1. The size of the trophozoite of Entamoeba histolytica is 12 to 60 rlm. It moves with the help of single-directional pseudopodia. It has a transparent ectoplasm and an endoplasm rich in granules. It has a spherical vesicular nucleus with a diameter of 4 to 7 At the same time, there is a single layer of evenly distributed and uniformly sized perinuclear chromatin granules at the edge of the thin nuclear membrane.

The nucleolus is small, 0.5 microns in size, often centered, and surrounded by fine, colorless filamentous structures. In sterile culture medium, trophozoites often have more than 2 nuclei. Trophozoites isolated from tissues of symptomatic patients often contain ingested red blood cells and sometimes white blood cells and bacteria.

The process of trophozoites forming cysts in the intestinal lumen is called encyslation

Trophozoites cannot form cysts in organs or the outside world outside the intestinal lumen. In the intestinal lumen, the trophozoites gradually shrink and stop moving, turning into a nearly spherical precyst, and then turn into a single-nucleated cyst and undergo secondary nuclear division.

There is a short rod-shaped nutrient storage structure in the cytoplasm called a chmmatoid body. The morphology of pseudochromosomes has significance in identifying insect species.

Trophozoites first adsorb to intestinal epithelial cells through lectins, and then secrete perforin and cysteine ​​proteases to destroy the intestinal mucosal epithelial barrier and penetrate cells, and finally kill the host intestinal epithelial cells and immune cells, causing ulcers.

Entamoeba histolytica infection can cause intestinal and extraintestinal amoebiasis.

(1) Intestinal amoebiasis

(2) Extraintestinal amoebiasis

Macrophages play an important role in amoeba killing and antigen presentation.

saline smear method

iodine smear method

In vitro culture

Nucleic acid diagnosis

Transmission and Epidemic Entamoebiasis histolytica has a worldwide distribution, with higher infection rates in tropical and subtropical regions such as India, Indonesia, the Sahara Desert, tropical Africa, and Central and South America.

The average infection rate of the Chinese population is about 0.949%, and the number of infected people is estimated to be 10.69 million, mainly in the northwest, southwest and north China. The infection rate in Yunnan, Guizhou, Xinjiang, Gansu and other places exceeds 2%.

The treatment of amoebiasis has two basic goals, one is to cure the invasive lesions inside and outside the intestines, and the other is to clear the cysts in the intestinal lumen.

Metronidazole is currently the drug of choice for the treatment of amebiasis. Metronogar is suitable for patients with acute or chronic invasive intestinal amoebiasis, and is almost 100% absorbed when taken orally.

Amebiasis is a worldwide public health problem. While treating the disease, comprehensive measures must be taken to prevent infection. Specific methods include harmless treatment of feces to kill cysts; protecting water sources and food , free from pollution; improve environmental sanitation and get rid of harmful insects; strengthen health education to improve self-protection capabilities

Female larvae suck blood, male larvae do not.

When a female sandfly stings a patient or infected animal host, macrophages containing amastigotes in the blood or skin are sucked into the stomach. After 24 hours, the amastigotes develop into early promastigotes.

At this time, the insect body takes on an oval shape and the flagellum begins to protrude from the body. After 48 hours, it develops into a thick and short promastigote or a fusiform promastigote. The body shape gradually changes from oval to a wide spindle or a spindle with a length exceeding 3 times the width. At this time, the flagellum also changes from short to long.

On the 3rd and 4th day, a large number of mature promastigotes appeared, their activity was significantly enhanced, and they reproduced by longitudinal binary fission. While the number increased sharply, the insects gradually moved to the forest fly's stomach, esophagus and pharynx.

One week later, a large number of infectious promastigotes accumulate in the mouth and beak. At this time, when the sandfly stings a healthy person, the promastigotes enter the human body along with the sandfly saliva.

When a female sandfly infected with promastigotes stings a human body and sucks blood, the promastigotes enter the subcutaneous tissue of the human body along with the saliva secreted by the sandflies.

Part of the promastigotes can be phagocytosed and eliminated by polymorphonuclear leukocytes, and part of them can be phagocytosed into human macrophages.

