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46 Cards in this Set

  • Front
  • Back
The helminths can live in the humans for years, decades.
General symptoms?
metabolic product of the helminth
- protein  allergisation  eozinophilia, urticaria, asthma
- food requirement of the helminths 
food withdrawal from the host  losing weight, anaemia
- mechanical effect
damage to the skin
- specific organ symptoms during the migration of the larva
intestinal obstruction
lymphatic vessels, blood vessels obstruction
- carcinogenesis (schistosoma)
Diagnosis of helmiths
- serology
- macroscopic examination
- microscopic examination 
- concentration methods:
- larva: larva migration test
- positive thermo-hydrotaxis of the larvas
- egg:
- flotation: specific weight of the media > egg
specific weight (supernatant)
- sedimentation: specific weight of the media < egg
specific weight (in the sediment)
- biopsy: - cysticercus in the muscle
Prevention
- washing hands
- washing vegetables, fruits
- avoid eating not sufficiently roasted, cooked meat … etc.
Therapy
- drugs usually inhibit one of the catalytic enzyme system of the helmiths
- they usually have wide spectrum
- eg: Mebendazole, Praziquntel, Thiabendazole
Nemathelminthes
- round worms
- separate - sexed
complete digestive system
Nematodes
- thread worm
- resistant, non cellular cuticle
- spindle or whip shape
Platyhelminthes
– flatworms
- hermaphroditic or separated sexed
uncomplete or lack of digestive system
Trematodes
- fluke
- leaf-shaped
- cellular epithelium
- pair of suckers
Cestodes
- tape worm
strobila (segments)  inside: complete male and female reproduction system
- no mouth  absorption
Entrobius vermicularis
- spin worm
"ab ano ad os"
World-wide distribution with the highest prevalence in temperate and cold climates and in crowded conditions
larva leaves the egg in the duodenum  migration into the colon  fertilization  gravid female goes down to the anus and the embryonated ovum is deposited on perianal skin (a few thousand/day)  itching  scratching  autoinfection
eggs are rarely found in faeces, they are more easily found in the perianal region
Scotch-tape smear can be used to pick up the eggs and must be made in the morning before defecation and bathing
Life cycle of
Enterobius vermicularis
da
da
Trichuris trichiura
- whip form
world-wide distribution, it is the third most common worm of man
geohelminth  egg is laid into the ground, in wet, worm soil the maturation of the egg takes place  release of the larva  infection with soil contaminated food (larva)
Treatment:
mebendazol
Ascaris lumbricoides
has a world-wide distribution and is most prevalent in tropical areas
25% of the world population harbours the parasite
geohelminth
infect. with soil contam. egg  larva leaves the egg in the duodenum  through the small intestine wall  blood stream  lung  alveolus  bronchus  trachea  pharynx  oesophagus small intestine sexually mature worm gravid female release the egg  with faeces in soil
immature or adult A. lumbricoides are sometimes passed in stools
adult males are 15-20 cm, femals are 20-35 cm
Diagnosis:
- detection of eggs in faeces
Treatment:
- mebendazol, levamizol
Ancylostoma duodenale, Necator americanus
hook worm
A. duodenale is prevalent in Southern Europe, North Africa, Northern Asia;
N. americanus is the predominant species in the Western and equatorial Africa
Many areas are endemic for both species
larva inf. through skin  blood stream  lung, pharynx, small intestine (sexually mature worm)  sucking blood (0.3-0.9 ml/day)
