T_11 Protozoários urogenitais e intestinais ★ Flashcards

1
Q

Como podemos dividir os Parasitas?

A

Protozoários – Parasitas unicelulares.
Metazoários - Pluricelurares

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2
Q

Qual é o protozoário urogenital que conheces?

A

TRICHOMONAS VAGINALIS

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3
Q

Caracteriza a estrutura e epidemiologia do Trichomonas vaginalis.

A

Physiology and Structure
T. vaginalis is not an intestinal protozoan; rather, it is the cause of urogenital infections.

The organism’s four cilia and short, undulating membrane are responsible for motility.

T. vaginalis exists only as a trophozoite and is found in the urethras and vaginas of women and the urethras and prostate glands of men.

Epidemiology
This parasite has worldwide distribution, with sexual intercourse as the primary mode of transmission.

Occasionally, infections have been transmitted by fomites (toilet articles, clothing), although this transmission is limited by the lability of the trophozoite form.

Infants may be infected by passage through the mother’s infected birth canal.

The prevalence of T. vaginalis in developed countries is reported to be 5% to 20% in women and 2% to 10% in men.

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4
Q

Em que formas podemos encontrar o Trichomonas vaginalis?

A

Só existe sob a forma de trofozoíto (forma vegetativa, forma e tamanho parecidos com um leucócito, mas com flagelos, permitindo o movimento e a sua distinção).

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5
Q

Qual é a manifestação clínica da infeção pro Trichomonas vaginalis?

A

A principal manifestação clínica, como o nome indica, é a vaginite, embora muitas infeções sejam assintomáticas.

Raramente, no homem, pode causar uretrite ou prostatite.

Most infected women are asymptomatic or have a scant, watery vaginal discharge.

Vaginitis may occur with more extensive inflammation and erosion of the epithelial lining that is associated with itching, burning, and painful urination.

Infection has also been associated with premature rupture of membranes, premature birth, other adverse pregnancy outcomes, and posthysterectomy cuff infections.

Men are primarily asymptomatic carriers who serve as a reservoir for infections in women.

However, men occasionally experience urethritis, prostatitis, and other urinary tract problems.

Neonates can acquire the organism via passage through the birth canal and reports have documented T. vaginalis as a cause of neonatal pneumonia and conjunctivitis.

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6
Q

Como é feito o diagnóstico da infeção por Trichomonas vaginalis?

A

O diagnóstico faz-se através da mobilidade da Trichomonas.

A colheita do exsudado vaginal é feita com zaragatoa e observa-se a mobilidade da Trichomonas.

Pode também ser utilizada a cultura, também com observação da mobilidade.

A imunofluorescência raramente é utilizada.

Também pode ser utilizada biologia molecular (PCR).

The microscopic examination of vaginal or urethral discharge for characteristic trophozoites is the diagnostic method of choice.

Stained (Giemsa, Papanicolaou) or unstained smears can be examined.

The diagnostic yield may be improved by culturing the organism (93% sensitivity) or using monoclonal fluorescent antibody staining (86% sensitivity).

A nucleic acid probe assay also is available commercially.

Serologic tests may be useful in epidemiologic surveillance.

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7
Q

Como é feito o tratamento da trichomoníase?

A

The drug of choice is metronidazole. Both male and female sex partners must be treated to avoid reinfection.

Resistance to metronidazole has been reported and may require retreatment with higher doses.

More recently, tinidazole has received FDA approval for treatment of trichomoniasis in adults and may be used as a first-line agent or for cases refractory to metronidazole.

Personal hygiene, avoidance of shared toilet articles and clothing, and safe sexual practices are important preventive actions.

Elimination of carriage in men is critical for the eradication of disease.

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8
Q

Quais são os protozoários intestinais que conheces?

