T15_Tremátodos ★ Flashcards
Que tremátodos conheces?
- Fasciolopsis buski
- Fasciola hepatica
- Clonorchis (Opisthorchis) sinensis
- Paragonimus westermani
- Schistosoma spp.
Características gerais dos tremátodos
- _____ dorso-ventralmente;
- Simetria _____, não _____;
- Quanto ao sexo, são _____;
- Tubo digestivo _____, _____ _____;
- Possuem _____ para _____ (uma na região oral, outra ventral) – estruturas utilizadas na _____ de espécie;
- Ovos geralmente _____, excepto _____ (corpo _____, sexos separados, ovos não operculados);
- Transmissão _____, excepto _____, a infeção pode ocorrer por _____ larvar _____ a partir do _____;
- ++ países _____ em _____;
- Ciclo de vida _____ (indireto), implicando quase sempre um _____ _____ como hospedeiro intermediário;
- Diagnóstico: deteção de ovos _____ _____, excepto _____ _____, que deposita ovos na _____ e _____ _____ ovos na expetoração ou fezes.
- Achatados dorso-ventralmente;
- Simetria bilateral, não segmentados;
- Quanto ao sexo, são Hermafroditas;
- Tubo digestivo incompleto, sem ânus;
- Possuem ventosas para fixação (uma na região oral, outra ventral) – estruturas utilizadas na identificação de espécie;
- Ovos geralmente operculados, excepto Schistosoma (corpo cilíndrico, sexos separados,ovos não operculados);
- Transmissão fecal-oral, excepto Schistosoma, a infeção pode ocorrer por penetração larvar transcutânea a partir do solo;
- ++ países tropicais em desenvolvimento;
- Ciclo de vida complexo (indireto), implicando quase sempre um molusco aquático como hospedeiro intermediário;
- Diagnóstico: deteção de ovos nas fezes, excepto Schistosoma haemotobium que deposita ovos na urina e Paragonimus westermani ovos na expetoração ou fezes.
Como podemos distinguir os tremátodos quanto aos tecidulares e os intra-vasculares?
Tecidulares:
* Fasciolopsis buski
* Fasciola hepatica
* Clonorchis (Opisthorchis) sinensis
* Paragonimus westermani
Intra-vasculares:
* Schistosoma mansoni
* Schistosoma japonicum
* Schistosoma haematobium
Caracteriza o Clonorchis sinensis
PHYSIOLOGY AND STRUCTURE
Clonorchis sinensis, also referred to as Opisthorchis sinensis, in the older literature, is commonly called the Chinese liver fluke.
It has a life cycle, which involves two intermediate hosts.
This trematode differs from other fluke cycles in that the eggs are eaten by the snail, and then **reproduction begins in the soft tissues of the snail.
C. sinensis also requires a second intermediate host, such as a freshwater fish, in which the cercariae encyst and develop into infective metacercariae.
When uncooked freshwater fish harboring metacercariae are eaten, flukes develop first in the duodenum and then migrate to the bile ducts, in which they become adults.
The adult fluke undergoes self-fertilization and begins producing eggs.
C. sinensis may survive in the biliary tract for as long as 50 years, producing approximately 2000 eggs per day. These eggs pass with feces and are once again eaten by snails, reinitiating the cycle.
EPIDEMIOLOGY
C. sinensis is found in China, Japan, Korea, and Vietnam, in which it is estimated to infect approximately 15 million people.
It is one of the most frequent infections seen among Asian refugees, and it can be traced to the consumption of raw, pickled, smoked, or dried freshwater fish that harbor the viable metacercariae.
Dogs, cats, and fish-eating mammals can also serve as reservoir hosts.
CLINICAL SYNDROMES
Infection in humans is usually mild and asymptomatic.
Severe infections with many flukes in the bile ducts produces:
* fever,
* diarrhea,
* epigastric pain,
* hepatomegaly,
* anorexia, and
* occasionally jaundice.
Biliary obstruction may occur, and chronic infection can result in adenocarcinoma of the bile ducts.
Invasion of the gallbladder may produce:
* cholecystitis,
* cholelithiasis, and impaired liver function,
* as well as liver abscesses.
LABORATORY DIAGNOSIS
The diagnosis is made by recovering the distinctive eggs from stool.
The eggs measure 27 to 35 μm × 12 to 19 μm and are characterized by a distinct operculum with prominent shoulders and a tiny knob at the posterior (abopercular) pole.
In mild infections, repeated examinations of stool or duodenal aspirates may be necessary.
In acute symptomatic infection, there are usually eosinophilia and an elevation of serum alkaline phosphatase levels.
Radiographic imaging procedures may detect abnormalities of the biliary tract.
