosis requires culture with:
alkaline media (like TCBS)
What about the V cholera vaccine?
It is of questionable value, and is not recommended by the WHO.
What will occur if you ingest enterotoxigenic E coli, and when? How much do you need to ingest?
Incubation 1-3 days
Diarrhea is watery but less profuse than cholera.
10^9
How can you test for enterotoxigenic E coli?

What antibiotics should be used?
ELISA for LT
DNA probe for LT or ST

No antibiotics
Does EPEC have LT or ST toxin?
Does it have cytotoxin?
No
Maybe
What does EPEC destroy?
Microvilli
Rate V. Cholera, EPEC and ETEC in severity of watery diarrhea.
How do you treat them?
V.Cholera>ETEC>EPEC
V.Cholera: tet or doxy
All three are treated with supportive care only.
What causes EPEC to be epidemic in infants?
Yet to acquire normal intestinal flora/no protective coating.
No specific immunity.
Vibrio parahemolyticus:
GNR or GPC:
Facultative _________
Haplophilic =
Produces heat stable cytotoxin
Is it invasive?
What type of food is it associated with?
GNR
Facultative anaerobic
Haplophilic = salt-requiring
Produces heat stable cytotoxin
Is it invasive? Yes, locally
What type of food is it associated with? Seafood
Vibrio parahemolyticus:
Incubation:
How long does diarrhea last?
What type of diarrhea?
What other types of infection can it cause?
Incubation: 1-2 days
diarrhea lasts: 3-4days
Type: ranges from watery to dysentery-like, often mild
What other types of infection can it cause? Wound infection/septicemia
What is one reason Vibrio illnesses peak in the summer?
Organism replication/water sports.
Vibrio parahemolyticus
What is needed to culture it?
What type of agar can be used?
What specific test can be performed to diagnose?
How do you treat it?
Not picked up on routine culture, need haplophilic, such as TCBS or CHROMagar.
Kangawa test
Supportive care.
What is the Kangawa test used for?
Diagosing Vibrio parahemolyticus
Kangawa test-organisms produce a theromostable direct hemolysin.
Produces hemolysis of human erythrocytes.
What antibiotics are used for Vibrio parahemolyticus?
None (of little use)
What is the most commonly diagnosed intestinal parasitic disease in the US?
How many life cycles does it have?
Giardia lamblia (intestinalis)
Two life cycle stages
Giardia lamblia
Describe the trophozoites, including motility, number of nuclei and level of resistance to the environment.
Bilaterally symmetrical, with 4 pairs of flagellae, cysts have 4 nuclei and are environmentally resistant.
What are the diagnostic stages and the infective stage of Giardia lamblia?
Diagnostic: Cyst and troph
Infective: Cyst
Where do cysts of Giardia lamblia exist? How do the trophozoites multiply?
What results from the adhered trophs and the resultig inflammatory response?
Cysts: Upper jej and duodenum
Trophs multiply via binary fission.
Impaired intestinal absorption
What is the incubation period of Giardia lamblia? How long do light infections last? Heavier infections? When might it become a chronic infection?
Incubation: 1-2weeks
Light infection: Asymptomatic
Heavier infection: 7-10 days
Chronic in immunecompromised
Which disease can the "string test" be used?
Giardia lamblia, when stool examinations were negative, so as to exam duodenal fluid.
How do you diagnose Giardia lamblia?
Repeat (to increase sensitivity) stool exam for cysts, fresh if looking for trophozoites.
ELISA or AB test: for cysts and trophozoites
When diagnosing Giardia lamblia, what does repeat stool exams improve, sensitivity or specificity?
What tests are good for detecting cysts and trophozoites?
Sensitivity
ELISA and Fluorescent AB test
Treatment of Giardia lamblia?
Prevention?
Metronidazole (flagyl)
Tinidizole
Nitazoxanide

