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Gastrointestinal System > Gastro-Intestinal Parasitic Infections > Flashcards

Gastro-Intestinal Parasitic Infections Flashcards

1
Q

Protozoa which causes infectious diarrhoea

A
  1. Entamoeba histolytica (Amoeba)
  2. Giardia lamblia (Flagellate)
  3. Cryptosporidium parvum (Coccidia)
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2
Q

AMOEBIASIS

A

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

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3
Q

Intestinal Amoebiasis

A

Asymptomatic_Carrier state = majorityof infectionsSymptomatic  Dysentery Non-dysenteric colitis Amoeboma Amoebic appendicitisComplications_  Perforation Peritonitis Haemorrhage Intussusception Strictures (due to fibrosis)

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4
Q

Extra-Intestinal Amoedbiasis

A

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
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5
Q

Amoebiasis:

Laboratory Diagnosis

A

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
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6
Q

Amoebiasis:

Treatment

A

DOC: Metronidazole. Also for eradication

  • Diloxanide in combination with metronidazole
  • Paramomycin- non invasive (E. histolytica)
  • Dihydroemetine- severe extra intestinal
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7
Q

Giardia lambliaEpidemiology

A

:  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

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8
Q

G. lamblia

Clinical Features

A

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

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9
Q

G. lamblia:

Laboratory diagnosis

A

Stool microscopy for cysts and trophozoites

Chronic infection- excretion is intermittent

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10
Q

G. lamblia:

Treatment and Control/Prevention

A

Quinacrine hydrochloride, metronidazole, tinidazole, furazolidone, and paromomycin
 Hygiene – sewerage systems
 Water should be filtered or boiled, chlorine not always sufficient

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11
Q

Cryptosporidium parvum

Epidemiology

A

Seen commonly in patients with HIV/AIDS

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12
Q

Cryptosporidium parvum

Life Cycle

A

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

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13
Q

Cryptosporidium parvum:

Treatment

A

_In the immunocompetent patient, the disease is self-limited and antiparasitic therapy is not warrantedRehydration may be required in small childrenIn the immunocompromised host, the severity and chronicity of the diarrheawarrant therapeutic intervention. There is no uniformly effectiveanticryptosporidial agent available. Paromomycin, macrolides, nitozoxanideThe only uniformly successful approach has been the reversal of underlyingimmunologic abnormalities

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14
Q

List the Helminths/Worms

A

Ascaris lumbricoides

Enterobius vermicularis

Trichuris trichiura

Hookworms: Ancylostoma duodenale/Necator americanus

Strongyloides stercolaris

Taenia saginata and Taenia solium

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15
Q

PHYLUM: NEMATODA

“THE ROUNDWORMS”

A

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

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16
Q

A. lumbricoides

Epidemiology

A

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
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17
Q

A. lumbricoides

Life Cycle

A

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.

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18
Q

A. lumbricoides

Clinical Presentation

A 
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

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19
Q

A. lumbricoides

Laboratory Diagnosis

A

Find ova/worms in stool

Fertile ovum: 60 x 45 μm

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20
Q

A. lumbricoides

Treatment and Prevention

A

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
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21
Q

Enterobius vermicularis:

Epidemiology

A

Pinworm/Threadworm”  Distribution: worldwide; group infections; common in children.  Highest prevalence in temperate & cold
climates (fewer changes of clothing) & crowded conditions

22
Q

Enterobius vermicularis:

Life Cycle

A

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.

23
Q

Enterobius vermicularis:

Types of Infection

A

Autoinfection

Retroinfection

24
Q

Autoinfection

A

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.

25
Q

Retroinfection

A

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

26
Q

Enterobius vermicularis

DIAGNOSIS

A

Find eggs in stool (rarely) /perianal swabs
or scrapings/swabs under fingernails  May find adult worms around anus at
night  Cellophane tape method

27
Q

E. vermicularis

Treatment

A

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

28
Q

E. vermicularis

Control

A

 Treat whole family/group
 Chemotherapy + education, short
fingernails.  Repeat courses of treatment

29
Q

Trichuris trichura

Epidemiology

A

Whipworm

Worldwide distribution

Males: 30-45mm, coiled posterior end, attenuated anterior end

30
Q

Trichuris trichura

Life Cycle

A

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

31
Q

Trichuris trichura

Clinical presentation

A

Heavy infections: spread
throughout colon to rectum

Severe dysentery with blood & mucus in stool & rectal prolapse

32
Q

Trichuris trichura

Dx and Tx

A

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

33
Q

Hookworms

A

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

34
Q

Hookworms

Lifecycle

A 
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
35
Q

Hookworm

Clinical presentation

A

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

36
Q

Hookworm

Diagnosis

A

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.

37
Q

Hookworm

Treatment

A

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

38
Q

Hookworm

Control

A

Man = only reservoir of infection

Better sanitation & barrier
protection against larval penetration
wear shoes

39
Q

Strongyloides stercoralis

Epidemoilogy

A

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)

40
Q

Life cycle types for S.

A

Parasitic Form

Free-living form

Autinfections

41
Q

Parasitic form

A

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.

42
Q

Free-living form

A

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.

43
Q

Autoinfections

A

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

44
Q

Clinical Presentation

A

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

45
Q

Strongyloides stercoralis

Diagnosis

A

Finding adults or rhabditiform larvae in stool or duodenal aspirate Larvae have a short buccal cavity (vs Hookworm)
TREATMENT CONTROL M

46
Q

Treatment

A 
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
47
Q

Control

A 
Man is most important host
Reservoir hosts: dogs & primates
Strongyloides thrives in damp, warm
soil, especially in overcrowded
conditions
48
Q

Cestodes

A

Long, ribbon-like helminth
 T. saginata: beef tapeworm
 T. solium: pork tapeworm
Eggs: round, with a thick, radially striated shel

49
Q

Taenia saginata

A

Transmission: inadequately cooked meat Symptoms: Majority asymptomatic
Epigastric discomfort, nausea, weight loss,
diarrhea, irritability
Diagnosis: proglottids in stool Rx: praziquantel/niclosamide

50
Q

Taenia solium

A

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

Gastrointestinal System (14 decks)

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