T12 e 13_ Protozoários do sangue e tecidos ★ Flashcards
Quais são os agentes etiológicos da malária?
- Plasmodium falciparum
- Plasmodium vivax
- Plasmodium malariae
- Plasmodium ovale
- Plasmodium knowlesi
Os plasmódios são _____
Coccídeos
Caracteriza o ciclo de vida do Plasmodium
Tem 2 ciclos de vida:
* No mosquito
* No humano
- O mosquito (Anopheles) introduz no ser humano, por via hematogénea, os esporozoítos, através da sua saliva
- Os esporozoítos são transportados até ao fígado (hepatócitos), onde ocorre reprodução assexuada - ciclo exoeritrocítico (fora do eritrócito), com duração de 8-25 dias, sendo que pode ficar numa fase refratéria, durante meses a nos (no P. ovale e P. vivax - hipnozoítos, que irão causar doença muito depois da inoculação)
- Dá-se a rutura dos hepatócitos, com libertação de merozoítos para a corrente sanguínea, onde se ligam a recetores específicos nos eritrócitos - início do ciclo eritrocítico
- Há 2 vias a partir daqui. A assexuada (+ comum) e a sexuada.
- Na via assexuada, há uma série de estadios de evolução do merozoíto (“ring, trophozoite, schizont”), culminando na lise do eritrócito e libertação de ainda mais merozoítos (até 24), que repetiram esta fase do ciclo.
- Na via sexuada, também dentro do eritrócito, alguns merozoítos, evoluem para gametócitos, macho e fêmea.
- Estes gametócitos são ingeridos pelo vetor (mosquito) e dar-se-à dentro dele o ciclo sexuado do Plasmodium
Plasmodia are coccidian or sporozoan (Apicomplexa) parasites of blood cells, and as seen with other coccidia, they require two hosts: the mosquito for the sexual reproductive stages and humans and other animals for the asexual reproductive stages. Infection with Plasmodium spp. (i.e., malaria) accounts for 216 million episodes with approximately
500,000 deaths annually, 90% of which are in Africa.
The five species of plasmodia that infect humans are P. falciparum, P. knowlesi, P. vivax, P. ovale, and P. malariae. These species share a common life cycle.
Human infection is initiated by the bite of an Anopheles mosquito, which introduces infectious plasmodia sporozoites via its saliva into the circulatory system.
The sporozoites are carried to the parenchymal cells of the liver, in which asexual reproduction (schizogony) occurs.
This phase of growth is termed the exoerythrocytic cycle and lasts 8 to 25 days, depending on the plasmodial species.
Some species (e.g., P. vivax, P. ovale) can establish a dormant hepatic phase in which the sporozoites (called hypnozoites or sleeping forms) do not divide. The presence of these viable plasmodia can lead to the relapse of infections months to years after the initial clinical disease (relapsing malaria).
The hepatocytes eventually rupture, liberating the plasmodia (termed merozoites at this stage), which in turn attach to specific receptors on the surface of erythrocytes and enter the cells, initiating the erythrocytic cycle.
Asexual replication progresses through a series of stages (ring, trophozoite, schizont) that culminates in the rupture of the erythrocyte, releasing up to 24 merozoites, which initiates another cycle of replication by infecting other erythrocytes.
Some merozoites also develop within erythrocytes into male and female gametocytes.
If a mosquito ingests mature male and female gametocytes during a blood meal, the sexual reproductive cycle of malaria can be initiated, with the eventual production of sporozoites infectious for humans.
This sexual reproductive stage within the mosquito is necessary for the maintenance of malaria within a population.
Most malaria seen in the United States is acquired by visitors or residents of countries with endemic disease (imported malaria).
However, the appropriate vector, the Anopheles mosquito, is found in several sections of the United States, and domestic transmission of disease has been observed (introduced malaria).
In addition to transmission by mosquitos, malaria can be acquired by:
* blood transfusions from an infected donor (transfusion malaria).
This type of transmission can also occur among narcotic addicts who share needles and syringes (“mainline” malaria).
Congenital acquisition, although rare, also is a possible mode of transmission (congenital malaria).
A malária é transmitida via _____
mosquito Anopheles fêmea que tem distribuição mundial, mas maisor prevalência nos climas tropicais do Hemisfério Sul. Pica sobretudo ao final da tarde/noite.