Improved sanitation and chlorination of water supply
Which bug will survive even in chlorinated water?
Cryptosporidium parvum
** Many US water treatment plants are inadequate**
Both the diagnostic and infective stage are the thick wall oocyte.
Cryptosporidium parvum
Cryptosporidium parvum
Is it invasive?
Does it cause cell lysis?
What does loss of microvilli and inflammatory response lead to?
Locally invasive
Does NOT cause cell lysis
SECRETORY, and (osmotic) malabsorptive diarrhea
Cryptosporidium parvum
How long does it last?
How do you treat it?
Lasts up to 20 days!!
Only treat the immunocomprimised, with paromycin and spiramycin.
Chronic secretory diarrhea may make you suspect:
Cryptosporidium parvum
Cryptosporidium parvum
How can you get it?
How can you diagnose?
Ingestion of sporolated oocyte which releases sporozoites following exposure to intestinal enzymes.
Diagnose via identifying oocytes in feces using acid fast stain, and monoclonal fluorescent ab
Sporolated oocyte ingested-> sporozoites released after exposure to intestinal enzymes -> asexual reproduction leads to the release of 8 merozoites that repeat the cycle.
Cryptosporidium parvum
Oocysts are autofluorescent unlike cryptosporidium parvum.
Cyclospora cayentanesis
In Cyclospora cayentanesis is the diarrhea worse or less persistant than cryptosporidium parvum?
What is diagnostic?
What is infective?
Less persistant
Diagnostic: unsporulated oocyst in feces, infectious 5 days later.
Sporulated oocyst.
A patient has had chronic intermittent diarrhea for 3 weeks. There is no fever or vomiting and no blood in the stool. The patient travels to Latin America and Eastern Europe frequently, most recently 2 weeks ago. (2)
Cryptosporidium parvum or Giardia lamblia
Patient has just returned today from Latin America following a 2 day buisness trip where he reports eating several meals of fish that he bought from street vendors around his hotel. He feels very ill with PROFUSE watery diarrhea and vomiting.
Vibrio cholera
12 to 72 hour incubation
Profuse diarrhea wiht abdominal distension, and vomiting.
Vibrio cholera
Several members of a single family are ill with abdominal cramps and watery diarrhea. They just returned from visiting friends on the East Coast of the US where they consumed raw oysters 48 hours ago.
Norovirus or Vibrio parahemolyticus
Where does replication of rotavirus take place?
Who is most often afflicted?
In the differentiated epi of the small intestines.
Usually confined to children.
How does rotavirus manifest in older children adults?
Usually mild or asymptomatic
Acute onset of diarrhea and vomiting, often PROJECTILE, following 1-4 day incubation period.
Rotavirus
*Severe in immunodeficient or malnourished children*
Pyrexia=
Intussusception=
Pyrexia=Fever
Intussusception=intestinal blockages caused by part of intestine sliding into another part.
What doess the RotaTec vaccine (live oral) contain? How many doses? Age?
5 live reassorted rotaviruses
3 doses
Btwn ages 6-32 weeks
Once you have had rotavirus can you get it again?
Route of transmission?
Treatment of rotavirus?
Yes, bc immunity is serotype specific.
Fecal-oral
Rehydration
Name that virus....
Watery diarrhea w/o fecal leukocytes or blood.
Agglutination tests, ELISA, or EM can be used to detect virus in feces
ROTAVIRUS
Who does Norovirus typically infect? How is it transmitted?
Typically infects children and adults.
Fecal-oral transmission, contaminated food and water, shellfish, aerosolized vomitus.
Incubation time 2 days.
Clinical signs are vairable and non descript.
Resistant to in vitro culture.
Norovirus
Primary site of viral replication is the jejunal mucosal epithelium.
Epi cells become vacuolated and cuboidal but remain intact.
Immune response of intraepithelial lymphocytes and neutrophils occurs.
Norovirus
What is the best way to detect Norovirus?
How is Norovirus treated?
Remember that it has a tendency to present in families/institutions.
Use PCR
Oral fluids
What are the primary and secondary most important causes of epidemic infantile darrhea?
Primary: EPEC (enteropahtogenic E coli)
Secondary: Adenovirus
Pathogenesis is probably similar to Rotavirus.
Clinical signs are similar to Rotavirus but this has a longer incubation period and more protracted clinical course (8-12 days)
Adenovirus
Can you be a carrier of adenovirus and be asymptomatic?
How can you treat adeonvirus?
What are the most common serotypes causing diarrhea in young children?
Yes, it is common.