A coproantigen ELISA has been developed and has displayed high specificity and sensitivity, whereas ELISA assays for circulating antibodies show high sensitivity but low specificity.
Nucleic acid amplification test (NAAT) platforms have been developed that detect and discriminate between fish-borne zoonoses caused by opisthorchids and members of the related family Heterophyidae, based on mitochondrial and ribosomal sequences.
TREATMENT, PREVENTION, AND CONTROL
The drug of choice is praziquantel.
Prevention of infection is accomplished by not eating uncooked fish and by implementing proper sanitation policies, including the disposal of human, dog, and cat feces in adequately protected sites so that they cannot contaminate water supplies with the intermediate snail and fish hosts.
Como é o ciclo de vida do Clonorchis sinensis?
It has a life cycle, which involves two intermediate hosts.
This trematode differs from other fluke cycles in that the eggs are eaten by the snail, and then **reproduction begins in the soft tissues of the snail.
C. sinensis also requires a second intermediate host, such as a freshwater fish, in which the cercariae encyst and develop into infective metacercariae.
When uncooked freshwater fish harboring metacercariae are eaten, flukes develop first in the duodenum and then migrate to the bile ducts, in which they become adults.
The adult fluke undergoes self-fertilization and begins producing eggs.
C. sinensis may survive in the biliary tract for as long as 50 years, producing approximately 2000 eggs per day. These eggs pass with feces and are once again eaten by snails, reinitiating the cycle.
Associas a Chinese liver fluke a que organismo?
Clonorchis sinensis
O Clonorchis sinensis tem tropismo para os ___ ____, podendo, em infeções crónicas causar um _____ das ____ ____.
A invasão deste orgão pode produzir também:
1. _____
2. _____
3. _____
4. _____
O Clonorchis sinensis tem tropismo para os ductos biliares, podendo, em infeções crónicas causar um adenocarcinoma das vias biliares
A invasão deste orgão pode produzir também:
1. Colecistite
2. Colelitíase
3. Disfunção hepática
4. Abcessos hepáticos
CLINICAL SYNDROMES
Infection in humans is usually mild and asymptomatic.
Severe infections with many flukes in the bile ducts produces:
* fever,
* diarrhea,
* epigastric pain,
* hepatomegaly,
* anorexia, and
* occasionally jaundice.
Biliary obstruction may occur, and chronic infection can result in adenocarcinoma of the bile ducts.
Invasion of the gallbladder may produce:
* cholecystitis,
* cholelithiasis, and impaired liver function,
* as well as liver abscesses.
O Fasciolopsis buski, também conhecido por “____ ____ Fluke”, é mais prevalente nas regiões ____ e ___ da Ásia, dado ser o região endémica do seu hospedeiro intermediário o ____ do género ____ e ____.
O Fasciola hepatica, também conhecido por “____ ____ Fluke”, é mais prevalente ____, o seu hospedeiro intermediário é o ____ do género ____.
O vetor biológico de ambos são __ ____ ____.
Quantos aos hospedeiros definitivos o ____ ____ tem os ovinos, ruminantes e humanos e o ____ ____ tem o porco, cão, coelho, humano.
O Fasciolopsis buski, também conhecido por “Giant Intestinal Fluke”, é mais prevalente nas regiões Oriental e Sul da Ásia, dado ser o região endémica do seu hospedeiro intermediário o molusco do género Segmentina e Hippeutis.
O Fasciola hepatica, também conhecido por “Sheep Liver Fluke”, é mais prevalente mundialmente, o seu hospedeiro intermediário é o molusco do género Lymnae.
O vetor biológico de ambos são as plantas aquáticas.
Quantos aos hospedeiros definitivos o Fasciola hepatica tem os ovinos, ruminantes e humanos e o Fasciolopsis buski tem o porco, cão, coelho e humano.
Caracteriza o ciclo de vida do Fasciolopsis buski
This large intestinal fluke has a typical life cycle.
Humans ingest the encysted larval stage (metacercaria) when they peel the husks from aquatic vegetation (e.g., water chestnuts) with their teeth.
The metacercariae are scraped from the husk, swallowed, and develop into immature flukes in the duodenum.
The fluke attaches to the mucosa of the small intestine with two muscular suckers, develops into an adult form, and undergoes self-fertilization.
Egg production is initiated 3 months after the initial infection with the metacercariae.
The operculated eggs pass in feces to water, in which the operculum at the top of the eggshell pops open, liberating a free-swimming larval stage (miracidium).
Glands at the pointed anterior end of the miracidium produce lytic substances that allow the penetration of the soft tissues of snails.
In the snail tissue, the miracidium develops through a series of stages by asexual germ cell propagation.
The final stage (cercaria) in the snail is a free-swimming form that, after release from the snail, encysts on the aquatic vegetation, becoming the metacercariae, or infective stage.
