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86 Cards in this Set

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GI Parasitic Infections
General
Predominately found in the developing world

Afflicts those where poor sanitation, contaminated food and water are part of the immediate environment

A few of these infections endemic to the developed world (Giardia, cryptosporidium, less commonly cysticercosis and amebae, rarely helminths)

Occasionally infect travelers, particularly those staying for long-terms in poorly developed areas
Intestinal Protozoa
Entamoeba histolytica

Giardia lamblia

Cryptosporidium

Others: Cyclospora, Isospora, Microsporida
Entamoeba histolytica

Epidemiology
Worldwide distribution: Most in Central/South America, Africa, Indian subcontinent

3rd leading parasitic cause of death in developing nations (10% of world population infected with Entamoeba)

In developed world: Think of in Institutionalized, recent immigrants, and gay males
Entamoeba histolytica

Transmission
Fecal-oral: through contaminated food and water; person-to-person spread may occur
Entamoeba dispar
Non-pathogenic, morphologically indistinguishable; need isoenzyme electrophoresis or specific stool antigen tests to differentiate

Much asymptomatic infection attributed to E. histolytica is probably due to E. dispar
Entamoeba histolytica

Life Cycle
Ingested cysts (environmentally resistant) transform to trophozoites upon exposure to stomach acid that colonize and in some individuals subsequently invade intestinal mucosa.

In most the infection is asymptomatic.

In some it invades the intestinal mucosa causing colitis and less commonly, through hematogenous or direct spread, distant infection

Trophozoites can divide and transform to infective cysts in asymptomatic carriers or symptomatic patients that are pasted in the stool
Entamoeba histolytica

Clinical Presentation
Invasive Bowel Disease

Extraintestinal manifestations
- Hepatic involvement/abscess >> rarely lung, pericardium, brain
- Rarely Vaginitis, skin ulcerations
Entamoeba histolytica

Invasive Bowel Disease
AKA intestinal amebiasis
Most common manifestation of infection
Dysentery, abdominal tenderness, fever

Chronic colitis may mimic Inflammatory Bowel Disease
Entamoeba histolytica

Complications of Invasive Bowel Disease
stricture, ameboma, hemorrhage, perforation, intussusception
Entamoeba histolytica

Virulence Factors
Galactosamine adherence lectin

Proteinases

Lysis of WBC’s
Amebiasis

Intestinal Diagnosis
3 stool exams (90% sensitive) for cysts or trophozoites esp. w/ RBC

Stool antigen detection (differentiates from E. dispar)

most with positive serum serologies by day 7. Titers remain positive for years, despite treatment (IHA)
Amebiasis

Extraintestinal Diagnosis
clinical picture, + serologies, “anchovy paste” aspirate

Note: aspiration of amebic cysts free of:
1. WBCs since amebae cytolytic
2. Amebae, since activity peripheral in the abscess
Amebiasis

Treatment
Invasive disease: metronidazole (Flagyl)
- Affects only trophozoites, NOT cysts

Intestinal cysts: paromomycin, iodoquinol
- Need to treat with these drugs subsequently to eliminate the cyst shedding state

NO therapy needed for E. dispar, or other commensals (E. hartmanni, E. polecki, E. ginigivalis, etc.)
Another name for Septra
TMP/SMX
36 yo previously healthy man bacpacked in Colorado mountains x 2 weeks
On 4th day of trip developed diarrhea. Improved with loperamide (Imodium.) One week later, diarrhea recurred, again improved.
Returned to NC feeling well. One week after return --> malaise, copious diarrhea, without fever. Some improvement with TMP/SMX but still having 5-7 loose stools per day, nausea.
Weight loss 7lbs.

NAME THAT DISEASE
Giardia
Giardia Lambia

Epidemiology
Worldwide distribution

Most common enteric parasite in USA and Canada

Cysts found in surface waters where mammalian reservoirs frequent (beaver the prototype)

Prevalence of infection approaches 30% in childhood in some developing nations

Sporadic infection in US seen in outdoor adventurers. Small epidemics seen associated with day-care or swimming pools.
Giardia Lambia

Transmission
water >> food, person-to-person, zoonosis (dog or cat)
Giardia Lambia

Life Cycle
1. trophozoite or freely living stage
2. cyst

Ingested cysts transform to trophozoites upon exposure to gastric acid and attach to small intestinal villi where they cause a malabsorptive diarrhea.