A. duodenale cause a daily blood loss of 0,15 ml compared to 0,03 ml for N.americanus.
adults live in the small intestine attached to intestinal mucosa where they feed on villous tissue sucking blood
Hypocromic, microcytic anemia is the main clinical manifestation of the disease
epigastric pain and eosinophilia are often observed
Hypoproteinemia, malnutrition occur in heavily infected people
Treatment:
- mebendazole or albendazole
Ancylostoma duodenale, Necator americanus life cycle
das
das
Strongyloides stercoralis
geohelminth
Endemic in tropics, subtropics and warm moist climates Widespread in Eastern Europe and in the Mediterranean region
About 1% of the world population infected
The infection is acquired by skin contact with contaminated soil
filariform larva through the skin  blood-lung  small intestine  sexually mature worm  egg:
 rhabditiform larva  leaving with faeces  soil  maturation  filariform larva filariform larva lung (autoinfection)
Eggs are excreted with faeces in the external environment, transform into either filariform larvae (L3, the infective stage) (the direct development cycle) or into free-living adult males and females in the soil (the indirect development cycle)
Strongyloides stercoralis
In the indirect development cycle several reproductive cycle of the free-living forms can occur - they produce eggs (40-70 µm) which can develop into rhabditiform larvae and into infectious third stage larvae
Filariform larvae (L3) penetrate the skin by releasing hydrolitic enzymes
enter dermal vessels and migrate through the blood or lymphatic channels to the hearth and lungs
In the lungs the larvae break out of the capillaries into alveolar spaces, migrate up the respiratory tract into the pharynx
they are then swallowed, reaching the small intestine
During this process, larvae moult to the fourth stage (L4) and only females develop into adults
Strongyloides stercoralis
infections may persist for over 30 years
In the intestinal lumen rhabditiform larvae may directly transform in filariform larvae
here they may penetrate the colonic mucosa or the perianal skin causing autoinfection.
Autoinfection explains the long duration of the infection and the possible multiplication within the host (hyperinfection)
Disease:
Symptoms depend on: the host immune system and the moulting regulatory mechanisms of the parasite
chronic infection and hyperinfection (with or without dissemination)
Light infections may be asymptomatic usually with eosinophilia
Strongyloides stercoralis
patients may complain about mild gastrointestinal symptoms (light intermittent abdominal pain and diarrhea), or pruritus of anal skin or larva currens
heavy infections are characterized by more severe intestinal symptoms (nausea, vomiting, diarrhea), frequently with malabsorption, gastrointestinal bledding, jejunal perforation, paralytic ileus, granulomatous hepatitis, eosinophilic ascites often with marked eosinophilia.
Diagnosis:
infection is diagnosed by the presence in faeces of first-stage
rhabditoid larvae
Antibody detection is usefull in patients with hypereosinophilia and negative stool examination
Immunodiagnosis by indirect immunofluorescence
Treatment:
- thiabendazole and ivermectine
life cycle of the Toxocara (cati, canis)
Toxocara (cati, canis)
– geohelminth
- Human toxocariasis is caused by nematodes of the genus Toxocara - final host: cat, dog  gravid female vacate the eggs in the gut  with faeces into the soil  maturation in the soil  larva in human  granulomatosus infection (liver, brain)
especially T.canis (common roundworm of dogs).
- the infection is acquired from ingestion of embryonated eggs released in the soil - after ingestion, L2 larvae begin a somatic migration to the lungs, liver, eye, CNS.