After the promastigote enters the macrophage, it gradually becomes round, loses the external part of its flagellum, and transforms into the amastigote stage.

At this time, worm-containing vacuoles are formed in macrophages. Amastigotes can not only survive in macrophages, but also divide and reproduce. Massive proliferation of amastigotes eventually leads to macrophage rupture.

The free amastigotes enter other macrophages and repeat the above proliferation process.

fever

Swelling of the spleen, liver, and lymph nodes

anemia

Common complications

The main clinical manifestation is lymphadenopathy in multiple parts of the body, especially in the groin and thigh, followed by the neck, armpit and upper trochlea, and thirdly behind the ear, supraclavicle and armpit, with no obvious local tenderness or redness. Leishmania can often be detected when lymph nodes are removed and serially sectioned. The general condition of most patients is good, but a few may have low-grade fever and fatigue. The liver and spleen are rarely palpable, and eosinophils are often increased. Most patients with this disease can recover on their own.

Many skin nodules containing Leishmania appear on the patient's face, limbs or trunk. The nodules are granulomas of varying sizes or dark papules. They are common on the face and neck, and some resemble tumor-type leprosy.

Cutaneous leishmaniasis is found in the Karamay region of Xinjiang, my country. It mainly includes four types of skin diseases: papules, plaques, ulcers and nodular prurigo. A few of them are pustules and impetigo-like.

puncture examination

skin biopsy

Antibody testing

Circulating Antigen Test

PCR method

Rapid test strip method

The pentavalent zinc agent sodium zinc gluconate, the domestic preparation is Sdbiihexonas, has good efficacy.

For a small number of patients who are ineffective after repeated treatments with pentamidine, they can be treated with aromatic pentamidine such as pentamidine or stilbamidine, or used in combination with pentavalent diazepam for better results.

Killing of Sick Dogs Sick dogs should be checked regularly, detected early, and hunted early. Hunting and killing sick dogs is the key to the prevention and control of canine leishmaniasis in endemic areas.

After the blood film is stained with Giemsa or Reiter's stain, the nucleus appears purple-red, the cytoplasm appears sky blue to dark blue, and malaria pigment appears brown, tan, or dark brown.

The sporozoites that invade the liver cells are slender in shape, about 11 microns in length and 1.0 microns in diameter. They are often bent into a C-shape or S-shape. The front end is slightly thinner, the top is flatter, the back end is blunt, and the body surface is smooth.

The epidermis consists of an outer membrane, a double inner membrane, and a layer of subepidermal microtubules.

Submembranous microtubules extend from the polar ring backward to the nucleus or terminate slightly beyond the nucleus. The weak movement of the worm may be caused by the expansion and contraction of microtubules under the membrane.

There are 3 to 4 polar rings on the top of the front end of the sporozoite. The cell has one nucleus and is elongated. There is a pair of electron-dense rod-like bodies (rhoptry), which may open to the top ring. In front or behind the nucleus, there are a large number of micronemes, which are round, oval or elongated.

The sporozoites that invade the liver cells gradually turn into a round shape and continue to grow in size. The nucleus begins to divide, but the cytoplasm of the parasite has not yet divided. At this time, the parasite enters the early schizont stage or is called the immature schizont stage.

Subsequently, the nucleus divides repeatedly, and the cytoplasm also divides accordingly. Each nucleus is surrounded by part of the cytoplasm, forming a merozoite, which is a mature schizont.

Finally, the merozoites released by the hepatocytes enter the peripheral blood, invade red blood cells, and initiate the development of intraerythrozoic Plasmodium.

trophozoite

Schizont

gametophyte

extraerythrocytic phase

intraerythrocytic phase

The five species of malaria parasites that parasitize the human body have basically the same life cycle and require two hosts, humans and Anopheles mosquitoes. In the human body, it parasitizes in liver cells and red blood cells and undergoes schizogony. In red blood cells, in addition to schizoite proliferation, some merozoites form gametocytes and begin the initial development of sexual reproduction. In the mosquito, gamelogony is completed, followed by spore multiplication.