Some trophozoites transform to environmentally resistant cyst which are passed in the stool
Giardia Lambia

Clinical Presentation
Incubation period: 7-14 days

Manifestation of infection vary widely from asymptomatic to acutely symptomatic, to chronic diarrhea with malabsorption

Weight loss, nausea, abdominal pain, steatorrhea, FLATULENCE common

Symptomatic infection more common in children

Noninflammatory diarrhea. No blood, mucous in stool. No fever.
Giardia

Diagnosis
Microscopic exam of stool for cysts, trophozoites
- “gold standard”
- Identifies 50-70% of infections with 1 stool, 90%+ with 3 stools

Fecal suspension ELISA for antigen > 90% sensitive

Microscopic exam of duodenal fluid (Entero-Test or string test), duodenal aspirate, tissue
- Difficult to do
Giardia

Treatment
Metronidazole
- divided doses x 7 days

Quiacrine (if cannot tolerate metronidazole)
- drug production d/c in USA in 1992
Giardia

Prevention
Water prurification

Good sanitation, hand washing
Giardia

DDX
viruses

noninvasive bacteria

cryptosporidiosis

Cyclospora

tropical sprue
Cryptosporidium parvum

Epidemiology
Coccidian parasite

Worldwide distribution

Recognized as a veterinary pathogen 1907, 1st human case 1976

Can cause disease in immunocompetent and immunocompromised host
Cryptosporidium parvum
Intracellular pathogen; microvilli
Oocysts move into intestine where excyst to sporozoites;

Oocysts resistant to disinfection; ID50 is 130 cysts or so

Pathogenesis of diarrhea unclear; microvilli atrophied and blunted.

Sporozoites seen along apical surfaces of intestinal epithelial cells
Cryptosporidium parvum

Transmission
water>>fecal-oral>person-person

Occasionally person to person or zoonotic
Cryptosporidium parvum

Outbreaks
Outbreaks seen in day-care settings, swimming pool associated, and food-borne (apple cider, fresh vegetables)

A few waterborne outbreaks described that are of huge dimensions. Not eliminated by water treatment. Transmission through water distribution systems in these cases.

Agriculture, particularly cattle implicated. Calves probably the most important shedders.
How do you get cryptosporidium out of water?
need to boil the water

chlorination is not good enough
Cryptosporidium

Clinical Presentation
7-10 day incubation period

Diarrhea, crampy abdominal pain

Varies from intermittent, scant to continuous, watery, voluminous (up to 17L/day)

Self-limited in immunocompetent

Can be devastating in immunocompromised, particularly AIDS patients
- Chronic infection with uncontrolled diarrhea, abdominal pain and weight loss; cholangitis, cholecystitis occurs
Cryptosporidium

Diagnosis
Microscopic (modified Acid Fast Stain)

ELISA stool antigen detection
Cryptosporidium

Treatment
NO TREATMENT

Currently, no widely accepted palliative or curative therapy
- Anti-motility agents (Lomotil) somewhat effective in alleviating symptoms

- Antiretroviral therapy to control HIV and reconstitute immunity helps
Isospora belli
Intestinal Protozoa

Tropical and subtropical climates; AIDS patients

Occasionally infects travelers

Diarrheal illness

Treat with TMP/SXT
Cyclospora
Intestinal Protozoa

Coccidial: Acid fast organism

Some developed world outbreaks with imported fresh fruits (raspberries)

Treat with TMP/SXT
Microsporidia
Intestinal Protozoa

Opportunist in AIDS patients.

Can cause cholecystitis, cholangitis
Helminths
Roundworms (nematodes), tapeworms (cestodes) and flukes (trematodes)

Complex life cycle, generally with two or more hosts

Most worms CANNOT reproduce within human host (therefore, need intermediate host or environment).

Little or no eosinophilia from intestinal adult worm, though eosinophilia the rule with migration of larvae prior to development of adult or with worm invasion of deep tissues
Anoter name for nematodes
roundworms
Anoter name for cestodes
tapeworms
Anoter name for trematodes
flukes
Name the nematodes
Ascaris

Enterobius

Hookworm
- Necator americanus
- Ancylostoma duodenale

Strongyloides
Nematodes
Over 500,000 species

Elongated, bilaterally symmetric bodies containing an intestinal tract and a large body cavity.

