GI Tract Infections Fall13 Student Version

8/13/2019 GI Tract Infections Fall13 Student Version

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Chapter 22 GI infections

Chapter 24 CNS infections

Chapter 25 Eye infections

Chapter 26 Skin infections

Case studies due Nov 26th

Cases 31,36,38,53,58,72,78

Student Presentations Dec 3rd(groups 1-5) andDec 5th(groups 6-10)

Final Exam Tues Dec 10th7:30-9:30 AM


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Gastrointestinal Tract infections

Chapter 22


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DiarrheaIncrease in fluid and electrolyte loss into the lumen of the gut

Gastroenteritis

nausea, vomiting & diarrhea

May also present with abdominal discomfort, cramps, & fever

Common causes

Campylobacter jejuni

Escherichia coli

Salmonella spp.

Viruses: Rarer causes

Bacillus cereus

Clostridium perfringens

Food poisoning

Disease caused by ingestion of food contaminated with a toxin

Dysentery

Diarrhea with blood and mucus in feces

Abdominal pain, cramps and feverare common

Common causes

Entamoeba histolytica - amoebic dysentery

Shigellaspp.bacterial dysentery


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Pathogenesis Preformed toxins

Present with short incubation with vomiting

C. botulinumand S. aureus

Toxins produced in the gut

Longer incubation period with marked vomiting

V. choleraeand Enterotoxigenic E. coli

Tissue Invasion

Entoamoeba histolytica, Salmonella spp., Enteroinvasive E. coli

Parasitism

Protozoa and worms

Preforation

Infection or trauma allows gut flora to escape

Results in intra-abdominal disease or systemic sepsis


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Enteric Pathogens

Enteric bacteriarod-shaped Gram-negative bacteria;

most occur normally or pathogenically in intestines ofhumans and other animals

Escherichia

Klebsiella Salmonella

Shigella


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Enterobacteriaciae

G- rods which ferment glucose; oxidase negative

Facultative anaerobes

Serotypes

O antigens- LPS

H antigens- flagellar

Kantigens- capsular or fimbriae


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EPEC

Developing countries

Destroy gut microvilli

No Toxins

Use bundle forming pili and intimin (adhesin)to attach to and disrupt epithelial cell in smallintestine

EnteropathogenicE. coli


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Entertoxigenic E. coliETEC

The major cause of travelersdiarrhea and diarrheal disease inchildren in developing countries

Transmitted by food or water contaminated with human or animalfeces

Self limiting

Two toxins which stimulate the lining of the intestines to secreteexcessive fluid

Watery diarrhea, abdominal cramping, low-grade fever, andnausea

Illness occurs 1-3 daysdays after exposure and last 3-4days onaverage


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Treatment Replace liquids

Anti-mobility agents may reduce number of bowel movement

but can prolong disease and should be avoided in cases ofbloody diarrhea and fever. Kaolin-pectin compounds or

lactobacillus do not slow or relieve symptoms

Avoid milk products, because temporary lactose intolerance is

common after intestinal illness Wash your hands often to reduce the chance of transmitting

the pathogen to someone else.

Some doctors recommend a BRAT' diet: bananas, rice,

applesauce and toast.

Withhold food for 24 hours in moderate to severe cases,

allowing only lukewarm clear liquids. Slowly add soft foods.

Visit your doctor if the diarrhea is painful, is severe, contains

blood or is accompanied by a high fever.


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EnterohemorrhagicE. coliEHEC or VTEC (verotoxigenic)

Serotype 0157:H7 is most common type (ID = 10 cells)

Produce verotoxin (Shiga toxin) which binds to gut mucosal and kidneyleading to damage and hemorrhage

Symptoms

Acute bloody diarrhea with severe abdominal cramps with little or nofever which last approximately 1 week


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May cause hemorrhagic (HC) and hemolytic-uremic syndrome(HUS) associated with hemolytic anemia, thrombocytopenia andacute renal failure in 5% of infections and the principal cause ofacute renal failure in children under 5.