A
  • Entamoeba histolytica
  • Giardia spp. (duodenalis) (lamblia e intestinalis)
  • Dientamoeba fragilis
  • Neobalantidium coli
  • Sarcocystis spp.
  • Cryptosporidium spp.
  • Cyclospora spp.
  • Cytoisospora belli

A negrito os referidos na aula

A itálico referidos como causadores de doença no imunodeprimido e crianças mas não taõ relevantes para nós (últimos 3)

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9
Q

Qual é a principal via de contaminação dos protozoários intestinais?

A

Fecal-oral

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10
Q

Caracteriza a epidemiologia da Entamoeba histolytica

A
  • Mais prevalente em países em desenvolvimento com climas tropicais.
  • Dada a transmissão fecal oral, o mau saneamento básico e reservatórios contaminados são fatores predisponentes à transmissão do parasita.
  • A maioria dos indivíduos infetados são assintomáticos, e funcionam como reservatórios da doença.
  • Dado o perfil do sistema digestivo humano o trofozoíto não sobrevive a ingestão e passagem no estômago, daí a forma infetante ser o quisto.
  • Transmissão sexual, por práticas anais-orais, também encontra a sua prevalência em áreas endémicas deste parasita.
  • O trofozoíto em situações raras, pode causar amebíase cutânea, por inoculção direta, nomeadamente em encontros sexuais.

Cyst and trophozoite forms of E. histolytica are detected in fecal specimens from infected patients.

Trophozoites can also be found in the crypts of the large intestine. In freshly passed stools, actively motile trophozoites can be seen, whereas in formed stools, the cysts are usually the only form recognized.

For the diagnosis of amebiasis, distinguishing between the E. histolytica trophozoites and cysts and those of commensal amebae, such as E. coli, is important.

E. histolytica has a worldwide distribution.

Although it is found in cold areas such as Alaska, Canada, and Eastern Europe, its incidence is highest in tropical and subtropical regions that have poor sanitation and contaminated water.

The average prevalence of infection in these areas is 10% to 15%, with as
many as 50% of the population infected in some areas.

Many of the infected individuals are asymptomatic carriers who represent a reservoir for the spread of E. histolytica to others.

Patients infected with E. histolytica pass noninfectious trophozoites and the infectious cysts in their stools.

The trophozoites cannot survive in the external environment or in transport through the stomach if ingested. Therefore the main source of water and food contamination is the asymptomatic carrier who passes cysts.

This is a particular problem in hospitals for the mentally ill, military and refugee camps, prisons, and crowded day-care centers.

Flies and cockroaches also can serve as mechanical vectors for the transmission of E. histolytica cysts. Sewage containing cysts can contaminate water systems, wells, springs, and agricultural areas in which human waste is used as fertilizer.

Finally, cysts can be transmitted by oral-anal sexual practices, with amebiasis prevalent in homosexual populations.

Direct trophozoite transmission in sexual encounters can produce cutaneous amebiasis.

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11
Q

Quais são as formas estruturais da Entamoeba histolytica? Distingue-as caracterizando o processo patogénico da infeção por este organismo.

A
  • A forma de quisto (infetante) entra no organismo (via oral) e desce até ao estômago. {o trofozoíto até pode entrar, mas vai morrer no ambiente ácido do estômago}
  • O baixo pH vai estimular mudanças no quisto, que, aos chegar ao duodeno, liberta os trofozoítos (forma patogénica - que causa a doença)
  • Estes seres vão causar a necrose do intestino grosso
  • Também causam a lise de células do SImune, como os neutrófilos, por alterações da permeabilidade da membrana dos mesmos levando a, um aumento da [Ca2+] intracelular, e consequente lise, com libertação de mediadores inflamatórias e exponencialização da destruição tecidual local.
  • Causam úlceras em forma de frasco (triangulares, base larga e vértice (luminal) mais apertado)
  • Tudo o que for Amebíase extraintestinal, vai ser sempre causada por trofozoítos.
  • Amebae are found only in environments that have a low oxygen pressure because the protozoa are killed by ambient oxygen concentrations.

Cyst and trophozoite forms of E. histolytica are detected in fecal specimens from infected patients.