Disease:
the clinical presentation depends on the number of larvae ingested and the degree of allergic response
two major syndromes have been identified:

Visceral Larva Migrans (VLM) characterized by fever, malaise, leucocytosis with hypereosinophilia, hepatomegaly, cough, myalgias, high titers of isohaemagglutinins, other manifestation: myocarditis, encephalitis and pneumonia
- Ocular Larva Migrans (OLM) characterised by retinal granulomas and uveitis  blindness Diagnosis:
- western-blot analysis
- detection of
Trichinella spiralis
Trichinella spiralis
spiralis - pork meat
eating cyst beating meat (encysted larva)  release of the larva  maturation  copulation  gravid female under the mucous membrane of the the small intestine  larva born  lymphatics, blood vessels  encystation in muscle  infective for years
the cyst is formed outside by a fibrous capsule and inside by an eosinophil infiltration around the tightly coiled larvae
Disease: trichinellosis
massive infection may cause acute enteritis
myalgia, fever, periorbital oedema
the migration and the later muscle encystation of larvae may be asymptomatic or cause serious generalized disease with possible miocardial and brain pathology
Diagnosis:
is based on serology and
on finding of larvae in the striated muscle biopsy
Treatment:
- tiabendazol
Wuchereria bancrofti and Brugia malayi
Vector:
Wuchereria bancrofti: mosquitoes of the genus Culex, Anopheles and Aedes
Brugia malayi: mosquitoes of the genus Mansonia, Anopheles and Aedes
bite  filariform larva  lymph. node for 1 year (inflamm. in the lymph. node  elephanthiasis)  microfilaria  circulation in the blood during the night  back to the mosquito
lymphatic filariases have a wide geographic distribution W. bancrofti and B. malayi infect ~128 milion people - and about 43 milion have symptoms
B. malayi infection is endemic in Asia (China, Corea, India, Indonesia, Malaysia, Philippines, Sri Lanka)
W. bancrofti has a larger distribution : China, India, Indonesia, Japan, Malaysia, Philippines, South-East Asia, Sri Lanka, Tropical Africa, Central and South America, Pacific Islands
Microfilariae are usually nocturnally periodic but sub-periodic strains of B. malayi and W. bancrofti are observed
human round worms life cycle
Lymphatic filariasis
adults live in the lymphatic vessels and lymphnodes where they cause dilatation
inflammatory infiltrates and blockage of the lymphatic circulation
adenolymphangitis, orchitis, epididimitis associated with fever are the commonest manifestation of the acute stage of the infection
eosinophilia is frequent at this stage
lymphoedema particularly of the legs and scrotum
hydrocoeles and chyluria are the result of the progression of the disease
genital manifestations are frequent in W.bancrofti infections while they are rare during B.malayi infections
Treatment: - diethylcarbamazine
- ivermectine, albendazole used alone or in combination
Loa-Loa
the infection is endemic in West and Central Africa, especially in Angola, Cameroun, Congo, Eq. Guinea, Gabon, Nigeria, RCA, Zaire
vector: Chrysops fly
after injection larvae develop into adults in 6 months and may live for 17 years in the organism
bite  migration in the subcutis  gravid female  microfilaria  blood circul. during the day  the most typical: conjunctiva
Microfilariae are present in blood without periodicity, count is mandatory before therapy
Diagnosis:
microfilariae can be demonstrated in blood with fluorochromes: Acridine orange stain
direct diagnosis by observation of microfilariae in blood
indirect diagnostic tests: IF
cross-reaction with other nematode infections limits the
usefulness of serology in these patients
immunodiagnosis by indirect immunofluorescence, antigen: frozen sections of Dirofilaria immitis
Treatment:
- diethilcarbamazin
Oncocerca volvulus
onchocerciasis occurs especially in Tropical Africa - high endemicity in B. Faso and Ghana
vector: Simulium genus - black fly
migration in the subcutis  eye  blindness
- O. volvulus: the larvae enter the host tissues - and develop to adults in subcutaneous nodules in about 1 year
Adults live for 8-10 years in nodules
females contain eggs and larvae in different stages of development
after being released by the adult female microfilariae escape to the subcutaneous tissues and the eye and can be recovered with blood-free skin snips
Disease:
"river blindness" due to the presence of microfilariae in the ocular structures
other clinical manifestations: pruritic dermatitis with lichenification and thickening of skin
Diagnosis:
by fresh examination of blood-free skin snips
biopsies must be kept in saline for 1 to 3 hours to allow migration of microfilariae.
Dracunculus medinensis
drinking water (copepods with the larva)  larva migration  subcutis - cutis  with the help of toxin  vesicle formation  in the water bursts  worm in the water  uterus bursts  larva in the water  copepodes eat them
life cycle of human tape worms
Taenia saginata , Taenia solium
Taenia saginata - cattle
Taenia solium – pig
Taeniasis: world-wide distribution. T. saginata is prevalent in regions where cattle are raised: Africa, Middle-East, Central and South America, Europa and Asia
T. solium is prevalent in Central and South America (expecially in Mexico), Africa, South-Est Asia, Eastern Europe, Micronesia
Taeniasis occurs when raw or undercooked unfrozen beef (T.saginata) or pork (T.solium) are eaten.
