Gastro-Intestinal Parasitic Infections Flashcards
Protozoa which causes infectious diarrhoea
- Entamoeba histolytica (Amoeba)
- Giardia lamblia (Flagellate)
- Cryptosporidium parvum (Coccidia)
AMOEBIASIS
Entamoeba:
Several protozoan species in the genus Entamoeba colonize humans, but not all of them are associated with
disease
Entamoeba histolytica is well recognized as a pathogenic amoeba,
associated with intestinal and extraintestinal infections
The other species are important because they may be confused with E. histolytica in diagnostic investigations (E. dispar, E. moshkovshii)
AMOEBIASIS
Entamoeba
E. histolytica is transmitted via the faecal-oral route through
contaminated water or food
Only 10% of patients infected with E. histolytica develop severe
dysentery and complications (e.g. amoebic liver abscess); 90%
asymptomatic
Intestinal Amoebiasis
Asymptomatic_Carrier state = majorityof infectionsSymptomatic Dysentery Non-dysenteric colitis Amoeboma Amoebic appendicitisComplications_ Perforation Peritonitis Haemorrhage Intussusception Strictures (due to fibrosis)
Extra-Intestinal Amoedbiasis
Hepatic invasion:
- Necrotic areas
- Liver abscess
Complications of liver abscess:
- Rupture
- Extension to lungs, skin etc.
- Haematogenous spread to other organs
Cutaneous: -Direct migration from bowel lesion -Commonest site is perineum Other organs: lungs, brain etc. without liver involvement intestinal
Amoebiasis:
Laboratory Diagnosis
Microscopic identification:
- Cysts and trophozoites in the stool
- Edge of abscess – look for organism
Immunodiagnosis:
-Antibody detection is most useful in extra-intestinal disease (e.g. amoebic liver abscess)when organisms are not found on stool examination
- E. histolytica - specific antibodies may persist for years after successful treatment, sothe presence of antibodies does not necessarily indicate acute or current infection. Inaddition, these tests provide limited information in patients from endemic areas
- Antigen detection may be useful as an adjunct to microscopic diagnosis in detectingparasites and can distinguish between pathogenic and nonpathogenic infections
Amoebiasis:
Treatment
DOC: Metronidazole. Also for eradication
- Diloxanide in combination with metronidazole
- Paramomycin- non invasive (E. histolytica)
- Dihydroemetine- severe extra intestinal
Giardia lambliaEpidemiology
: Also referred to as G. intestinalis/duodenalis
World wide; cysts are the infective form. They survive in the environment under adverse environmental conditions
Transmission is via ingestion of contaminated
water or food, or direct person-to-person spread via the faecal-oral route
Children below 10 years of age, especially those
in overcrowded surroundings Clinical cases in adults are sporadic and outbreaks sometimes occur in travelers
G. lamblia
Clinical Features
Vary from asymptomatic (>2/3) Sudden onset of explosive diarrhea, bloating, abdominal pains & weight loss
The stool is foul-smelling, greasy in appearance, and floats. It is devoid of blood or mucus.