Trophozoites can also be found in the crypts of the large intestine. In freshly passed stools, actively motile trophozoites can be seen, whereas in formed stools, the cysts are usually the only form recognized.

For the diagnosis of amebiasis, distinguishing between the E. histolytica trophozoites and cysts and those of commensal amebae, such as E. coli, is important.

After ingestion, the cysts pass through the stomach, in which exposure to gastric acid stimulates the release of the pathogenic trophozoite in the duodenum.

The trophozoites divide and produce extensive local necrosis in the large intestine. The basis for this tissue destruction is incompletely understood, although it is attributed to production of a cytotoxin.

Attachment of E. histolytica trophozoites to host cells via a galactose-inhibitable adherence protein is required for cytolysis and tissue necrosis to occur.

The lysis of colonic epithelial cells, human neutrophils, lymphocytes, and monocytes by trophozoites is associated with a lethal alteration of host cell membrane permeability, resulting in an irreversible increase in intracellular calcium levels.

The release of toxic neutrophil constituents after the lysis of neutrophils may contribute to the tissue destruction.

Flask-shaped ulcerations of the intestinal mucosa are present with inflammation, hemorrhage, and secondary bacterial infection.

Invasion into the deeper mucosa with extension into the peritoneal cavity may occur. This can lead to secondary involvement of other organs, primarily the liver but also the lungs, brain, and heart.

Extraintestinal amebiasis is associated with trophozoites.

Amebae are found only in environments that have a low oxygen pressure because the protozoa are killed by ambient oxygen concentrations.

Lectin binding, zymodeme analysis, genome deoxyribonucleic acid (DNA) analysis, and staining with specific monoclonal antibodies have been used as markers to identify invasive strains of E. histolytica.

It is now recognized that the ameba morphologically identified as E. histolyticais actually four distinct species.

The pathogenic species is E. histolytica, and the nonpathogenic species are E. dispar, E. moshkovskii, and E. bangladeshi.

The zymodeme profiles and biochemical, molecular, and immunologic differences are stable and support the existence of four species. Of note, these four species are morphologically indistinguishable from one another.

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12
Q

Qual é o local extraintestinal primordial da Amebíase?

A

Fígado, causa abcessos hepáticos, e o responsável é sempre o trofozoíto.

Porquê?
Os trofozoítos no sangue são removidos pelo fígado alojando-se aí.

Os abcessos tendencialmente formam-se no lobo direito, causndo dor no hipocôndrio direito, hepatoesplenomegália e elevação do diafragma.

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13
Q

Caracteriza a clínica da Entamoeba histolytica

A

Infeção por Entamoeba histolytica, vamos ter 3 possíveis outcomes:
* Portador (assintomático), a maioria
* Amebíase Intestinal = Disenteria amebiana
* Amebíase Extraintestinal

Para ser portador:
1. A estirpe de E.histolytica tem de ter baixa virulência
2. Inocular pouca quantidade
3. O SImune estar intacto

A Disenteria amebiana causa sintomas relacionados com a destruição local do intestino grosso:
* Dor abdominal
* Cólica
* Colite com diarreia
* Nos casos mais severas, grandes quantidades de fezes sanguinolentas

Amebíase extraintestinal, caracteriza-se por uma disseminação sistémica do trofozoíto e terá como consequências:
* Febre
* Leucocitose
* Rigor

O principal órgão extraintestinal afetado é o fígado

The outcome of infection may result in a carrier state, intestinal amebiasis, or extraintestinal amebiasis.

If the strain of E. histolytica has a low virulence, if the inoculum is low, or if the patient’s immune system is intact, the organisms may reproduce, and cysts may be passed in stool specimens with no clinical symptoms.

Although infections with E. histolytica may be asymptomatic, most asymptomatic individuals are infected with the noninvasive E. dispar or
E. moshkovskii, as characterized by specific isoenzyme profiles (zymodemes), DNA-based assays, their susceptibility to complement-mediated lysis, and their failure to agglutinate in the presence of the lectin concanavalin A.