The glycogen storage of Plasmodium in the intraerythrocytic stage is very small, and glucose is the main energy source of Plasmodium in the intraerythrocytic stage. Parasitism of Plasmodium causes changes in the red blood cell membrane, which enhances the active transport of glucose through the membrane, or removes certain factors that inhibit transport, so that Plasmodium can continuously obtain glucose from the host's plasma for metabolism.

The free amino acids obtained by Plasmodium are mainly from the hydrolysis products of hemoglobin in red blood cells, as well as amino acids and organic matter from the host's plasma and red blood cells.

Plasmodium has no lipid storage, nor can it synthesize fatty acids and cholesterol, and is completely dependent on the host's supply.

It refers to the time between the invasion of Plasmodium into the human body and the emergence of clinical symptoms, including the time for the development of protozoa in the outer red blood cell stage and the time required for the protozoa to proliferate to a certain number in the intraerythrocytic stage through offspring cleavage.

The length of the incubation period is closely related to the strain of protozoa that enters the human body, the number of spores and the body's immunity.

A typical malaria attack is characterized by three consecutive stages: chills, high fever, and fever-reducing sweating.

The attack is caused by intraerythrocytic schizophrenia. After several generations of intraerythrocytic schizophrenia, the density of protozoa in the blood reaches the fever threshold.

Since intraerythrocytic schizoid proliferation is the basis of malaria attacks, the attacks are cyclical, and this cycle is consistent with the intraerythrocytic schizoid proliferation cycle.

As the body's immunity against malaria parasites gradually increases, a large number of protozoa are eliminated and the attack can stop on its own.

After the initial attack of malaria has stopped, if the patient is not reinfected, a malaria attack may occur just because a small amount of remaining intraerythrocytic Plasmodium parasites in the body reproduce in large numbers under certain conditions, which is called resurgence of malaria.

Rekindling is related to the decline of host resistance and specific immunity and the antigenic variation of Plasmodium

Relapse of malaria refers to a patient with an initial onset of malaria who has eliminated the intraerythrocytic malaria parasites and has not been infected by mosquito-borne infections. After several weeks to more than a year, another malaria attack occurs, which is called relapse.

After several malaria attacks, anemia may occur, especially in falciparum malaria.

In addition to the direct destruction of red blood cells by Plasmodium, the cause of anemia is also related to the following factors

In patients with the first episode, the spleen usually begins to swell 3 to 4 days after the attack. In those who do not heal for a long time or have repeated infections, the splenomegaly is very obvious and can reach below the umbilical cord. The main causes are splenic congestion and mononuclear-macrophage proliferation. With aggressive antimalarial treatment in the early stage, the disease can return to normal size. In chronic patients, due to the thickening of the splenic capsule, the high degree of tissue fibrosis and the hardening of the texture, the spleen cannot return to normal despite radical antimalarial treatment.

innate resistance

innate immunity

adaptive immunity

Thick and thin blood film staining microscopy is still the most commonly used method at present, but this method has relatively high professional requirements for the microscopist.

Circulating Antibody Testing

Circulating Antigen Test

Malaria is one of the diseases that seriously endangers human health

Source of infection

malaria vector

Susceptible groups

Preventive measures include mosquito control and preventive medication

Currently, the only preventive drug that can kill liver-stage malaria parasites and dormant parasites is primaquine.

Preventive antimalarial drugs include chloroquine. In areas where chloroquine-resistant falciparum malaria is endemic, mefloquine can be used.

According to the effect of antimalarial drugs on different parasite stages of Plasmodium, they can be divided into anti-relapse drugs that kill the extra-erythrocytic schizonts and dormants, such as primaquine; anti-clinical drugs that kill the proliferative phase of intra-erythrocytic schizonts. Seizure drugs, such as chloroquine, pyronaridine, and artemisinin.

Trophozoites refer to parasites that divide and reproduce within intermediate host cells, including tachyzoites and bradyzoites.