Transmission is from undercooked ground beef, raw milk, sewage-contaminated swimming pools and in day-care centers

Must request stool specimen to be grown on sorbitol-MacConkey(SMAC) agar- E. coliO157:H7 differs from most other strains of E.

coliin being unable to ferment sorbitol No treatment for common symptoms, HUS must be treated in

intensive care and blood transfusions and kidney dialysisperformed


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Enteroinvasive E. coliEIEC

Attach to mucosa of colon; invade by endocytosis using plasmid

associated genes

Invade mucosa, divide, spread and destroy epithelium causing

inflammation, necrosis and ulceration

Watery diarrhea that progresses to dysentery: blood and mucus

found in diarrhea. Fever, abdominal cramps, malaise, vomiting


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Salmonella Motile, G- rods Acute gastroenteritis

S. enterica

Invades M cells, mucosal epithelial cells,

stimulates production of fluids Inflammatory response confines infection to GI

tract but causes prostaglandinrelease which

results in diarrhea

In patients with sickle cell anemia or cancer cancause septicemialeading to osteomyelitis,

pneumonia, meningitis

8-24 hrs nausea, vomiting, abdominal pain and

diarrhea, low-grade fever and chills

Self-limitinginfection; antibiotics & anti-

diarrheals can prolong illness

Infectious for 2 weeks post symptoms


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More Severe Infections: Septicemia-Fever

S. typhi and S. paratyphi

Invade tissue and infect macrophages which carry them tospleen, liver & bone marrow. Liver>bile>gall bladder> intestine

10 day incubation, fever, anorexia, dull frontal headache, cough,constipation, abdominal pain fever which increases to 104oC.Normal CBC

Spread for 1-2 weeks fever, malaise, confusion,hepatosplenomegaly, neutropenia, faint rash

3rdweek: High fever, hemorrhage, ulceration and perforation-peritonitis, liver necrosis, endocarditis, meningitis, empyema,osteomyelitis, pyelonephritis

Treat with antibiotics Fatality rate is 2-10%


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Shigella Shigellosis: Bacterial (bacillary) dysentery

Mild (S. sonnei), Moderate (S. flexneriandboydii), Severe (S. dysenteriae)

Similar mode of infection to Salmonella Infects PMNs & macrophages & triggers

apoptosis Uses hemolysin and outer membrane protein

to coat itself in actin

Shiga toxin causes damage to intestinal andglomerular enodothelial cells (Verotoxin) Can lead to HUS 2-3 days after exposure, fever, cramping and

watery diarrhea. The fluid loss is extensive andcan be life threatening. The number of stoolsdecreases but gradually has mucus PMNs andblood with severe lower abdominal pains

Transmitted by fecal oral route, fomites, flies,food and water, close contact


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Membrane ruffles surround a

Shigella flexneribacterium as it

invades an epithelial cell.

The initial contact between

molecules on the pathogens

and the host cells surface

triggers activities in the host

cell that eventually lead to

rearrangements of the cellsplasma membrane and its

cytoskeleton

Eventually, the pathogen is

wrapped up by the membraneand internalized. (Electron micrographcourtesy of Pascale Cossart, Institut Pasteur; reprinted

from Science276:720, by permission of the American

Association for the Advancement of Science.)


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Non- enterics

C l b j j i d C f


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Curved, G-rods

One of the most common causes of acute enteritis

2 million in US/yr

Often in chicken, other meats (cutting board) and milk, dog feces Heat labile enterotoxin; invasive causing abscesses

C. fetushas paracrystalline structure called S-layer

Acute enteritis: Causes fever, cramps, profuse diarrhea even bloody, canmimic acute appendicitis

Begins 3-4 days after infection and Last 1-7 days In neonates and pregnant women infection can lead to meningitis

In debilitated adults bacteremia is not uncommon

C. fetusis more common in summer

Confirmation

needs special stool culture (Campy BAP)

Treatment

Liquids and in severe cases Erythromycin

Campylobacterjejuni and C. fetus

Ch l
http://images.google.com/imgres?imgurl=www.cdc.gov/ncidod/eid/vol5no1/altek2b.jpg&imgrefurl=http://www.cdc.gov/ncidod/eid/vol5no1/altekruseG.htm&h=406&w=616&sz=34&tbnid=XTdh731THGYJ:&tbnh=88&tbnw=133&prev=/images?q=Campylobacter&hl=en&lr=&ie=UTF-8&oe=UTF-8


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CholeraVibrio choleraeserogroup O139 Major cause of epidemic diarrhea in developing

countries

Cholera toxin (review from earlier this semester)

Transmission

Contaminated drinking water or food

Fecal contamination of water or streetvendor food

Uncooked shellfish

Mild to severe disease which presents withprofuse watery diarrhea (1L/hr), vomiting and legcramps, circulatory collapse (tachycardia,hypotension), renal failure and death

Treatment is rehydration

Confirmation: Vibrios on a dark-field microscopyof stool sample

www louisianasportsman com


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Article by Don

Shoopman

Vibrio vulnificus is a bacterium in the same family as those that cause cholera,according to the Centers for Disease Control and Prevention. It lives in warm seawaterand is part of a group of Vibrios that are called halophilic because they require salt.