Detection of carriers of E. histolytica in areas with a low endemicity is
important for epidemiologic purposes.

Patients with intestinal amebiasis develop clinical symptoms related to the localized tissue destruction in the large intestine.
These include abdominal pain, cramping, and colitis with diarrhea.

More severe disease is characterized by numerous bloody stools per day.

Systemic signs of infection (fever, leukocytosis, rigors) are present in patients with extraintestinal amebiasis.

The liver is primarily involved because trophozoites in the blood are removed as they pass through this organ.

Abscess formation is common. The right lobe is most commonly involved. Pain over the liver with hepatomegaly and elevation of the diaphragm is observed

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14
Q

Extra - Dx laboratorial e tratamento da Amebíase

A

The identification of E. histolytica trophozoites and cysts in stools and trophozoites in tissue is diagnostic of amebic infection.

Care must be taken to distinguish between these amebae and commensal amebae, as well as between these amebae and polymorphonuclear leukocytes.

Microscopic examination of stool specimens is inherently insensitive because the protozoa are not usually distributed homogeneously in the specimen, and the parasites are concentrated in the intestinal ulcers and at the margins of the abscess, not in the stool or the necrotic center of the abscess.

For this reason, multiple stool specimens should be collected.

Extraintestinal amebiasis is sometimes diagnosed using scanning procedures for the liver and other organs.
Specific serologic tests, together with microscopic examination of the abscess material, can confirm the diagnosis.

Virtually all patients with hepatic amebiasis and most patients (more than 80%) with intestinal disease have positive serologic findings at the time of clinical presentation.

This may be less useful in endemic areas in which the prevalence of positive serologic results is higher.

Examinations of stool specimens are frequently negative in extraintestinal disease.

In addition to conventional microscopic and serologic tests, researchers have developed several immunologic tests for the detection of fecal antigen, as well as polymerase chain reaction (PCR) and DNA-probe assays for the detection of pathogenic strains of E. histolytica (versus nonpathogenic E. dispar and E. moshkovskii). These newer diagnostic approaches are now commercially available.

Acute, fulminating amebiasis is treated with metronidazole, followed by iodoquinol, diloxanide furoate, or paromomycin.

Asymptomatic carriage can be eradicated with iodoquinol, diloxanide furoate, or paromomycin.

As already noted, human infection results from the ingestion of food or water contaminated with human feces or as a result of specific sexual practices.

The elimination of the cycle of infection requires the introduction of adequate sanitation measures and education about the routes of transmission.

The chlorination and filtration of water supplies may limit the spread of these and other enteric protozoal infections but are not possible in many developing countries.

Physicians should alert travelers to developing countries about the risks associated with the consumption of water (including ice cubes), unpeeled fruits, and raw vegetables. Water should be boiled and fruits and vegetables thoroughly cleaned before consumption.

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15
Q

Caracteriza o Neobalantidium coli

A
  1. Protozoário intestinal
  2. 2 formas: Quisto-infetante , Trofozoíto- patogénica
  3. Trofozoíto é ciliado!
  4. Distribuição universal, sendo o porco o principal reservatório e a transmissão fecal oral
  5. Clínica - Disenteria (semelhante à amebíase, com a diferença de não ter entidade clínicas extraintestinais
  6. Diagnóstico faz-se por obsevação microscópica de quistos e trofozoítos nas fezes, sendo que estes são maiores e ciliados em relação aos outros protozoários intestinais
  7. Tratamento - tetraciclina, com possível alternativa de Metronidazol + iodoquinol

The intestinal protozoan N. coli is the only member of the Ciliophora group that is pathogenic for humans.

Disease produced by N. coli is similar to amebiasis because the organisms elaborate proteolytic and cytotoxic substances that mediate tissue invasion and intestinal ulceration.

Physiology and Structure
The life cycle of N. coli is simple, involving ingestion of infectious cysts, excystation, and invasion of trophozoites into the mucosal lining of the large intestine, cecum, and terminal ileum.

