GIT Helminths Flashcards
Necator americanus, Strongyloides stercolaris, Trichuris trichiura, Ascaris lumbroides, Enterobius vermicularis
Anatomy of GIT
Mouth Oesophagus Stomach Small intestines - duodenum, jejenum Large inestines - ascending, transverse, descending Rectum, anus Liver, gall bladder, pancreas
Trematodes
Flukes
- Classify depending on location found
- – Blood flukes, liver flukes, lung flukes, intestinal flukes
Intestinal cestodes
Tapeworms -- Species: Taenia solium T. saginata Diphyllobothrium Hymenolepis Dipylidium caninum Echinococcus Spirometra Taenia multiceps
Nematodes
Ascaris lumbricoides - ascariasis
Trichuris trichuria - whipworm - trichuriasis
Necator americanus + Ancylostoma duodenale - hookworms
Enterobius vermicularis - pinworm - entrobiasis
Strongyloides stercoralis - strongyloidiasis
Ascariasis - life cycle
Begins with eggs maturing in soil
human ingests eggs via food/drink/contaminated hands
Larvae burrow out of GI lumen into venous blood -> right heart -> lungs
Mature and live in lungs until coughed up
Then goes back to GIT
Why do ascaris prefer the lungs to develop?
Maybe higher O2 conc’n in lungs compared to GIT
Definitive host of acaris
humans; they mate there reaching final form
Why do they prefer hatching in soil?
Body temp too high
Risk factors - Ascariasis
Poor sanitation
Warm weather
Early illness ascariasis - symptoms due to
- lung migration
Late illness ascariasis - symptoms due to
- worm burden
Early infection - Eosinophils levels
When the body recognizes larvae moving in the blood, Eosinophilic levels rise in blood and lung tissue.
IgE - mediator of immune response causes what symptoms
–immune response causes transient cough, wheezing, chest pain, hemoptysis
Sputum sample
–Eosinophils in areas they shouldn’t be in
or
–Charcot-Leyden Crystals (sign of high burden of Eosinophils)
Late infection of ascaris is often asymptomatic (T/F)
True
Diagnosis of Ascariasis
Colonoscopy findings, feces observation (OAP)
Symptoms - Ascariasis
nausea
Abd pain
Diarrhoea
Ascariasis fertilized eggs distinguished from unfertilized eggs, how?
They are round rather than elongated and have a thicker cell wall.
Ascaris - fertilile egg
Round/ovoidal with thick shell; mammilated coat
Ascaris - infertile egg
Elongated, triangular, kidney shaped; thin shell; mammilated covering missing
Complications
Bowel blockage - heavy infection
Worms crawling to biliary tree - blocks biliary flow = biliary sepsis
Worms moving to peritoneum carrying fecal content - peritonitis
Treatment- Ascariasis
Albendazole, mebendazole, pyrantel
Surgery for obstruction
Trichuriasis - pathogen and egg shape
Trichuris trichiura
Long void, two clear bulbs on each end, football shaped
Trichuriasis transmission and complication
Soil; fecal oral
Rectal prolapse - occurs when rectum loses attachment to internal body and protrudes from anus
Trichuriasis pathogenesis
- eggs are ingested and travel to the intestines
- the larvae emerge and take up residence
- They become either male or female adults
- Adult worm resembles a bull whip - one side thick and other thin - thin side burrows into gut - fat end remains out in gut
- Eggs passed into stool
Eggs sit in soil for 3-5 wks for maturation to become fertile (T/F)
True
Risk factors and treatment - Trichuriasis
Poor sanitation
Warm weather to nurture eggs
-Mebendazole + Albendazole
Clinical presentation - Trichuriasis -Illness severity correlates with worm burden (T/F)
True
Light infection symptoms - Trichuriasis
-Asymptomatic
Moderate infection symptoms - Trichuriasis
- Nausea
- Abd pain
- Diarrhoea
Heavy infection - symptoms
- anemia, growth stunting, rectal prolapse (due to tenesmus-irritation of worms)
Host may/may not respond to infection (T/F)
True
Host may not respond to infection due to?
Heads of worm buried in mucosa
Antigen presentation occurs where?
Antigen persentation to gut associated lymphatic tissue (GALT)
Eosinophilia usually mild so immunization is unclear in Trichuriasis (T/F)
True
Life cycle - hookworms
Burrow into epidermis until they penetrate dermis
Move to vascular supply -> heart -> lungs
Maturation in lungs (same as ascaris)
When coughed up -> stomach -> jejunum (SI) - reproduction
Eggs must exit body to complete life cycle
Virulence factors - hookworms
Mouthparts to hold on to intestines - keeps from swept away with feces and sucks blood
Transmission - hookworms
Fecal, soil, skin; not oral
Anthroponosis in dogs
Related to dog hookworm
Unholy trinity - lung issues
- Overlaps Trichuris, Ascaris, hookworm
Human hookworm
Necator americanus
Risk factors - Necator
- poor sanitation
- warm weather
- bare skin
- Impoverished persons affected
When does high worm burden occur in hookworm infections?
Penetration to GIT in late infection
Skin migration in hookworms referred to as?
Cutaneous Larva migrans
Larva migrans
Worms moving through the skin for a few days
IgE comes to respond to invaders - histamine released to local tissues, causes itchiness = secondary infection
IgE response in local tissues causes what symptoms in hookworm infection?