The CDC reports that Vibrio vulnificuscauses infection in the skin when open wounds

are exposed to warm seawater, infections that may lead to skin breakdown andulceration. The highest incidences are between May and September.

Also, people with immune disorders are at higher risk for invasion of the organism intothe bloodstream and potentially fatal complications, the CDC said.

Vibrio vulnificuscan cause disease in those who eat contaminated seafood, also.Healthy people who ingest Vibrio vulnificussuffer from vomiting, diarrhea andabdominal pain while immunocompromised persons, particularly those with chronic

liver disease, face a severe and life-threatening illness characterized by fever and chills,decreased blood pressure and blistering skin lesions. Vibrio vulnificusbloodstreaminfections are fatal about 50 percent of the time.

www.louisianasportsman.com


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Vibrioparahaemolyticus

Cramps, nausea, vomiting, fever and chills within 24 hrs of

ingestion and only last 3 days

Undercooked shellfish

Heat Stable Cytotoxin

Yersinia enterocolitica

Colder regions

Invades ileum; necrosis of PeyersPatches

Present with entercolitis and mesenteric adenitis

(inflammation of lymph nodes in the abdomen)

Confused with appendicitis in children


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Clostridium perfringens boxcarshaped rods

Common form

Endospores survive cooking and germinate to produce enterotoxin (a-toxin) in

large intestine 50%of people who ingest spores will suffer from food poisoning 8-24 hrs later

Clinically can test for enterotoxin by latex agglutination assay

Rare form

Beta-toxin-producing strains cause a necrotizing disease of the small intestineresulting in pain and diarrhea

Risk factors:

People on a

undercooked

Co-infectionwithAscaris lumbricoides

Enteritis necroticans orpig-belmainly occurs in New Guinea

The bowel wall becomes necrotic and perforated allowing for dissemination Treat with penicillin G and bowel is re-sectioned

15-45% fatality rate

Causes gangrene in soft tissue wounds


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Clostridium difficile Occurs after treatment with

clindamycin or other broad-spectrum antibiotic which inhibitsthe growth of normal facultativegram negative bacteria

More common in children orhospitalized patient

Colonic mucosa covered with afibrinous yellow pseudomembrane

Suspect if have taken antibioticwithin last 2 months or if diarrheaoccurs within 72 hrs ofhospitalization

It produces two exotoxins

Cytotoxin Enterotoxin

Non-invasive(does not go intobloodstream)


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C. difficile Pseudomembranous Colitis: Pseudomembranous inflammation

occurs when an epithelial surface becomes destroyed. The ensuing

acute inflammatory response produces a fibrinopurulent exudate asthe body attempts to cover the wound with a substitute (pseudo)

membrane.

Pseudomembranous colitis is usually the result of Clostridium difficile

infection following heavy antibiotic therapy that destroys normalbowel flora, allowing the Clostridiumto proliferate.


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Staphylococcal infections

30 different types of Staph that infect

humans

Staphylococcus aureus most

prevalent

Can infect most parts of the body

Causes:

Boils

Impetigo

Cellulitis

Scalded skin syndrome Toxic Shock Syndrome

Food poisoning

F d i i


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Food poisoningstaphyloenterotoxicosis; staphyloenterotoxemia

50% produce enterotoxins (heat-stable)

8 different enterotoxins (A-E) Symptoms

Severe vomiting within 3-6 hrs after eating poultry or eggproducts

salads such as egg, tuna, chicken, potato, macaroni; bakery

products such as cream-filled pastries, cream pies, chocolateclairs; sandwich fillings; milk and dairy products.

Recover within 24 hrs

Detect toxin using latex agglutination test

Infective dose-a toxin dose of less than 1.0 microgram in

contaminated food will produce symptoms of staphylococcalintoxication

Botulism


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Botulism Three types

Food borne-ingestion of neurotoxin Outbreaks associated with home processing of

food: Sausages, meat products, canned vegetables

and seafood products

Infant-ingestion of spores Affects infants under 12 months of age under 12 months of age.