After staining with Giemsa stain, it can be seen that the cytoplasm is blue and the nucleus is purple-red, located in the center of the insect body; between the nucleus and the tip, there are light red particles, called parakaryosomes, which are parasites inside the cell. It is spindle-shaped or oval-shaped and reproduces by endo-budding method. It usually contains several to more than 20 worms. This collection of rapidly proliferating worms surrounded by the host cell membrane is called a pseudocyst (pseudocyst), which contains worms called tachyzoites

Round or oval, with a tough, elastic wall. The cyst contains several to hundreds of trophozoites. The trophozoites in the cyst are called bradyzoites and can continue to proliferate. Their shape is similar to tachyzoites, but the body is smaller and the nucleus is slightly posterior.

Round or oval, with two layers of smooth and transparent cyst walls, which are filled with uniform small particles. The mature oocyst contains 2 sporangia, each containing 4 crescent-shaped sporozoites.

It develops and proliferates in the villous epithelial cells of the feline small intestine. The mature schizont is oblong and contains 4 to 29 merozoites, usually 10 to 15, arranged in a fan-like shape. The merozoites are shaped like a crescent. Shape, sharp at the front and blunt at the back

The free merozoites of gametocytes invade other intestinal epithelial cells and develop into gametocytes, which then develop into gametocytes.

Gametophytes are divided into male and female. Female gametes are larger in size, with nuclei dyed deep red and cytoplasm dark blue; male gametophytes are smaller in size and mature into 12-32 male gametes with tapered ends.

Male and female gametes fertilize and combine to develop into zygotes, which then develop into oocysts

在猫科动物体内完成有性生殖,同时也进行无性生殖，因此猫是弓形虫的终宿主兼中间宿主

在人或其他动物体内只能完成无性生殖,为中间宿主

有性生殖只限于猫科动物小肠上皮细胞内,称肠内期发 育;无性生殖阶段可在肠外其他组织的有核细胞内进行，称肠外期发育

When a cat or feline eats animal internal organs or meat tissue, it swallows the cysts or tachyzoites (in the host's pseudocyst) containing Toxoplasma gondii into the digestive tract and becomes infected.

In addition, infection can also be acquired by eating or drinking food or water contaminated with mature oocysts.

The bradyzoites in the cysts, the sporozoites in the oocysts and the tachyzoites escape from the small intestinal lumen and mainly invade the small intestinal epithelial cells in the ileum to develop and proliferate. After 3 to 7 days, the parasites in the epithelial cells will undergo fission. The merozoites proliferate to form schizonts, which release merozoites after maturity and invade new epithelial cells to form the second and third generation schizonts. After several generations of multiplication, some merozoites develop into female and male gametophytes, which continue to develop into female , male gametes.

The male and female gametes are fertilized and become zygotes, which eventually form oocysts. The oocysts break through the epithelial cells and enter the intestinal lumen, and are excreted with feces. In a suitable temperature and humidity environment, they develop into infectious mature oocysts in 2 to 4 days.

The time it takes for a cat to excrete oocysts after ingesting parasites at different stages of development is also different. Usually, it takes about 3 to 10 days to excrete oocysts after ingesting cysts, while it takes about 19 to 48 days to excrete oocysts after ingesting false cysts or oocysts. . Infected cats can excrete 10 million oocysts every day for 10 to 20 days.

Mature oocysts are an important stage of infection.

When oocysts in cat feces or cysts or pseudocysts in animal tissues are swallowed by intermediate hosts such as humans, cattle, sheep, pigs, etc., sporozoites, bradyzoites or tachyzoites respectively escape in their intestines. , then invades the menstrual blood or lymph of the intestinal wall, enters the cells of the mononuclear macrophage system, and spreads to various organs and tissues throughout the body, such as the brain, lymph nodes, liver, heart, lungs, tongue, muscles, etc., enters the cells and develops and proliferates , forming a false cyst.

When the tachyzoites multiply to a certain number, the cell membrane ruptures, and the tachyzoites invade new tissue cells and multiply repeatedly. The invasion of host cells by tachyzoites is an active process, including three stages: adhesion, penetration and vesicle formation.

In a body with normal immune function, after some tachyzoites invade host cells (especially brain, eye, and skeletal muscle cells), the proliferation rate of the parasite slows down and transforms into bradyzoites, which secrete cystic substances to form cysts.