Transient cough, wheezing, chest pain, hemoptysis - increase in eosinophils
Clinical manifestations - hookworm infection
CLM rash
Loeffler’s
GI upset
Iron deficiency anemia
Dog hookworm species
Ancylostoma brazilliense
Ancylostoma life cycle
Dog poops depositing eggs
Walking by and larvae burrow in skin
Clinical manifestation - Ancylostoma
Creeping eruption - itchy response, IgE response
Won’t penetrate - will remain under skin until death
Diagnosis of hookwoms
Ova and Parasite test - eggs are smooth, lobes of embryo inside
Treatment - Necator americanus
Albendazole
Ivermectin
Both oral and well absorbed - to tissues
Late infection treatment - hookworms
Antihistamines for itching
Iron repletion for growth restriction
Prevention - hookworms
Shoes
Are vaccines possible - hookworms?
Possible, since there is tissue migration can do humoral response
Strongyloidiasis etiology
Strongyloides stercoralis
Strongyloides stercolaris - life cycle
- Enters via skin - dermis penetration
- Moves to heart -> lungs -> respiratory tree -> oesophagus -> intestine
- Maturation in duodenum/bronchus
- Eggs hatch to larvae -> move to bowel lumen
- Larvae metamorphose in bowel - feces - to filiform larvae (infectious larvae)
New host infection occurs via which route?
Larvae passed in feces
Autoinfection
primary host infection in away that completes life cycle
Autoinfection occurs in strongyloides how?
Stays on skin/rectal area when wiping
Infectious larvae in stool penetrates the rectal wall
How are strongyloides different from other roundworms?
They have a free living cycle in soil and can also complete their cycle in humans
Risk factors - strongyloides
Poor sanitation
Warm weather
Bare skin/ direct contact with feces
- fatal in immunocompromised + newborns
Clinical features - early illness - Strongyloides
Skin and lung migration
Clinical features - late illness - Strongyloides
Immunosuppression = high worm burden
Skin migration
Rash (Larva currens) - pruritic, IgE mediated
Infection shorter than cutaneous migrans
Lung migration pathogenesis
Larvae reaches lungs
IgE migration to lungs - causes immune response which leads to transient cough, wheezing, chest pain, hemoptysis
—Eosinophil in blood/ Charcot-Leyden
Late infection symptoms - Strongyloides
Nausea
Abd pain
Diarrhea
Hyperinfection - causation
- if autoinfection causes strongyloides to persist; can occur for yrs/decades
- Causes decrease in T lymphocytes
-depletion of T lymphocytes will cause lowered immunity which leads to hyperinfection
Hyperinfection risk factors
-immunosuppresion heavy - chemo, organ transplant
Hyperinfection - clinical features
(worms reproduce faster due to low immune response and migrate to ectopic sites carrying fecal bacteria from gut)
- causes infection from bacteria in blood = sepsis
- death
Chronic auto-infection symptoms
Larva currens on exam - butt cheeks
- blood test +ve high eosinophils
Diagnosis - Strongyloides early infection
- biopsy of bowel wall = worms
- OAP - false negatives, worms few in num hard to find
- Serology - ELISA - good if patient has good immune system (cause worms go to blood)
Hyperinfection - Diagnosis
GNR in blood, low eosinophils
Larvae in sputum - lung migration
Serology - too late to help - long waiting time
Treatment - early infection
Ivermectin preferred over albendazole
Treat patient before immunosuppression
Treatment - hyperinfection
Add ivermectin + albendazole
Reduce immunesuppression
Broad spectrum antibiotics for sepsis
Prevention - Strongyloides
Wear shoes
Good indicators of strongyloides hyperinfection - symptoms
Pneumonia + sepsis
Enterobius vermicularis
Pinworm
Transmission - Enterobius vermicularis
- Food contaminated with eggs
- Eggs on skin/fingers
- Eggs in bedding/underwear
Anthroponosis
Pathogen only lives in humans, includes enterobius
Eggs visualization
small, flat on one side, dome on the other
Life cycle - pinworm
- when consumed stomach juices allow them to hatch
- cecum - where they have reached maturiy
- Female fertilized and moves to rectum = crawl out through anus along perianal skin and leave goo behind which is microscopic - sticky eggs are irritating so it becomes itchy
Pinworms must exit body to complete life cycle
Yes they move to perianal space
Children are affected by pinworm more often (T/F)
True
Symptoms
Often asymptomatic
Itchy butt/pruritis ani in heavy infection
Young kids symptoms
Irritability, wet beds, insomnia
Perianal rash in kids can occur due to
Perianal rash, - can be due to eggs themsevles/ due to secondary infection /superinfection - on the superficial area
Vaginal discharge occurs why?
Migration of worms to vagina
Immune response - pinworms
None - since they dont invade tissue - hides from GALT
-Eosinophil - no response - no vaccine
Standard sign of pinworms
Pruritis ani
Diagnosis
Cellophane tape prep in morning
Fingernail scrapings
Adult female can be seen outside perianal area at night
Treatment - enterobius
Albendazole - penetrates tissue
Pyrantel pamoate - stays in gut
Both highly effective
Prevention - enterobius
Keep hands clean