- transfusões sanguíneas (malária tranfusional)
- Uso de seringas, na população narcótica (“mainline” malaria)
- Muito raro, mas possível, também pode haver malária congénita
O Plasmodium falciparum causa a febre _______ . Justifica. Que outras coisas pode causar?
Terçã Maligna
* “Terçã” porque a febre aparece de 48h em 48h (aparece no 1 dia e volta a reaparecer ao 3 dia). “Maligna” porque este é dos quadros mais graves associados à malária, e o que mata com mais frequência.
* Este é o agente com o período de incubação mais curto.
* É o responsável pelos quadros mais graves da doença, porque consegue realizar multiparasitismo (mais do que um parasita pode invadir um eritrócito) e atingir um grande número de eritrócitos afetados.
* Com isto, podem-se originar microembolias, devido à presença dos parasitas e restos de células, que podem atingir vários órgãos, nomeadamente:
O cérebro, causando a malária cerebral que pode levar ao coma ou à morte.
Ou o rim, podendo causar insuficiência renal, hemoglobinúria que pode dar síndrome nefrótico, ou até morte
The incubation period of P. falciparum is the shortest of all the plasmodia, ranging from 7 to 10 days, and does not extend for months to years.
After the early influenza-like symptoms, P. falciparum rapidly produces daily (quotidian) chills and fever and severe nausea, vomiting, and diarrhea.
The periodicity of the attacks then becomes tertian (36 to 48 hours), and fulminating disease develops.
The term malignant tertian malaria is appropriate for this infection. Because the symptoms of this type of malaria are similar to those of intestinal infections, the nausea, vomiting, and diarrhea have led to the observation that malaria is “the malignant mimic.”
Although any malaria infection may be fatal, *P. falciparum is the most likely to result in death if left untreated.
The increased numbers of erythrocytes infected and destroyed result in toxic cellular debris, adherence of RBCs to vascular endothelium and to adjacent RBCs, and formation of capillary plugging by masses of RBCs, platelets, leukocytes, and malarial pigment.
Involvement of the brain (cerebral malaria) is most often seen in P. falciparum infection.
Capillary plugging from an accumulation of malarial pigment and masses of cells can result in coma and death.
Kidney damage is also associated with P. falciparum malaria, resulting in an illness called blackwater fever. (BWF is a condition characterized by massive hemolysis after treatment for acute malaria, with clinical symptoms that include hemoglobinuria, anemia, jaundice, and fever (1–3). The name of the syndrome relates to the presence of dark urine noted in affected patients.)
Intravascular hemolysis with rapid destruction of RBCs produces a marked hemoglobinuria and can result in acute renal failure, tubular necrosis, nephrotic syndrome, and death.
Liver involvement is characterized by abdominal pain, vomiting of bile, severe diarrhea, and rapid dehydration.
O P. vivax e o P. ovale, destacam-se dos restantes agentes do género pela formação de ______. Apresentando clinicamente uma febre ______
- Hipnozoítos hepáticos
-
Terçã benigna
corresponde a uma quadro mais ligeiro (apesar de raramente poderem causar quadros graves) que o do P.falciparum.
A particularidade destes agentes é que apresentam formas latentes, os hipnozoítos hepáticos, que persistem durante muito tempo no fígado (ficam latentes), pelo que a pessoa poderá ter recidivas meses ou anos após a infeção.
São entidades clinicamente semelhantes sendo que, caso não sejam tratadas, as infeções por P. ovale duram cerca de 1 ano, enquanto que por P.vivaz ficam latentes durante muitos anos.
O P. malariae causa a febre ______. Tendo como particularidade a sua patogenicidade, caracteriza-a.
Febre quartã, uma febre que reaparece de 72 em 72 horas.
O P. malariae também pode causar infeções que se prolongam no tempo,porque começam de forma muito ligeira (pode ser mesmo assintomática), pelo
que o quadro vai-se arrastando sem a pessoa perceber, originando uma infeção crónica (que normalmente não é um quadro grave).
Este agente atinge os eritrócitos adultos, mas não os deforma.
Qual é o Plasmodium que não deforma eritrócitos adultos?
P. malariae
Como efetuarias o Dx da malária?