- O Fasciolopsis burki inicia o seu ciclo de vida sob a forma de ____, nas ____ ____.
- O ser humano, ao ingeri-las consume também a forma infetante, que, no ____ vão desenvolver-se numa fascíola (fluke) ____.
- Esta fascíola, migra para o ____ ____ onde vai ancorar à ____ utilizando as suas 2 ____.
- Evolui para uma fascíola ____, com capacidade de ___-____.
- Os ___ _____ são libertados após __ mes(es) da inoculação da forma infetante.
- Estes são libertados através das ____, libertando uma ____ ____ (____)
- Glândulas na membrana deste estadio larvar vão produzir substâncias _____, permitindo a penetração no _____
- No ____ os ______ vão se desenvolver numa série de mltiplicações ____
- O estadio final, a _____ vai ser libertada sob a forma de _____, ancorando nas ____ _____ e tornando-se na _____. Reiniciado o ciclo.
- O Fasciolopsis burki inicia o seu ciclo de vida sob a forma de metacercária, nas plantas aquáticas.
- O ser humano, ao ingeri-las consume também a forma infetante, que, no duodeno vão desenvolver-se numa fascíola (fluke) imatura.
- Esta fascíola, migra para o intestino delgado onde vai ancorar à mucosa utilizando as suas 2 ventosas.
- Evolui para uma fascíola adulta, com capacidade de auto-fertilização.
- Os ovos operculados são libertados após 3 mes(es) da inoculação da forma infetante.
- Estes são libertados através das fezes, libertando uma larva nadadora (miracídios)
- Glândulas na membrana deste estadio larvar vão produzir substâncias líticas, permitindo a penetração no molusco
- No molusco os miracídios vão se desenvolver numa série de mltiplicações assexuadas
- O estadio final, a cercária vai ser libertada sob a forma de quisto, ancorando nas plantas aquáticas e tornando-se na metacercária - forma infetante. Reiniciado o ciclo.
O vetor do Fasciola hepatica é o _____
Segundo a aula*
Caramujo
Como é o ciclo de vida do Fasciola hepatica
Commonly called the sheep liver fluke, F. hepatica is a parasite of herbivores (particularly sheep and cattle) and humans.
Its life cycle (Fig. 75.4) is similar to that of F. buski, with human infection resulting from the ingestion of watercress that harbors the encysted metacercariae.
The larval flukes then migrate through the duodenal wall and across the peritoneal cavity, penetrate the liver capsule, pass through the liver parenchyma, and enter the bile ducts to become adult worms.
Approximately 3 to 4 months after the initial infection, the adult flukes start producing operculated eggs that are identical to those of F. buski, as seen in stool examination.
Qual é a grande diferença do ciclo de vida Fasciolopsis burki e o Fasciola hepatica? E como é que isso vai influenciar a clínica associada a cada um deles?
O F. buski tem o seu ciclo de vida (intra-humano) todo no trato gastrointestinal, enquanto que o F. hepatica, vai passar do duodeno, para o fígado e vias biliares. Levando a sintomatologias diferentes.
CLINICAL SYNDROMES - F. buski
The symptomatology of F. buski infection relates directly to the worm burden in the small intestine.
Attachment of the flukes in the small intestine can produce inflammation, ulceration, and hemorrhage.
Severe infections produce abdominal discomfort similar to that of a duodenal ulcer, as well as diarrhea. Stools may be profuse, a malabsorption syndrome similar to giardiasis is common, and intestinal obstruction can occur. Marked eosinophilia is also present.
Although death can occur, it is rare.
CLINICAL SYNDROMES - F. hepatica
Migration of the larval worm through the liver produces irritation of this tissue, tenderness, and hepatomegaly.
Pain in the right upper quadrant, chills, fever, and marked eosinophilia are commonly observed.
As the worms take up residence in the bile ducts, their mechanical irritation and toxic secretions produce hepatitis, hyperplasia of the epithelium, and biliary obstruction.
Some worms penetrate eroded areas in the ducts and invade the liver to produce necrotic foci referred to as liver rot.
In severe infections, secondary bacterial infection can occur, and portal cirrhosis is common.
Como fazemos a distinção laboratoria do Fasciolopsis buski do Fasciola hepática?
Não fazemos. Microscopicamente os ovos são iguais.