May be symptomatic for months and develop malabsorption
Untreated - subside after a few weeks
G. lamblia:
Laboratory diagnosis
Stool microscopy for cysts and trophozoites
Chronic infection- excretion is intermittent
G. lamblia:
Treatment and Control/Prevention
Quinacrine hydrochloride, metronidazole, tinidazole, furazolidone, and paromomycin
Hygiene – sewerage systems
Water should be filtered or boiled, chlorine not always sufficient
Cryptosporidium parvum
Epidemiology
Seen commonly in patients with HIV/AIDS
Cryptosporidium parvum
Life Cycle
C. parvum is found in many mammalian species
Has a direct fecal-oral life cycle & colonizes the
GIT Mature oocysts are infective when excreted in the
faeces and, if swallowed, immediately excyst to
release sporozoites which penetrate the surface
of epithelial cells and start to feed as trophozoites. Infectious dose is low and cysts are resistant to
chlorine – tap water is not safe in
immunecompromised Stool specimen stained with modified Ziehl Neelsen (ZN) stain showing cryptosporidia Cryptosporidium parvum
Cryptosporidium parvum:
Treatment
_In the immunocompetent patient, the disease is self-limited and antiparasitic therapy is not warrantedRehydration may be required in small childrenIn the immunocompromised host, the severity and chronicity of the diarrheawarrant therapeutic intervention. There is no uniformly effectiveanticryptosporidial agent available. Paromomycin, macrolides, nitozoxanideThe only uniformly successful approach has been the reversal of underlyingimmunologic abnormalities
List the Helminths/Worms
Ascaris lumbricoides
Enterobius vermicularis
Trichuris trichiura
Hookworms: Ancylostoma duodenale/Necator americanus
Strongyloides stercolaris
Taenia saginata and Taenia solium
PHYLUM: NEMATODA
“THE ROUNDWORMS”
Intestinal nematodes = Geohelminths
Soil-transmitted & part of development occurs
outside of host’s body
Frequency of infection is a general indication of
level of personal hygiene & sanitation in a
community
Morphology: Adult size range: 1-2 mm (Trichinella spiralis) to
35 cm (Ascaris lumbricoides) Separate sexes; males smaller Ova needs to develop in the external environment
into larval form
Ova infective/diagnostic form
Larval stage often causes pathology of disease
A. lumbricoides
Epidemiology
TRANSMISSION: By ingestion of ova in soil – via contaminated
hands/food/water By nightsoil fertilizer
Ascaris pneumonia: caused by migrating larvae damaging lungs Produces Löeffler’s syndrome: fever, cough, asthma, eosinophilia, IgE TRANSMISSION: By ingestion of ova in soil – via contaminated hands/food/water By nightsoil fertilizer “The common roundworm”: about a quarter of world’s population infected; cosmopolitan distribution
A. lumbricoides
Life Cycle
Adult inhabits small intestine; size: female 20-35cm & male 15- 25cm (ventrally curved tail) B: Produces ±200 000 eggs/day; C: Eggs passed out as immature ova. D: Ova embryonate in moist soil after ±3 weeks. E: Ova swallowed by host. F: Rhabditiform larva: hatches in small intestine; penetrates mucous membrane; G: Enters bloodstream & travels via right heart to lungs; burrows
through alveolar wall into
respiratory tract; H: Travels down oesophagus into small intestine.
A. lumbricoides
Clinical Presentation
Ascaris pneumonia: caused by migrating larvae damaging lungs Produces Löeffler’s syndrome: fever, cough, asthma, eosinophilia, IgE
Adult worms in small intestine: usually cause little pathology; but if heavy
infection: intestinal colic, obstruction & malnutrition Worms causing intestinal obstruction
Migration of larvae & wandering adults: larvae can wander into: brain/eye/liver
A. lumbricoides
Laboratory Diagnosis
Find ova/worms in stool
Fertile ovum: 60 x 45 μm
A. lumbricoides
Treatment and Prevention
Only effective for adult worms
DOC’s: Albendazole or Mebendazole or Pyrantel pamoate
Control:
Avoid soil pollution Control based on: Good personal hygiene Proper disposal of faeces Health education Chemotherapy
Enterobius vermicularis:
Epidemiology
Pinworm/Threadworm” Distribution: worldwide; group infections; common in children. Highest prevalence in temperate & cold
climates (fewer changes of clothing) & crowded conditions
Enterobius vermicularis:
Life Cycle
Adults in glandular crypts of caecum &
appendix
Mature female: life duration 37-93 days. Female migrates to anus when ovary full &
lays eggs on perianal skin.
Enterobius vermicularis:
Types of Infection
Autoinfection
Retroinfection
Autoinfection
Eggs lodge under fingernails or contaminate
food/ water/ clothing/ dust
Eggs ingested & larvae hatch in stomach;
grow rapidly to ±150µm.