Spores colonize & produce toxin in intestinal tractof infant Environmental sources such as soil, cistern water,

dust and foods Honey is the one dietary reservoir of C. botulinum

Infection of wound with spores Clostridium botulinum

G+ rod Endospore former Produces exotoxin (A,B,E,F affect humans)


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Symptoms of foodborne botulism (ingestion of toxin)

18 to 36 hours

marked lassitude and vertigo, usually followed by double vision andprogressive difficulty in speaking and swallowing.

Difficulty in breathing, weakness of other muscles, abdominaldistention

Clinical symptoms of infant botulism

poor feeding, lethargy, weakness, pooled oral secretions, and wail oraltered cry.

Loss of head control Recommended treatment is primarily supportive care.

Diagnosis: toxins in stool (sometimes in food)

Flaccid (floppy) paralysis

starts with the eyes and face, to the throat, chest and extremities.

When the diaphragm and chest muscles become fully involved,respiration is inhibited and death from asphyxia results.

Recommended treatment for foodborne botulism includes earlyadministration of botulinal antitoxin (available from CDC) and intensivesupportive care (including mechanical breathing assistance).


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Listeriosis Listeria monocytogenesis ingested with contaminated food

The gram positive coccobaccilus penetrates the epithelial cells that form thelumen, or intestinal lining and multiplies.

It is released into the underlying tissues and gains access toblood vessels Within the bloodstream the bacterium penetrates white blood cells, which spread

the infection through the body.

If the infected cells release the pathogen in the placenta of a pregnant woman or inthe brain, it can cause life-threatening infections.

Rotaviruses(Reoviridae)


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Rotaviruses(Reoviridae) the most common cause of severe diarrhea among

children

incubation period is approximately 2 days.

vomiting and watery diarrhea for 3 - 8 days, and fever andabdominal pain occur frequently.

Immunity after infection is incomplete, but repeatinfections tend to be less severe than the original infection.

A rotavirus has a characteristic wheel-likeappearancewhen viewed by electron microscopy (the name rotavirusis derived from the Latin rota, meaning wheel")

transmission is fecal-oral

transmission can occur through ingestion ofcontaminatedwater or food and contact with contaminated surfaces.

the disease has a winter seasonal pattern, with annual

epidemics occurring from November to April. The highest rates of illness occur among infants and young

children between age of 6 months and 2 yrs.

Treatment:Rehydration


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Helicobacter pylori Barry Marshall and Robin Warren of Perth,

Western Australia, discovered H. pyloriin 1983.

Uses several mechanism to invade Cytotoxin

Acid inhibiting protein

Adhesins

Urease Treatment

Proton pump inhibitor and 2 antibiotics:

Clarithromycin and amoxicillin

Endoscopy demonstrating two large

ulcers in the duodenal bulb, with

surrounding duodenitis.

H li b t l i


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Helicobacter pylori

Gram negative spiral-shapedbacterium

Found in the gastric mucous layer

Causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers

Approximately 2/3 of the world's population is infected with H. pylori. Most people are asymptomatic

H. pylorican cause chronic active, chronic persistent, and atrophic gastritis in adultsand children.

The most common ulcer symptom is gnawing or burning pain

occurs when the stomach is empty, between meals and in the early morninghours

last from minutes to hours and may be relieved by eating or by taking antacids


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The Urea Breath tests for the presence

of urease. The test becomes negative

shortly after eradication of the bacteria

from the stomach with antibiotics.

Endoscopy is an accurate test for

diagnosing H. pylori as well as the

inflammation and ulcers that it causes.

During endoscopy, small tissue samples

(biopsies) from the stomach lining can beobtained. These tissue samples are

placed on special slides containing urea

(e.g., CLO test slides). If the urea is broken

down by H. pylori in the biopsy, there is a

simple color change around the biopsysample on the slide. This means that

there is active infection with H. pylori in

the stomach.