Few are parasites of humans, however, infection with intestinal roundworms constitutes largest group of helminthic infections of humans.

Estimated worldwide: 1 billion cases ascariasis
Ascariasis
Very common intestinal parasitic infection
- Infects ¼ of the world population, ~1 billion!

Cosmopolitan distribution but more common in tropical regions. Now rare in US.

More common in children
Ascariasis

Transmission
Fecal-oral transmission via conatminated foods or soil contaminated hands
Ascaris lumbricoides
Female adult worms with very high egg output which can survive for long periods in the soil
Ascaris lumbricoides

Life Cycle
Ingested eggs hatch in small intestine.

Larva pass through intestinal wall into venous system to liver; then through heart to lungs.

In lungs larvae mature and pass into airways where they are then coughed up and swallowed.

Then complete develop into adult worms in small intestine.

During there passage through tissues (intestinal wall and lungs can cause inflammation with eosinophilia

One month to complete
Ascaris Lumbicoides

Pathogenesis and Clinical Disease
Asymptomatic infection common in light infections

Larval migratory phase: host reactions
- Pneumonitis: hypersensitivity reaction as parasite migrates through. Cough, wheezing, sob, fever, chills, malaise

Adult worms
- Vague crampy abdominal pain most common symptom
- Intestinal obstruction (1/500 infected persons/year)
- Aberrant migration can occur into bile ducts, appendix
> Causes fever, local pain
> If in bile duct jaundice, pancreatitis, hepatitis
Ascaris Lumbicoides

Diagnosis
Diagnosis through stool examination: ova or adult parasites. Easy to do because of large number of ova per adult female.

Adult worms passed per rectum or “coughed up” through retrograde migration from intestine to esophagus.

Obstructing biliary worms through endoscopy

Larvae migrating through lungs can be diagnosed from sputum exam
Ascaris Lumbicoides

Treatment
Choice
- Mebendazole
- Albendazole

Pyrantel pamoate
Ascaris Lumbicoides

Prevention
Improved sanitation

Sometimes mass treatment (periodic deworming)
Enterobius Vermicularis

Epidemiology
Most widely prevalent nematode of man

One nematode more prevalent in temperate than tropical climates

42 x 106 cases in USA each year

Host: human (predominately children)
- School, day care, congregate settings
Enterobius Vermicularis

Pathogenesis
Non-invasive; adults live in cecal area

Local allergic rxns to worm proteins

Susceptibility decrease with age --?immunity
Enterobius Vermicularis

Clinical Presentation
Most infections asymptomatic

Perianal itching with subsequent sleep disturbance

Very rarely, abnormal migrations: vaginitis, appendicitis, prostatitis
Enterobius Vermicularis

Diagnosis
"scotch-tape test"
Enterobius Vermicularis

Treatment
Mebendazole 1 dose or

Pyrantel pamoate 1 dose

Repeat dose at 2 weeks

May need to treat close contacts/family members
Hookworm Species
Species which produce human disease vary geographically:
- Ancylostoma duodenale
- Necator americanus

Common in tropics, subtropics, SE USA; rare in regions with < 40” inches annual rainfall.
Necator americanus
North and South America, Central Africa, Indonesia, South Pacific, parts of India

Hookworm
Ancylostoma duodenale
Mediterranean countries, Iran, India, Pakistan, Far East

Hookworm
Hookworms

Who is at risk?
Globally > 1 x 109 people infected

Risk for infection: skin exposures to fecally contaminated soil in endemic areas
- local residents of tropics
- occupational (infantry troops)
- recreational (tourists walking with barefoot or with open footwear)—especially cutaneous larva migrans: see below
Hookworms

Life Cycle
Infective larvae penetrate skin that contacts soil.

Migrates through systemic venous system to lung

Mature in lung, migrate up trachea and swallowed

Further mature into adults in small intestine. Attach to mucosa and cause slow, chronic blood loss and iron deficiency anemia.