Oral fluid and electrolyte replacement.

40 & 41
Salmonella has over 2000 serotypes.
"?" antigens are somatic
"?" antigens are flagellar
"?" antigens are capsular
"O"antigens are somatic
"H" antigens are flagellar
"Vi" antigens are capsular
Exclusively human pathogens producing typhoid fever, a systemic illness.
Produces enterocolitis in many species.
Salmonella typhi
Salmonella paratyphi A,B,C
Enterocolitis
is an inflammation of both the small and large intestine. However, most conditions are categorized as one or the other of the following:

Enteritis is the inflammation of the small intestine

Colitis is inflammation of the large intestine, especially the colon
Is typhoid fever the only cause of enteric fever?
No, there are multiple causes of enteric fever, and conditions that mimic it.
Describe the classic syndrome of enteric fever.
An acute illness w/ fever, headache, abdominal pain, relative bradycardia, splenomegaly and leucopenia.
Bacteria are ingested, attach to mannose-containing receptors on microvilli of ileum, Peyer's patches engulf bacteria, bacteria are passed via lymphatics and multipy intra and extracellularly. Bacteria get into blood stream via thoracic duct, multi-organ seeding, heavier reseeding of ileum, inflammation and necrosis around Peyer's patches.
Enteric Fevers-Typhoid Fever
In Enteric fevers (Typhoid Fever) bacteria can be found in the urine, feces and blood. In what order does it show up.
First in the blood, then urine and then feces. (shedding in urine and feces)
In Enteric fevers (Typhoid Fever) what is the incubation period?
What are the initial clinical signs?
What 'rises' like a stepladder?
3 to 50 days
Initial clinical signs: dry cough, epistaxis, anorexia, abdomenal tenderness, and headach.
Fever exhibits a step ladder rise.
Is diarrhea common in early in Enteric fevers (Typhoid Fever)
What occurs after the fever plateaus?
No
Hepato and splenomegaly
Rose Spots are seen on the front of the chest and upper abdomen in ~50% of cases
In Enteric fevers (Typhoid Fever) what are the mortality rates if treated and if not treated?
Treated <5%
Untreated ~20%
Relapse can occur in both groups
How is Typhoid Fever diagnosed definitively? How is it treated? For how long?
Isolation of organism in blood, ie serological typing.

Treatment is essential, but resistance is common. 14 days at minimum and at least 7 days after cessation of fever.
Chloramphenicol, Ampicillin, Cotrimoxazole, Ciprofloxacin
Identical to enteric fever except it does not generally extend beyond mesenteric lymph node to cause bacteremia.
Salmonella enterocolitis
Incubation is 8-48 hours
Clinical signs are nonspecific, but rarely include vomiting.
A persistent or high fever may indicate bacteremia.
Usually subsides in 2-3 days.
Salmonella enterocolitis
To treat Salmonella enterocolitis fluid and electrolyte replacement is recommended. What is contraindicated?
Antibiotics and antimotility agents are contraindicated. Ab can prolong carrier state (but are needed if evidence of systemic invasion is present)
Presumptive Diagnosis: Clinical signs and hx, fecal leukocytes and occasionally fecal blood.
Salmonella enterocolitis
Definitive Diagnosis: Fecal culture with microbiologic isolation, identification, and serotyping.
Differential Diagnoses: Shigellosis and Campylobacteriosis.
Salmonella enterocolitis
Infection follows ingestion of as little as 500 viable organisms.
Campylobacter jejuni
What is colonized in Campylobacter jejuni? Is it invasive? Is bacteremia common?
First the jejunum and ileum, and later the colon and rectum.
It is invasive, penetrating submucosa, lamina propria and mesenteric lymph nodes.
Bacteremia is rare.
Campylobacter jejuni Pathogenesis:
Mucosal ulceration is common
Cellular damage results from:
Direct cellular invasion and _______.
Production of a _______-like endotoxin.
Production of at least ______ cytotoxins.
Direct cellular invasion and DEATH.
Production of a CHOLERA-like endotoxin.
Production of at least TWO cytotoxins.
Differential Diagnosis of _________ _________:
Acute appendicitis
Shigellosis
Salmonellosis
Differential Diagnosis of Campylobacter jejuni:
Acute appendicitis
Shigellosis
Salmonellosis
Campylobacter jejuni
Incubation period:
Shedding lasts for:
1-7 days
3 weeks
Are fecal leukocytes/blood found in Campylobacter jejuni?
How is it definatively diagnosed? (specific requirements)
Yes