The trophozoite is covered with rows of hairlike cilia that aid in motility.

Morphologically more complex than amebae, N. coli has a funnel-like primitive mouth called a cytostome, which is a large and small nucleus involved in reproduction, food vacuoles, and two contractile vacuoles.

Epidemiology
N. coli is distributed worldwide. Swine and (less commonly) monkeys are the most important reservoirs. Infections are transmitted by the fecal-oral route; outbreaks are associated with contamination of water supplies with pig feces.
Person-to-person spread, including through food handlers, has been implicated in outbreaks. Risk factors associated with human disease include contact with swine and substandard hygienic conditions.

Clinical Syndromes
As with other protozoan parasites, asymptomatic carriage of N. coli can exist.
Symptomatic disease is characterized by:
* abdominal pain and tenderness,
* tenesmus,
* nausea,
* anorexia, and
* watery stools with blood and pus.

Ulceration of the intestinal mucosa, as with amebiasis, can be seen; a secondary complication caused by bacterial invasion into the eroded intestinal mucosa can occur.

Extraintestinal invasion of other organs is extremely rare in neobalantidiasis.

Laboratory Diagnosis
Microscopic examination of feces for trophozoites and cysts is performed. The trophozoite is very large, varying in length from 50 to 200μm and in width from 40 to 70μm. The surface is covered with cilia, and the prominent internal structure is a macronucleus. A micronucleusalso is present.
Two pulsating, contractile vacuoles also are seen in fresh preparations of the trophozoites. The cyst is smaller (40 to 60 μm in diameter), is surrounded by a clear refractile wall, and has a single nucleus in the
cytoplasm. N. coli is a large organism compared with other intestinal protozoa and is readily detected in fresh, wet microscopic preparations.

Treatment, Prevention, and Control
The drug of choice is tetracycline; iodoquinol and metronidazole are alternative antimicrobials. Actions for prevention and control are similar to those for amebiasis. Appropriate personal hygiene, maintenance of sanitary conditions, and the careful monitoring of pig feces are all important preventive measures.

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16
Q

Caracteriza a Giardia duodenalis

A
  1. Protozoário intestinal
  2. 2 formas: Quisto-infetante , Trofozoíto- patogénica
  3. Trofozoíto é FLAGELADO!
  4. Distribuição universal, com grande prevalência em crianças, sendo a distribuição na natureza - riachos e lagos contaminados o principal reservatório e a transmissão fecal oral.
  5. Clínica - Giardíase; diarreia e síndrome de má absorção (mais siintomáticos, ao contrário da amebíase não causa necrose tecidual, apenas liga-se às vilosidades, impedindo a absorção, causando a síndrome de má absorção, com diarreia)
  6. Diagnóstico faz-se por obsevação microscópica de quistos e trofozoítos nas fezes, sendo que dado o padrão de excreção deste organismos “em chuveiro”, uma amostra pode ter muitos organismos, como a seguinte pode não ter nenhum, daí ser necessárias amostras espaçadas de fezes, em dias alternados (segundas, quartas e sextas p.e.). Outra opção, mais rara é a observação de trofozoítos no suco duodenal.
  7. Pesquisa de Ag nas fezes da Giardia é atualmente a forma preferível de diagnóstico.
  8. The drug of choice is metronidazole or nitazoxanide with furazolidone, tinidazole, paromomycin, albendazole, or quinacrine all acceptable alternatives.

Physiology and Structure
Both cyst and trophozoite forms of G. duodenalis are detected in fecal specimens from infected patients.

Pathogenesis
Infection with G. duodenalis is initiated by ingestion of cysts.
The minimum infective dose for humans is estimated to be 10 to 25 cysts.
Gastric acid stimulates excystation with the release of trophozoites in the duodenum and jejunum, in which the organisms multiply by binary fission.
The trophozoites can attach to the intestinal villi by a prominent ventral sucking disk.
Although the tips of the villi may appear flattened, and inflammation of the mucosa with hyperplasia of lymphoid follicles may be observed, frank tissue necrosis does not occur.
In addition, metastatic spread of disease beyond the gastrointestinal tract is very rare.