Larvae travel to caecum & appendix.
Retroinfection
Eggs hatch on anal mucosa & larvae migrate
up bowel. Majority of infections: few/no symptoms Pruritus ani: gravid female migrates out of
anus; scratching results in secondary
infection Vulvitis & ectopic lesions in other organs Usually no eosinophilia/anaemia
Enterobius vermicularis
DIAGNOSIS
Find eggs in stool (rarely) /perianal swabs
or scrapings/swabs under fingernails May find adult worms around anus at
night Cellophane tape method
E. vermicularis
Treatment
Must treat whole family to avoid reinfection: from contaminated environment or asymptomatic family
member; often repeat courses of
treatment necessary. DOC: Albendazole. Also effective: Mebendazole / Pyrantel
pamoate
E. vermicularis
Control
Treat whole family/group
Chemotherapy + education, short
fingernails. Repeat courses of treatment
Trichuris trichura
Epidemiology
Whipworm
Worldwide distribution
Males: 30-45mm, coiled posterior end, attenuated anterior end
Trichuris trichura
Life Cycle
A: Adult inhabits caecum & appendix; anterior part buried in mucosa
Females produce 3000-8000 eggs/day
B, C, D: ova in stool; embryonation +21 days E & F: stool used as fertilizer and vegetables contaminated with ova
G: embryonated ova ingested; larvae hatch in
small intestine; attach to intestinal villi.
A: larvae in caecum develop into adults
Trichuris trichura
Clinical presentation
Heavy infections: spread
throughout colon to rectum
Severe dysentery with blood & mucus in stool & rectal prolapse
Trichuris trichura
Dx and Tx
Find ova in stool; Ova: 30-50 μm; barrel-shaped (tea tray), smooth shell & bile-stained;
frequently associated with Ascaris & Hookworm infections
Treatment & Control: same as Ascaris
Hookworms
2 species in man: Necator americanus & Ancylostoma duodenale
Distribution: Occur in all tropical & subtropical countries
Adult hookworms attach to small intestinal mucosa with the biting action of cutting mouth parts
Feed on villous tissue & suck blood. Leads to severe anaemia in 0.2% of infected individuals
Transmission via 2 routes:
- Skin: filariform larvae in soil contaminated by human faeces
- Orally: ingestion of contaminated food
Buccal capsule of Necator with 2 crescent-shaped
cutting plates
Buccal capsule of Ancylostoma containing two pairs of teeth
Hookworms
Lifecycle
A: adults are ivory white; attach to small intestinal mucosa with buccal capsules; live for 1-9 years. B: ova deposited into intestinal lumen & contain 2/4/8 blastomeres; Necator: Female produces ±9000 eggs/day Ancylostoma: ±30 000 eggs/day C: ova passed out in faeces D: rhabditiform larvae hatch in damp shaded soil; develop into filariform larvae: infective form for man. E: larvae penetrate host’s skin F: enter bloodstream G: carried to right heart, then lungs H: larvae penetrate alveoli; move up trachea I: down oesophagus to small intestine
Hookworm
Clinical presentation
Main symptom in chronic infections:
progressive iron deficiency anaemia
(hypochromic, microcytic); with
epigastric pain, but no wasting
Ground itch: irritating vesicular rash
at site of penetration of filariform
larvae
There may be an eosinophilia of 7-
14%
Migration of larvae in lung: cough,
asthma, fever, high eosinophilia, bronchitis
Hookworm
Diagnosis
Find ova in stool: 60-40 μm; thin,
transparent, colourless shell.
Stools may contain occult blood.
Can estimate worm load by egg count:2500 eggs/g stool = significant & associated
with symptoms
NB: With persistent anaemia: growth &
development of children is stunted.