Caso seja mesmo preciso distinguir ambas as formas clínicas fazemos uma recolha de bílis, e analisamos se há F. hepatica, se sim, confirma o dx desta espécie, se não é provavelmente F. buski
Características gerais do Paragonimus westermani
- Distribuição geográfica:
* ____ ____;
* ___;
* ____ ____;
* ____ ____ - Forma infetante: ____ em ____ __ ___ ___ ou outro ____
- Localização no homem: ____ ___/___ (penetração através do ____), podendo originar sintomatologia semelhante a ____ ____; também pode ocorrer calcificação ___ (____ ____)
- Diagnóstico: ____ __ ___ (elíptico, ___-___, revestimento espesso, ____) na ____ ou ____ (se deglutidos); técnicas de _____ (doença pulmonar/SNC); e ainda ____
- Distribuição geográfica:
* Extremo Oriente,
* China,
* Sudeste Asiático,
* América Latina - Forma infetante: metacercária em caranguejo de água doce ou outro crustáceo
- Localização no homem: cavidade pleural/pulmão (penetração através do diafragma), podendo originar sintomatologia semelhante a tuberculose pulmonar; também pode ocorrer calcificação cerebral (paragonimíase cerebral)
- Diagnóstico: deteção de ovos (elíptico, amarelo-acastanhado, revestimento espesso, operculado) na expectoração ou fezes (se deglutidos); técnicas de imagem (doença pulmonar/SNC); e ainda serologia
Como é o ciclo de vida do Paragonimus westermani
P. westermani, commonly called the lung fluke, is one of several species of Paragonimus that infect humans and many other animals.
Fig. 75.7 shows a familiar fluke life cycle from egg to snail to infective metacercaria.
The infective stage occurs in a second intermediate host: the muscles and gills of freshwater crabs and crayfish.
In humans who ingest infected meat, the larval worm hatches in the stomach and follows an extensive migration through the intestinal wall to the abdominal cavity, then through the diaphragm, and finally to the pleural cavity.
Adult worms reside in the lungs and produce eggs that are liberated from ruptured bronchioles and appear in sputum or, when swallowed, in feces.
Infection is initiated by ciliated, free-swimming, freshwater cercariae that penetrate intact skin, enter the circulation, and develop in the intrahepatic portal circulation (S. mansoni and S. japonicum) or in the vesical, prostatirectal, and uterine plexuses and veins (S. haematobium).
The female has a long, slender, cylindric body, whereas the shorter male, which appears cylindric, is actually flat. The cylindric appearance derives from folding the sides of the body to produce a groove, the gynecophoral canal, in which the female resides for fertilization.
Both sexes have oral and ventral suckers and an incomplete digestive system, which is typical of a fluke.
As the worms develop in the portal circulation, they elaborate a remarkable defense against host resistance.
They coat themselves with substances that the host recognizes as itself; consequently, there is little host response directed against their presence in blood vessels.
This protective mechanism accounts for chronic infections that may last 20 to 30 years or longer.
After developing in the portal vein, the male and female adult worms pair up and migrate to their final locations, where fertilization and egg production begin.
S. mansoni and S. japonicum are found in mesenteric veins and produce intestinal schistosomiasis; S. haematobium occurs in veins around the urinary bladder and causes vesicular schistosomiasis.
On reaching the submucosal venules of their respective locations, the worms initiate oviposition, which may continue at the rate of 300 to 3000 eggs daily for 4 to 35 years.
Although the host inflammatory response to the adult worms is minimal, the eggs elicit an intense inflammatory reaction, with mononuclear and polymorphonuclear cellular infiltrates and the formation of microabscesses.
In addition, the larvae inside the eggs produce enzymes that aid in tissue destruction and allow the eggs to pass through the mucosa and into the lumen of the bowel and bladder, where they are passed to the external environment in the feces and urine, respectively.
The eggs hatch quickly on reaching fresh water to release motile miracidia.
The miracidia then invade the appropriate snail host, where they develop into thousands of infectious cercariae.
The free-swimming cercariae are released into the water, where they are immediately infectious for humans and other mammals.
The infection is similar in all three species of human schistosomes in that disease results primarily from the host’s immune response to the eggs.
The very earliest signs and symptoms are caused by the penetration of the cercariae through the skin.
Immediate and delayed hypersensitivity to parasite antigens result in an intensely pruritic papular skin rash.
The onset of oviposition results in a symptom complex known as Katayama syndrome, which is marked by:
* fever,
* chills,
* cough,
* urticaria,
* arthralgias,
* lymphadenopathy,
* splenomegaly,
* and abdominal pain.
This syndrome is typically seen 1 to 2 months after primary exposure and may persist for 3 months or more. It is thought to result from the massive release of parasite antigens, with subsequent immune complex formation.
Associated laboratory abnormalities include leukocytosis, eosinophilia, and polyclonal gammopathy.
The more chronic and significant phase of schistosomiasis is caused by the presence of eggs in various tissues and the resulting formation of granulomas and fibrosis.
The retained eggs induce extensive inflammation and scarring, the clinical significance of which is directly related to the location and number of eggs.
Because of differences in some aspects of disease and epidemiology, these worms are discussed as separate species.