Epidemiology
The Giardia species has a worldwide distribution, and this organism has a sylvatic or “wilderness” distribution in many streams, lakes, and mountain resorts. This sylvatic distribution is maintained in reservoir animals such as beavers and muskrats. Giardiasis is acquired by the consumption of inadequately treated contaminated water, ingestion of contaminated uncooked vegetables or fruits, or person-to-person spread by the fecal-oral or oral-anal route.
The cyst stage is resistant to chlorine concentrations (1 to 2 parts per million) used in most water-treatment facilities. Thus adequate water treatment should include chemicals plus filtration.
Risk factors associated with Giardia infections include:
* poor sanitary conditions,
* travel to known endemic areas,
* consumption of inadequately treated water (e.g., from contaminated mountain streams),
* day-care centers,
* and oral-anal sexual practices.

Infections may occur in outbreak and endemic forms within day-care centers and other institutional settings and among family members of infected children. Scrupulous attention to handwashing and treatment of all infected individuals are important in controlling the spread of infection in these settings.

Clinical Syndromes
Giardia infection can result in either asymptomatic carriage (observed in approximately 50% of infected individuals) or symptomatic disease, ranging from mild diarrhea to a severe malabsorption syndrome.

The incubation period before symptomatic disease develops ranges from 1 to 4 weeks (average, 10 days). The onset of disease is sudden, with:
* foul-smelling, watery diarrhea,
* abdominal cramps,
* flatulence,
* and steatorrhea.

Blood and pus are rarely present in stool specimens, which is consistent with the absence of tissue destruction.

Spontaneous recovery generally occurs after 10 to 14 days, although a more chronic disease with multiple relapses may develop.
This is particularly a problem for patients with immunoglobulin A deficiency or intestinal diverticula.

Laboratory Diagnosis
With the onset of diarrhea and abdominal discomfort, stool specimens should be examined for cysts and trophozoites. The excretion of Giardia species may occur in “showers”, with many organisms present in the stool on a given day and few or none detected the next day.
For this reason, the physician should never accept the results of a single negative stool specimen as evidence that the patient is free of intestinal parasites.

One stool specimen per day for 3 days should be examined.

If stools remain persistently negative in a patient in whom giardiasis is highly suspected, additional specimens can be collected by duodenal aspiration, Entero-Test or string test, or biopsy of the upper small intestine.

In addition to conventional microscopy, several immunologic tests for the detection of fecal antigen are available commercially.
These tests include countercurrent immunoelectrophoresis, enzyme immunoassay, an immunochromatographic assay, and immunofluorescent staining. Reported sensitivities range from 88% to 98% and specificities from 87% to 100%. Numerous publications have documented the superior sensitivity of the immunoassay methods over that of routine microscopic examination of stool for the detection of Giardia. More recently, several molecular assays have been developed for the detection of G. duodenalis in clinical samples. Multiplex nucleic acid amplification test (NAAT) panels have been approved by the U.S. Food and Drug Administration (FDA) with reported sensitivities and specificities of 98% to 100% and 99%, respectively.

Treatment, Prevention, and Control
It is important to eradicate Giardia species from asymptomatic carriers and diseased patients.
The drug of choice is metronidazole or nitazoxanide with furazolidone, tinidazole, paromomycin, albendazole, or quinacrine all acceptable alternatives.

The prevention and control of giardiasis involves the avoidance of contaminated water and food, especially by the traveler and outdoorsman.
Protection is afforded by boiling drinking water from streams and lakes or in countries with a high incidence of endemic disease. Maintenance of properly functioning filtration systems in municipal water supplies also is
required because cysts are resistant to standard chlorination procedures.
Public health efforts should be made to identify the reservoir of infection to prevent spread of disease. In addition, high-risk sexual behavior should be avoided.