Culture with antibiotics, Skirrow's, Campy BAP
What disease are the following complications affiliated with?
Shedding for 3wks
Infrequent bacteremia
Severe intestinal hemorrhage, toxic megacolon, and uremic syndrome
Reactive arthritis & peripheral polyneuropathy (Guillain-Barre'syndrome) may appear 1-2 wks post recovery.
Campylobacter jejuni
Though Erythromycin is effective in treating Campylobacter jejuni, why is it only used in immunocompromised pt or in persistant infections?
Because by the time the organism is confirmed, patient is recovering.
How should you treat Campylobacter jejuni?
Supportive fluids and electrolytes.
Motile when grown at 25 degrees Celsius
Cold enrichment
Raw pork & chitterlings
Yersina (ent&psuedotb)
Yersinia is a member of enterobacteriaceae, however:
It grows poorly on MacConkey agar.
What is the most problematic type of Yersinia? and its most problematic serotype?
Enterocolitica, serotype 8
Salmonella, Campylobacter and Yersinia are all contracted via:
Ingestion of contaminated food
Penetration of the ileal mucosa leads to macrophage infection & mesenteric lymphadenitis via lymphatic transport.
Hepatic and splenic abscesses may develop.
Focal areas of mucosal ulceration with a marked pyogranulomatous (WBC & macrophage) inflammatory response is the typical lesion.
Yersinia
What are the usual clinical signs of Yersinia?
Bonus: what if it is severe?
Nonspecific, mild, not recognized.
Severe: Fever, abd pain, vomiting, diarrhea sometimes bloody, swelling & tenderness of mesenteric lymph nodes.
Which Yersinia is resistant to penicilin?
Enterolitica
How should you culture Yersinia?
How should you treat it?
CIN agar at room temp
Antimicrobials are not necessary but, can treat it with chloramphenicol, cephs, aminoglycosides, tets, and trimeth/sulf
List 6 causes of Dysentery
Shigella
EIEC
Campybacter jejuni
Salmonella enterica
Vibrio parahemolyticus
Entamoeba histolytica
List the Types of E coli GI infections:
EPEC
ETEC
EHEC
EIEC
EAEC
An 18 month old child is brought to your office with fever, bloody diarrhea and some vomiting. She has been drinking unpasteurized milk in the last 48 hrs. No other family members are ill. (3)
Enterohemorrhagic E Coli
Salmonella
Shigella
Campybacter
A patient calls and states that he and several family members are ill with severe vomiting. They ate at a church picnic 4 hours earlier.
Staph Aureus
12 yr old, abdomenal pain, diarrhea for 1-2wks. Something moving captured from stool, that mom thought was an earthworm. He had no fever cough or blood tinged sputum. His travel history was unremarkable and no other worms or larvae were seen on anal exam.
Intestinal Nematode
Maybe Strongyloides stercoralis or Trichuris trichiura
35 yr old man awoke with dry mouth and blurred vision. Rapid progression over 2 hours to diplopia, dysphagia and weakness. Difficulty speaking, previously healthy. In ER he is afebrile, bilateral ptosis, weak gag reflex, UE weakness but not LE. Sensation intact, mental status normal.
Botulism
Nematodes and Cestodes
Which are flat, which are round?
Nematodes are round
Cestodes are flat
List all of the nematodes. (6)
Ascaris lubricoides
Ancylostoma duodenale
Necator americanus
Strongyloides stercoralis
Trichuris trichiura
Enterobius vermicularis
List the four types of cestodes.
Dipylidium caninum
Diphyllobogthrium latum
Taenia saginata
Taenia solium
Pronounced eosinophilia
Treat with albendazole with mebendazole.
Clinical sign?
Ascaris lubricoides
Usually asymptomatic
Usually asymptomatic BUT may see:
Pneumonitis and biliary blockage resulting from migratory phase.
Intestinal stages may cause pain, nausea, blockage or penetration.
May see cholangitis if adults ascend biliary duct.
Ascaris lubricoides
Giant intestinal Worm, Common Roundworm
Ancylostoma duodenale & Necator americanus
___ found in Europe, north Africa and western Asia.
___ found in Africa, India, Far East, Australia, South and Central America and southern USA.
Ancylostoma duodenale found in Europe, north Africa and western Asia.