- Colhe-se um tubo de hemograma (ou punção do dedo)
- Faz-se o espregaço sanguíneo (FUNDAMENTAL para o Dx de espécie e quantificação do número de eritrócitos parasitados)
- Podemos também efetuar a pesquisa de Ag, permite um diagnóstico mais rápido e pode ser efetuado por qualquer profissional, de forma sensível. *Não invalida que posteriormente ter de ser sempre feito o esfregaço
A gota espessa é mais sensível para detetar a infeção, mas teremos sempre de efetuar o espregaço para detetar a espécie!
A anemia causada pelo Plasmodium, é uma anemia ______
Hemolítica, por lise dos eritrócitos
O que é o teste da gota espessa?
Teste para o diagnóstico de malária
A gota espessa é mais sensível para detetar a infeção, mas teremos sempre de efetuar o espregaço para detetar a espécie!
De que formas podemos efetuar a profilaxia da malária?
A profilaxia da malária é fundamental, quer para as pessoas residentes nas zonas de transmissão, quer para os viajantes (para o Brasil, Républica Dominicana, Tailândia,…).
As formas de profilaxia são:
* A quimioprofilaxia, ou seja, a toma de medicação antes, durante e após uma eventual infeção.
* O uso de repelentes e roupa protetora (evitar braços e pernas expostos), sobretudo à noite.
* E a colocação de redes nos quartos para proteção dos mosquitos.
Caracteriza a Toxoplasmose
T. gondii is a typical coccidian parasite related to Plasmodium, Cystoisospora, and other members of the Apicomplexa clade.
T. gondii is an intracellular parasite, and it is found in a wide variety of animals, including birds and humans. Only one species exists, and there appears to be little strain-to-strain variation.
The essential reservoir host of T. gondii is the common house cat and other felines.
PHYSIOLOGY AND STRUCTURE
Organisms develop in the intestinal cells of the cat and during an extraintestinal cycle with passage to the tissues via the bloodstream.
The organisms from the intestinal cycle are passed in cat feces and mature into infective cysts within 3 to 4 days in the external environment.
These oocysts are similar to those of Cystoisospora belli, which is the human intestinal protozoan parasite, and can be ingested by mice and other animals (including humans) and produce acute and chronic infection of various tissues, including brain.
Infection in cats is established when the tissues of infected rodents are eaten.
Some infective forms (trophozoites) of the oocyst develop as slender, crescentic types called tachyzoites.
These rapidly multiplying forms are responsible for the initial infection and tissue damage. Slow-growing, shorter forms, called bradyzoites, also develop and form cysts in chronic infections.
EPIDEMIOLOGY
Human infection with T. gondii is ubiquitous; however, it is increasingly apparent that certain immunocompromised individuals (patients with acquired immunodeficiency syndrome [AIDS]) are more likely to have severe manifestations.
The wide variety of animals that harbor the organism, such as carnivores, herbivores, and birds, accounts for the widespread transmission.
Human infection may be acquired in several ways:
* (1) ingestion of undercooked contaminated meat containing T. gondii cysts;
* (2) ingestion of oocysts from hands, food, soil, or water contaminated with cat feces;
* (3) organ transplantation or blood transfusion;
* (4) transplacental transmission;
* and (5) accidental inoculation of tachyzoites.
Serologic studies show an increased prevalence in human populations in which the consumption of uncooked meat or meat juices is popular. It is noteworthy that serologic tests of human and rodent populations are negative in the few geographic areas in which cats have not existed.
Outbreaks of toxoplasmosis in the United States are usually traced to
poorly cooked meat (e.g., hamburger) and contact with cat feces.
Transplacental infection can occur in pregnancy, either from infection acquired from meat and meat juices or from contact with cat feces. Transplacental infection from an infected mother has a devastating effect on the fetus.
Infection via contaminated blood or transplanted organs can occur but is not common.
The sharing of needles between intravenous drug users may also facilitate the transmission of Toxoplasma.
Although the rate of seroconversion is similar for individuals within a geographic location, the rate of severe infection is dramatically affected by the immune status of the individual.
Patients with defects in cell-mediated immunity, especially those who are infected with HIV or who have had an organ transplant or immunosuppressive therapy, are most likely to have disseminated or central nervous system (CNS) disease. Illness in this setting is generally believed to be caused by reactivation of previously latent infection rather than new exposure to the organism.
