Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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. |