P t d W


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Protozoa and Worms Protozoa

Giardia lamblia

Cryptosporidiumparvum Entamoeba histolytica

Cyclospora cayetansis- Travelers diarrhea (food)

Helminths

Nematodes

Ascaris lumbricoides

Trichinella spiralis (pork worm)

Trematodes

Taenia saginataand solium (beef tapeworm) and solium

(pork tape worm) Shistosoma(passes through intestine-inflammation)


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Giardiasis: Giardia lamblia (intestinalis) Fecal-Oral

Source usually water (rivers and

streams) Trophozoites from ingested cysts adhere to

the mucosa

Symptoms range from asymptomaticthrough acute watery diarrhea to chronicintermittent diarrhea

Present with diarrhea, abdominal pain,bloating, nausea, and vomiting

Acute symptoms occur 5-6 days after

infection and symptoms last 1-3 weeks Chronic Giardiasis is recurrent and results

in debilitating malabsorption

Treatment: Metronidazole

Giardia


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GiardiaCysts

See 2-4

nuclei

Trophozoites

Each cell as

two nuclei

with a largekarysome

Cryptosporidium parvum


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Cryptosporidium parvum Resistant to disinfectants like bleach due

to outer wall

Most common water-bornecause ofdiarrhea in US

Symptoms include diarrhea, stomachcramps, slight fever. Can beasymptomatic

Can be transferred sexually or fecal-oralroutes

Symptoms start 2-10 days after infection

In healthy individuals symptoms can lastup to 2 weeks in cycles

In immunocompromised individualsconcern for dehydration and spread toother organs such as digestive tract, lungsand conjunctiva

Crypto

Giardia

Oocyst is infectious stage

Develop in small intestine

Cryptosporidium


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CryptosporidiumWet mount- oocysts

Modified acid-fast stain will showbright red against a backgroundof blue-green fecal debris andyeast

Confirm with fluorescent antibodiesor ELISA

Entamoeba histolytica


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Entamoeba histolytica Trophozoite stage lives in colon: encysted form-infectious-oral

infection to small intestine where it destroys host tissue andRBC= amoebic colitis

1 in 10 who are infected become symptomatic

Mild: loose stools, stomach pain, stomach cramps

Severe: Bloody stools with mucus and pus, and fever(dysentery, colitis, toxic megacolon)

Rare: Disseminates and invades liver forming abscesses. Canalso spread to lungs and brain

Symptoms can occur from 1-4 weeks after infection

Treatment : Metronidazole

Ascariasis: Ascaris lumbricoides


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Ascariasis:Ascaris lumbricoides Infects 1 billion people world-wide

Larvae hatch in small intestine, migrate to liver andlungs. Return to intestine as adults via the trachea

and esophagus Commonly no acute symptoms

High worm burden can lead to abdominal pain dueto intestinal obstruction

Migrating larvae may occlude biliary tract or lead tooral expulsion

Lung phase the larvae migrate into lungs and lead tocough, dyspnea, hemoptysis, eosinophilicpneumonitis- Loefflerssyndrome

Specimens

Stool: look for eggs

Sputum or gastric aspirate: larvae

On occasion adult worms are passed in stool orthrough nose or mouth

Treatment: albendazole

Hookworms


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Hookworms Ancylostoma duodenale and Necator americanus

Both are found in Asia, Africa and the America but N. americanus ispredominant in Americas and Australia whileA. duodenale is prevalent in theMiddle East, North Africa and Southern Europe

Eggs are passed in stool, the larvae grow in feces or soil and become filariformwhich infect by penetration of skin and carried to the heart and lungs, ascend topharynx and are swallowed, in the intestine they mature in the lumen byhooking into the intestinal wall

Most worms are expelled between 1-2 yrs after infection

Clinical features Iron deficiency anemia (caused by blood loss at site of attachment) may be

accompanied by cardiac complications

Nutritional symptoms may occur

Local skin irritation-ground itch may occur at site of penetration

Pulmonary complications like with Ascaris during migration

Lab test Stool sample: eggs cant differentiate these two species,larvae is what can

be used to differentiate the two species

Treatment: elsewhere is none;US albendazole


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Enterobius vermicularis pinworms


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Enterobius vermicularis pinworms Female worms live in colon- lay eggs

which reach perianal skin

Pinworm eggs are infective within a

few hours after being deposited onthe skin. They can survive up to 2weeks on clothing, bedding, or otherobjects. You or your children canbecome infected after accidentallyingesting infective pinworm eggs fromcontaminated surfaces or fingers

Severe itching (pruritus)

Detect by using Scotch Tape


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Infections of the liver Schistosoma mansoni

Adult worms live in

mesenteric vessels andeggs are swept into hepaticcirculation and becometrapped in the sinuses ofthe liver

Hepatomegaly and fibrosis Echinococcus granulosus

Hydatid cysts

Malaria

Leishmaniasis

Ascariasis

Entamoeba histolytica

GI Tract Infections Fall13 Student Version

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