- in the muscle "cystisercus"  human infected by eating the meat  small intestine larva maturation  mature worm  egg filled segments break off 
pass out with faeces  pork or cattle  embryo  blood stream  muscle  cysticercus
T. saginata
T. solium scolex
T. saginata may measure 9 m, whereas T. solium may reach 6 m
T. saginata scolex is square, 1-2 mm in diameter with 4 suckers
T. solium scolex has a rostellum with hooklets
symptoms include abdominal discomfort or pain, abdominal distension, nausea, diarrhoea, malaise, anxiety, anorexia
Echinococcus granulosus
dog), E. multilocularis (fox) - final host
distribution with a higher prevalence in South-America (Argentina, Uruguay), Europe (mediterranean bassin), Northern Africa, Middle East, South-Central and East Asia
intermed. host: cattle, pig
- accid. intermed. host: human
Disease:
hydatidosis is caused by the larval stage of E. granulosus
after ingestion of eggs the onchospheres penetrate the intestinal mucosa and reach host organs (mainly liver and lung) where they encyst within a week reaching 1 cm in diameter in about 5 months
the cysts (2 to 30 cm) are constituted by an external acellular cuticule and an inner cellular "germinal" layer (10-25 µ) that produces the brood capsules containing 6-12 protoscolices or single protoscolices
the larvae (scolices) develop from the germinal layer
the mature protoscolices have 4 suckers and a rostellum with hooklets and can be observed in the hydatid fluid
Echinococcus granulosus
Echinococcus granulosus
spontaneous or surgical rupture of the cyst can originate a secondary hydatidosis - - the liver is the most common site of development of cysts (50-75%)
pulmonary infection is observed in about 20-30% of patients
any other organ can be affected: nervous system, heart, bones, spleen eyes, muscles are the most common sites
Diagnosis:
the presence of isolated hooklets is diagnostic for hydatidosis
lesions can be detected by CT scan or echography
ELISA, Western Blot
Treatment:
is based on surgical and/or medical therapy (albendazole)
Echinococcus multilocularis
multilocularis (E. multilocularis) The “small fox tapeworm”
- prevalent in North America (Alaska and northern Canada), in Europe (France, Switzerland, Austria and Germany), in Asia (from the White Sea to the Behring strait in the north and from Turkey, through Afghanistan, Iran, India, China, Mongolia to north Japan in the south)
causes alveolar echinococcosis (AE) in intermediate hosts
parasites red and arctic foxes (dogs and cats are the definitive hosts)
definitive hosts are always carnivores
in the definitive hosts the adult tapeworm, consisting of 2 to 6 proglottids, lives attached to the luminal surface of the small intestine
it is assumed that the intermediate host acquires the infections through the ingestion of contaminated fruits and vegetables
Echinococcus multilocularis
When the intermediate hosts (predominantly rodents or other small mammals, or, accidentally, humans) ingest eggs, the onchosphere hatches from the egg in the duodenum
the activated oncosphere penetrates the small intestine, enters blood vessels and reaches primarily the liver via the portal vein
in the liver the oncosphere proliferates into the metacestode surrounded by an inner germinative membrane and an outer laminated layer
the lifecycle is completed when an intermediate host carrier of viable protoscolices within the cysts, is devoured by a definite host
Echinococcus multilocularis
Disease: - the liver is the organ primarily affected
metastases are mainly observed in cases of advanced disease and may affect almost any organ
the disease either spreads via direct contact or via blood vessels
secondary AE mostly affects the brain, the lungs, soft tissue, the spine and other bony structures
the disease is primarily characterized by an expansive and infiltrative growth in the liver
clinical features may be absent for many years and mostly become apparent in advanced disease
they may include hepatomegaly, jaundice, abdominal pain, weight loss, fever and manifestations of secondarily affected organs.