Necator americanus found in Africa, India, Far East, Australia, South and Central America and southern USA.
Ancylostoma duodenale & Necator americanus are both examples of
Hookworms
Life cycle of _________
Direcgt with Pulmonary migration. Cutaneous penetration of 3rd stage larvae. Adults in small intestine.
Hookworms
(Ancylostoma duodenale & Necator americanus)
Adults feed on intestinal mucosa and blood of host. Iron-deficient anemia, melena, chronic diarrhea and retarded growth may occur in heavy infection.
Hookworms
(Ancylostoma duodenale & Necator americanus)
Cutaneous larval migrans, a marked dermatitis, may occur at the site of larval penetration of skin.
ID via ova in feces.
Treat with Thiabendazole, Mebendazole, Pyrantel pamoate, or Levamisole
Hookworms
(Ancylostoma duodenale & Necator americanus)
Parthogenesis

Cutaneous larval migrans, a marked dermatitis, may occur at the site of larval penetration of the skin as with hookworm infection.
Strongyloides stercoralis
Adults live in Sml In & feed on blood & mucosa.
May see profuse diarrhea, fluid loss, electrolyte imbalances & malabsorption in heavy infection.
Autoinfection in immunocompromised patients may result in "hyperinfection", a potentially fatal disease syndrome.
Strongyloides stercoralis
Fecal exam for larvae
Treat with Thiabendazole, Mebendazole, Pyrantel pamoate.
Strongyloides stercoralis
Trichuris trichiura are:
Whipworms (type of roundworm)
Direct life cycle, no migration, larva mature in intestinal mucosa.
Trichuris trichiura (whipworms)
Adults embed anterior portion into colonic epi through a parasite induced syncytium of fused epi cells.
Posterior portion of worm remains in lumen to release ova.
Trichuris trichiura (whipworms)
Clinical Signs: Usually little disease, may cause chronic diarrhea, intestinal discomfort and rectal prolapse.
Diagnosis: Fecal exam for ova, with POLAR PLUGS
Trichuris trichiura (whipworms)
Repeated infections result in sensitization to worm antigens.
Scratching facilitates host reinfections.
Enterobius vermicularis
(Pinworm, Threadworm, Seat Worm)
Adults located in descending colon, adults cause few lesions.
"I can't think of a more compelling reason to stay away from children."
Enterobius vermicularis
(Pinworm, Threadworm, Seat Worm)
ID and Treatment of Enterobius vermicularis (Pinworm, Threadworm, Seat Worm)
ID ova or adult on perianal region, NOT fecal exam.
Pyrantel pamoate, otherwise known as PinRid
Launder bedding
Check family members
Infection via flea ingestion
Intestinal cestode
Proglottids or egg packets in feces
Treat with Praziquantel
Dipylidium caninum
Dog tapeworm
Infection via undercooked fish.
Symptoms: Usually asymptomatic, but may see pernicous anemia due to B12 deficiency.
May grow to 30-40 ft
ID via eggs and proglottids in feces.
Treat via praziquantel
Diphyllobothrium latum
Infection via undercooked beef (15m) or pork (4m).
Mature in intestine due to scolex, takes 10-12 wks
Taenia saginata
Taenia solium
Few clinical signs.
Cysticerci cause a variety of lesions which may be severe depending on location.
ID via proglottids or ova in feces.
Treat with praziquantel.
Taenia saginata & Taenia solium
Cysticercosis
Infection in pigs and man w/ larval stages of parasitic cestode, Taenia solium.
Often has serious complications.
(formerly known as flux or the bloody flux) is an infection of the digestive system that results in severe diarrhea containing mucus and blood in the feces and is typically the result of unsanitary water containing micro-organisms which cause significant inflammation of the intestinal lining.
Dysentery
Two colonic bugs that can cause hemolytic uremic syndrome?
Shigella Type 1
Enterohemorrhagic E coli
Only requires 10-100 organisms for infection to occur.
Shigella
The presence of blood and a large number of fecal leukocytes in a febrile patient is highly suggestive of:
Treatment is limited to fluid and electrolyte replacement, and possibly dialysis:
Shigella
Bacteria attach to colonic mucosal epithelium and are endocytosed.
Bacteria multiply in the epithelial cells leading to cell death and rupture with spread to adjacent cells and lamina propria, but rarely invade past the wall of the colon.
Capillary thrombosis in lamina propria leads to mucosal infarction and sloughing.
Shigella
What species of Shigella produces cytotoxic enterotoxin Shiga toxin?
Which type of Shigella accounts for 60-80% of cases in the US and industrialized world.
Group A Shigella dysenteriae