Eggs passed into stool. Eggs hatch in soil into infective larvae

Gotta have stool in soil!
Hookworms

US epidemiologic problems
Hookworm in the US WAS a major problem in the Southeast and Appalachian mountains.

No shoes

Privies

Reflective of general poor sanitary conditions

Whole families were affected. Iron deficiency anemia was profound causing asthenia in all and developmental delay in children.
When is eosinophilia seen in hookworm infections?
with migration
Hookworms

Clinical
Initial intestinal infection with abd pain and eosinophilia

Chronic infestation with high worm burden: symptoms of iron deficiency anemia and hypoalbuminemia (protein-losing enteropathy)

Malnutrition

Eosinophilia with lung migration. Pulmonary symptoms tend to be milder than ascaris during migration
cutaneous larva migrans from worm penetration (Coolies itch)
Hookworms

Diagnosis
eggs in stool (larvae (if stool not fresh) may resemble strongyloides)
Hookworms

Therapy
mebendazole, albendazole, pyrantel pamoate
Hookworms

Prevention
Shoes, sanitary disposal of feces (proper latrines) and chemotherapy
Cutaneous Larva Migrans
Dog, cat hookworm most common cause

Pathogenesis: Larvae hatch in soil after eggs pass in canine, feline feces. Penetrate, migrate in skin producing inflammatory rxn along cutaneous tract. Pulmonary involvement also occurs.

Clinical disease: pruritic, serpiginous lesions develop 1 week post-contact with infected soil

Prevention: shoes

Treatment: topical thiabendazole
Strongyloides Stercoralis

Epidemiology
Over 200 x 106 persons infected worldwide

Same distribution as hookworm

Parasite likes warm, moist soil

Chronic infections, lasting up to 40 years, documented: probably because of autoinfection—see below.
Strongyloides Stercoralis

Life Cycle
Strongy eggs can “hatch” before leaving intestine and larvae can mature in and around rectum/anus—larvae than can penetrate perianal skin: cutaneous larvae curans

Basically the same life cycle as hook worm but note autoinfection can occur
Strongyloides Stercoralis

Pathogenesis
Adult worms embedded in small intestinal mucosa lead to local inflammation

Larvae --> tissue inflammation during migration

Penetrating larvae may carry enteric bacteria
Strongyloides Stercoralis

Clinical Presentation
Intestinal phase

Migratory phase

Hyperinfection syndrome
Strongyloides Stercoralis

Intestinal Phase
diarrhea and malabsorption (esp. in heavy infection)
Strongyloides Stercoralis

Migratory Phase
granulomatous colitis, hepatomegaly, pneumonitis and eosinophilia, fever, recurrent serpentine urticarial rash, “larva currens”
Strongyloides Stercoralis

Hyperinfection Syndrome
severe manifestations of above, septicemia, high mortality rate

associated with gram negative bacteria

Essentially disseminated strongyloides
Strongyloides Stercoralis

Treatment
Ivermectin

Thiabendazole
Strongyloides Stercoralis

Diagnosis
eggs in stool (larvae (if stool not fresh))
GI Trematodes
Blood Flukes

Liver Flukes

Intestinal Flukes

Lung Flukes
Blood Flukes
Schistosomiasis
Liver Flukes
Clonorchiasis
Intestinal Flukes
Fasciolopsiasis
Lung Flukes
Paragonimiasis
How do cestodes cause disease?
Adult tapeworms cause little or no symptomatic disease

Larval (cysticercal) tapeworms responsible for serious disease
- Cysticercal phase usually seen in INTERMEDIATE host.
- However if human ingests eggs rather than tissue phase cysticerci will cause result in intermediate cysticerci in muscles and brain.
- From brain seizures.

Little or no eosinophilia
List the Taeniasis
T. saginata = beef tapeworm

T. solium = pork tapeworm
Which Taeniasis cause cysticercosis?
T. solium ... seizures
Where is T. solium found?
Endemic in Latin America, Africa, Middle East, Central Asia.
Diphyllobothriasis
Fish Tapeworm

Causes Vitamin B12 deficiency
List the Cestodes
Taeniasis

Diphyllobothriasis
Characteristics of Cestodes
Hermaphroditic flatworm parasites

Some primarily human pathogens, others have animals as natural hosts but can also cause human infection

Lack a digestive system and actively transport host nutrients