Diagnosis:
computed tomography (CT) and magnetic-resonance-imaging (MRI) are used
for serology ELISA
Treatment:
The only curative treatment for AE to date is total surgical resection combined with chemotherapy
benzimidazoles
Hymenolepis nana
Cosmopolitan, is endemic in both temperate and tropical regions but most prevalent in conditions of poor sanitation
- swallowed eggs - maturing in intestine – developing the helmith
human flukes life cycle
Paragonimus westermani
infection occurs in Asia (especially in China, Corea, India, Japan, Laos, Philippines, Sri Lanka, Taiwan, Thailand, Vietnam), Central-West Africa, South America (Ecuador, Peru, Venezuela)
- eating infected raw crab – excystation in small intestine – migration to lung - maturation of helmith in lung
coughing the eggs – swallowing – faeces containing eggs
Disease:
pneumonia
caoughing, bloody sputum
Treatment:
praziquantel
Fasciola hepatica
F. hepatica infection is found in rural areas of temperate and tropical regions, related to cattle herding
High prevalence is described in Europe and Latin America
The adults live in biliary ducts for up to 10 years
larva  excystation in the duodenum  larva through the gut wall  hepar  liver  maturate worm  egg in the bile duct  pass out with faeces  fresh water (miracidium)  snail  plants  human
after excistation in the small intestine, metacercariae penetrate the intestinal wall , cross the liver parenchima to the bile ducts
eggs can be found in faeces 3-4 months after penetration.
Diagnosis:
the diagnosis is confirmed by the presence of eggs in faeces
serology is useful when the clinical picture is compatible and eggs are not found
Schistosoma - Bilharsiasis
Schistosoma - Bilharsiasis
S. mansoni - intermediate host are snails (Biomphalaria)
S. japonicum - intermediate host are snails (Onchomelania)
S. haematobium - intermediate host of S. haematobium are snails (Bulinus)
cercarae are the infective forms
fresh water cercaria  larva penetration through the skin  blood stream  liver: maturation  ven. plexus  eggs through the lumen wall  pass out  snail  cercaria
S. mansoni:.
geographical distribution: is endemic in 43 countries in Africa and Brazil, Suriname, Venezuela and in the Caribbean
adult schistosomes live in pairs in the portal system and in the mesenteric venules
each female lays about 300 eggs per day
viable eggs contain the motile larva, the miracidium
after breaking the shell the ciliated miracidium moves in the water and reaches the mollusca
Schistosoma Disease:
hepatosplenic schistosomiasis occurs in S. mansoni and S. japonicum infections
it results by eggs embolization in hepatic venules
formation of granulomas and portal fibrosis
hepatosplenomegaly and hepatic insufficiency
Diagnosis:
- serological tests
S. japonicum:
geographic distribution: Southeast Asia and western Pacific countries (including China, the Philipines and Indonesia)
adult schistosomes live in pairs in the portal system and in mesenteric venules
each female may lay up to 2.000-3.000 eggs per day S. haematobium:
after encountering the skin, the cercariae penetrate and lose the tail transforming into schistosomulae
is reported from 54 countries in Africa
adult schistosomes live in pairs in the pelvic veins (especially in the venous plexus surrounding the bladder)
each female lays about 150 eggs per day
S. japonicum:
Disease:
eggs are the main agent of pathology inducing granuloma formation
bladder wall enlargement, haematuria
hyperplasia of the mucosa due to the presence of granuloma fibrosis and calcification follow with polips formation in bladder and urether stenosis
hydronephrosis and possibly cancer are late complications of the infection
damage of the seminal vescicles seems to correlate with the degree of the obstructive uropathy
Diagnosis:
identification of eggs in urinary sediment
viable eggs contain a motile miracidium
eggs can occasionally be found in faeces
ELISA, IF, RIA
Treatment:- praziquantel