CLINICAL SYNDROMES
Most T. gondii infections are benign and asymptomatic, with symptoms occurring as the parasite moves from the blood to tissues, in which it becomes an intracellular parasite.
When symptomatic disease occurs, the infection is characterized by cell destruction, reproduction of more organisms, and eventual cyst formation.
Many tissues may be affected; however, the organism has a particular predilection for cells of the lung, heart, lymphoid organs, and CNS, including the eye.
Symptoms of acute disease include:
* chills,
* fever,
* headaches,
* myalgia,
* lymphadenitis, and
* fatigue;
(the symptoms occasionally resemble those of infectious mononucleosis).
In chronic disease, the signs and symptoms include:
* lymphadenitis,
* occasionally a rash,
* evidence of hepatitis,
* encephalomyelitis,
* and myocarditis.
* In some of the cases, chorioretinitis appears and may lead to blindness.
Congenital infection with T. gondii also occurs in infants born to mothers infected during pregnancy. If infection occurs in the first trimester, the result is spontaneous abortion, stillbirth, or severe disease.
Manifestations in the infant infected after the first trimester include:
* epilepsy,
* encephalitis,
* microcephaly,
* intracranial calcifications,
* hydrocephalus,
* psychomotor or mental retardation,
* chorioretinitis, blindness,
* anemia,
* jaundice,
* rash,
* pneumonia,
* diarrhea,
* and hypothermia.
Infants may be asymptomatic at birth only to develop disease months to years later. Most often these children develop chorioretinitis with or without blindness or other neurologic problems, including retardation, seizures, microcephaly, and hearing loss.
In immunocompromised older patients, a different spectrum of disease is seen. Reactivation of latent toxoplasmosis is a special problem for these people. The presenting symptoms of Toxoplasma infection in immunocompromised patients are usually neurologic, most frequently consistent with diffuse encephalopathy, meningoencephalitis, or cerebral mass lesions.
Reactivation of cerebral toxoplasmosis has emerged as a major cause of encephalitis in patients with AIDS. The disease is usually multifocal, with more than one mass lesion appearing in the brain at the same time. Symptoms are related to the location of the lesions and may include hemiparesis, seizures, visual impairment, confusion, and lethargy.
Other sites of infection that have been reported include the eye, lung, and testes. Although disease is seen predominantly in patients with AIDS, it also may occur with similar manifestations in other immunocompromised patients, in particular those undergoing solid organ transplantation.
Qual é o hospedeiro definitivo do Toxoplasma gondii?
O gato
O gato é hospedeiro definitivo, quer dizer que tem forma adulta e definitiva do parasita, eliminando nas fezes oocistos imaturos. Estes oocistos tornam-se maduros ao fim de 3-4 dias, e podemos contaminar-nos. A questão temporal da maturação dos oocistos é muito importante, pois pessoas que têm gatos e eliminam as fezes diariamente têm menores taxas de contaminação pois os oocistos não têm tempo de amadurecer e tornar-se infeciosos.
Tens uma doente grávida com um marido imunocomprometido, que te dizem viver com os seus 3 gatos. O quê que vais aconselhar?
Remoção das fezes diariamente
O gato é hospedeiro definitivo do Toxoplasma gondii, quer dizer que tem forma adulta e definitiva do parasita, eliminando nas fezes oocistos imaturos.
Estes oocistos tornam-se maduros ao fim de 3-4 dias, e podemos contaminar-nos. A questão temporal da maturação dos oocistos é muito importante, pois pessoas que têm gatos e eliminam as fezes diariamente têm menores taxas de contaminação pois os oocistos não têm tempo de amadurecer e tornar-se infeciosos.
Organisms develop in the intestinal cells of the cat and during an extraintestinal cycle with passage to the tissues via the bloodstream.
The organisms from the intestinal cycle are passed in cat feces and mature into infective cysts within 3 to 4 days in the external environment.
These oocysts are similar to those of Cystoisospora belli, which is the human intestinal protozoan parasite, and can be ingested by mice and other animals (including humans) and produce acute and chronic infection of various tissues, including brain.
Infection in cats is established when the tissues of infected rodents are eaten.
Some infective forms (trophozoites) of the oocyst develop as slender, crescentic types called tachyzoites.
These rapidly multiplying forms are responsible for the initial infection and tissue damage. Slow-growing, shorter forms, called bradyzoites, also develop and form cysts in chronic infections.