Hookworm
Treatment
Eliminate parasites AND treat anaemia
Light asymptomatic infections in adults in endemic areas: often left untreated
Should always treat children if possible
DOC’s: Albendazole (effective vs both species) or Mebendazole or Pyrantel pamoate
Treatment of anaemia: administer
iron by mouth
Hookworm
Control
Man = only reservoir of infection
Better sanitation & barrier
protection against larval penetration
wear shoes
Strongyloides stercoralis
Epidemoilogy
Distribution: worldwide; endemic in tropics & subtropics; warm moist climates About 1% of world’s population infected
Infections may persist for over 30 years
2 forms: parasitic & free-living
Female adult parasitic worm: ±2,5mm
Male exists, but disappears from bowel soon after fertilization of ova
Females can produce eggs parthenogenetically (non-sexual
reproduction)
Life cycle types for S.
Parasitic Form
Free-living form
Autinfections
Parasitic form
Parasitic form: A: Female adults in crypts of small intestine;eggs
hatch within epithelium & liberate larvae into
lumen. B: rhabditiform larvae in faeces = diagnostic
stage.
C: develop into infective filariform larvae. D: release hydrolytic enzymes & penetrate host’s
skin & follow same route as hookworm larvae. A: reach small intestine & mature into adults.
Free-living form
E: larvae develop into free-living male &
female adult worms.
F: copulate in soil & produce eggs; can
undergo several reproductive cycles.
G: eggs hatch in soil; rhabditiform become
filariform larvae.
H: infective form for man; acquired by skin
contact with contaminated soil.
Autoinfections
Filariform larvae are not passed out in stool reinvade bowel/perianal skin/ intestine or lodge in bronchial epithelium &
produce further progeny
Leads to build up of worm population
If host’s immune defences are lowered, then
rapid increase in worm burden &
hyperinfection results
Clinical Presentation
Larvae penetrate skin: haemorrhage & pruritus (itching) Majority of infections in endemic areas are asymptomatic Transient pneumonitis: as larvae pass through lungs Heavy infections: watery, mucus diarrhoea & malabsorption
Hyperinfections: Peritonitis, meningitis, encephalitis & pneumonitis
Eosinophilia disappears & indicates a poor prognosis
Massive strongyloidiasis can be lethal Portion of intestinal mucosa: showing extensive damage &
multiple haemorrhages
Larva currens: rapid linear eruption; occurs around anus & on trunk Caused by larvae migrating under skin
Strongyloides stercoralis
Diagnosis
Finding adults or rhabditiform larvae in stool or duodenal aspirate Larvae have a short buccal cavity (vs Hookworm)
TREATMENT CONTROL M
Treatment
Always treat Strongyloides, even if asymptomatic Should be looked for & treated in the immunosuppressed DOC: Albendazole, Thiabendazole & Mebendazole also effective Ivermectin proved more effective in recent studies
Control
Man is most important host Reservoir hosts: dogs & primates Strongyloides thrives in damp, warm soil, especially in overcrowded conditions
Cestodes
Long, ribbon-like helminth
T. saginata: beef tapeworm
T. solium: pork tapeworm
Eggs: round, with a thick, radially striated shel
Taenia saginata
Transmission: inadequately cooked meat Symptoms: Majority asymptomatic
Epigastric discomfort, nausea, weight loss,
diarrhea, irritability
Diagnosis: proglottids in stool Rx: praziquantel/niclosamide
Taenia solium
Transmission: Inadequately cooked meat
Symptoms: Similar to T. saginata
Cysticerci: brain, muscle, heart, liver, subcutaneous tissue with ingestion of eggs Cysticercosis in CNS: mild to severe (neurological abnormalities)
Diagnosis: proglottids in stool
Cysticercosis: suspicion (travel to endemic areas, neurological symptoms, subcutaneous nodules),
radiology, biopsy, specific Abs in blood Treatment: Aggressive approach for neurocysticercosis→ mortality approaches 50%. Seizure control a first
priority! DOC: Praziquantel/albendazole
Corticosteroids: ↓ inflammatory response