Group D Shigella sonnei
Incubation 1-3 days
An intense inflammatory infiltrate consisting primarily of neutrophils results following cell destruction.
Fecal leukocytes are prominent, as are blood and mucus.
Shigella
How to treat Shigella
Fluids:
Anti-motility:
Antibiotics:
Sensitivity testing:
Dialysis:
Fluids and electrolytes.
Anti-motility contraindicated
Antibiotics in severe case or immunocompromised
Sensitivity testing if ab are going to be given
Dialysis, may be necessary if hemolytic uremic syndrome.
What age group has 70% of all Shigella infections?
How is Shigella most often transmitted?
Children under the age of 15.
Fecal oral transmission
Is EHEC invasive?
What toxins does it produce?
EHEC is non-invasive
2 toxins:
Stx-1 is essentially identical to Shiga toxin and is neutralized by Shiga toxin antiserum.
Stx-2 is not neutralized by Shiga toxin antiserum
Stx-1 is essentially identical to Shiga toxin and is neutralized by Shiga toxin antiserum.
Stx-2 is not neutralized by Shiga toxin antiserum
Enterohemorrhagic E coli (EHEC)
*Both toxins are cytotoxic to vascular endothelial cells leading to microangiopathy, hemorrhagic colitis and hemolytic uremic syndrome.
Clinical Manifestations
Asymptomatic, Hemorrhagic Colitis, Hemolytic Uremic Syndrome.
Enterohemorrhagic E coli
EHEC
Where does Shiga toxin bind?

How can you detect Shiga toxin antigen?
Renal glomeruli, mesangial and tubular cells.

ELISA
Should be suspected in cases with bloody diarrhea w/o fecal leukocytes or pyrexia. Definative diagnosis requires microbilogical culture with isolation of the suspect organism using sorbital-MacConkey agar followed by serotyping.
Enterohemorrhagic E coli
What treatment is used for Enterohemorrhagic E coli?
Fluid/electrolytes
Antibiotic therapy is CONTRINDICATED
Dialysis may be needed if HUS
Shigella and enteroinvasive E coli are similar in that they are not:
They are not lactose fermenters
Very similar in terms of pathogenesis and clinical features to Shigella.
Majority of EIEC isolates are of serotype O124 although other serotypes may be involved.
Enteroinvasive E coli
The most important parasitic amoeba of man.
Third leading cause of parasitic death in developing countries.
Entamoeba histolytica
Where can the cysts from Entamoeba histolytica be found?
Stool
Lungs
Liver
Brain
E. histolytica and E. dispar
Which is the pathogenic form?
Microscopically, what is the only way to distinguish between them?
E. histolytica
E. histolytica may have ingested RBC's.
Histologically the amoebae are clearly evident along with necrosis and a granulomatous inflammatory response.
Amoebic abscesses in liver are not uncommon.
"Anchovie paste" aspirate from amoebic liver abscess.
Entamoeba histolytica
Varies from asymptomatic infection with cyst passage to acute amebic dysentery
Entamoeba histolytica
Asymptomatic-iodoquinol, paromomycin, or diloxanide furoate.
Symptomatic-metronidazole, tinidazole followed by drugs for asymptomatic
Entamoeba histolytica
In Entamoeba histolytica it is important to remember you need two drugs so you treat for:
Cyst and trophozoite form
GPB motile, strict anaerobes
Enterotoxin A
Cytotoxin B
Bowel movement inhibited
Clostridium difficile
When is Clostridium difficile normal?
What is it typically caused by?
Are fecal leukocytes typical?
It is commensual in infants but not in adults.
Offending antibiotic.
Yes.
How is Clostridium difficile diagnosed and treated?
ELISA, endoscopy for pseudomembranous membrane.
Discontinue offending Ab, and if severe use Vanco or Metronidiazole.
Acute illness with gastrointestinal or neurological manifestations affecting two or more people who have shared a meal in the previous week.
Foood Borne Diseases
When is the toxin associated with the followng, formed?
Staph aureus
Bacillus cereus
Clostridium botulinum
Clostridium perfringens
Preformed toxin (Intoxication)
Staph aureus
Bacillus cereus
Clostridium botulinum
Produced in Vivo
Clostridium perfringens
Clostridium difficile and perfringens are both
Gram pos and anaerobic
Large anerobic, rectangular, gram pos rods, form spores, replicate rapidly, double zone of hemolysis, produces lecithinase.
CLOSTRIDIUM PERFRINGENS
In Clostridium perfringens, what is often fatal, and what type of clostridium perfringens is it typically associated with?
Pigbel, also known as enteritis necroticans. It is associated with Type C. Deaths are caused by infection and necrosis of the intestines and from resulting septicemia.
What is the most common disease causing type of clostridium perfringens?
clostridium perfringens is food borne, what type of food?
Type A

Meat
How should clostridium perfringens be treated?
Fluids and electrolytes
A double zone of hemolysis is caused by:
clostridium perfringens
What should you know about Bacillus cereus?
GPR, aerobic, motile, sporeforming.
Emitic-heat and acid resistant, vomiting w/in 6hrs
Diarrheal-enterotoxin, watery
GPC, aerobic, catalase and coagulase positive.
Onset w/in 2-6 hours.
Staph Aureus
In staph aureus, what causes the vomiting and diarrhea? What are the typical foods involved?
Is there a fever?
Enterotoxins (A-E)
Typical foods are eggs and dairy.
No fever.
How many toxins are there in Clostridium botulinum? Which most often affect humans? How do they each act?
8 toxins
A, B, E most often
They are antigenically distinct but functionally identical. They block the neuro-transmitter acetylcholine causing flaccid paralysis
Begins 1-2 days after toxin ingestion
Initial vomiting/nausea
Oculomotor muscles are first affected with drooping eyelids, vertigo, blurred vision.
Progressive descending motor paralysis
Diff w/ speech/swallowing
Recovery may be slow and agnonizing.
Clostridium botulism
Are nerve palsies associated with botulism bilateral or unilateral.
Bilateral/Symmetric
What are the two routes to botulism infection?
Food borne or wound infection
Typical foods are honey and canned foods.
How is Clostridium botulism diagnosed and treated?
Anti-toxin neutralization test in mice, but don't wait.

Treat with polyvalent antitoxin, the monovalent only works if you know the right one, Intenstive support care, prophylax others.
Listeria monocytogenes is the only aerobic, gram positive _________.
Coccobacillus
Listeria monocytogenes most often affects the following groups.
Pregnant/fetus
Immunocompromised
Leukemic patients
Diabetic, cirrhotic, asthmatic, and ulcerative colitiis
Elderly
How do you treat Listeria monocytogenes?
Penicillin, ampicillin w/ or w/out gentamycin.
Erythromycin is also effective.
Is Listeria monocytogenes intra or extracellular? How does it evade antibody exposure? It is primarily a disease of the ?
Intracellular, in macrophages.
Evades antibody exposure by using macrophage membrane surface as coating agent.
Immunocompromised.
What is the typical issue/outcome in Listeria monocytogenes in the following.
Early Onset Neonatal Disease.
Late Onset Neonatal Disease.
Adult Disease.
(granulomatosis infantiseptica) has a high mortality if not treated rapidly, multi organ involvement and neningitis.
Late neonatal-meningitis/ meningoencephalitis, septicemia
Adult-Flu-like disease at 2-8 weeks post exposure.