Cysts can survive in the host for months, years, or longer. When the body's immune function is low or immunosuppressants are used for a long time, the cysts in the tissue can rupture and release bradyzoites. After the bradyzoites enter the bloodstream, they can invade other new tissue cells and continue to develop and proliferate into tachyzoites.

Tachyzoites and cysts are the main infection stages of transmission between intermediate hosts or between intermediate hosts and definitive hosts.

The pathogenic effect of Toxoplasma gondii is related to the genotype of Toxoplasma gondii, the virulence of the strain and the immune status of the host.

Toxoplasma gondii can be divided into highly virulent strains and attenuated strains based on their invasiveness, proliferation rate, cyst formation, and lethality to the host in mice.

Tachyzoites are the main pathogenic stage of acute infection with Toxoplasma gondii. They parasitize and rapidly proliferate in cells, destroying cells. After escaping, tachyzoites invade adjacent cells. Repeatedly, they cause tissue inflammatory reactions, edema, and mononuclear disease. Cells and a few multinucleated cells infiltrate.

Intracystic bradyzoites are a major stage of chronic infection. The cysts increase in size due to the proliferation of bradyzoites, squeezing the organs and causing dysfunction. The cyst can rupture, releasing bradyzoites. Most of the rare bradyzoites are destroyed by the host immune system, and some of the bradyzoites can invade new cells and form cysts.

After the host is infected with Toxoplasma gondii, it can produce effective protective immunity under normal circumstances and inhibit the proliferation of the parasite. The body generally has no obvious symptoms. Toxoplasmosis only occurs when the body is immune deficient or has low immune function.

Toxoplasma gondii infection is usually asymptomatic, but congenital infection and acquired infection in immunocompromised individuals often cause severe toxoplasmosis.

Congenital toxoplasmosis: A pregnant woman is infected with Toxoplasma gondii for the first time during pregnancy, and the parasite can be transmitted to the fetus through the placenta.

Acquired toxoplasmosis: In individuals with normal immunity, infected individuals generally have no obvious clinical manifestations and no specific symptoms and signs.

Patients in the acute infection stage often present with low-grade fever, headache, superficial lymph node enlargement, etc., which are more common in submandibular and posterior cervical lymph nodes. Toxoplasma gondii often affects the brain and eyes, causing damage to the central nervous system, such as encephalitis, meningoencephalitis, epilepsy and mental disorders. Retinochoroiditis is the most common form of toxoplasmic eye disease, and adults present with sudden vision loss. Infants and young children can see hand injuries. Eye-catching syndrome, slow reaction to external things, strabismus, iridocyclitis, uveitis, etc. may also occur, most of which are bilateral lesions.

If patients with latent infection suffer from immunodeficiency diseases such as AIDS, or receive long-term chemotherapy or immunosuppressive treatment for malignant tumors, organ transplants, etc., the patient's immune function may be low, inducing activation of latent infection and transforming into acute or subacute infection. , resulting in severe systemic toxoplasmosis, most of which died due to concurrent toxoplasmic encephalitis

The immune response mediated by macrophages, Thl cells, NK cells, neutrophils and dendritic cells (DC) plays a leading role.

Human infection with Toxoplasma gondii can induce the production of specific antibodies. IgM and IgA increase in the early stage of infection, and the former gradually disappears after 4 months, but there are also cases that are positive for a longer period of time; the latter disappears faster. One month after infection, IgM is gradually replaced by high-titer IgG, and remains so for a long time. The waxing and waning of IgM and IgG antibodies is called seroconversion, and the titers of IgM and IgG antibodies and the affinity of IgG are dynamically monitored. , helps to determine the time of Toxoplasma gondii infection in pregnant women and the probability of fetal involvement, and provides an important basis for clinical treatment.

It can be passed to the fetus through the placenta, so neonatal serum tests often show positive results. This antibody usually disappears 5 to 10 months after birth.

Whether in adults or newborns, antibodies play an insignificant role in immune protection against Toxoplasma gondii infection.

smear staining

Animal inoculation isolation method or cell culture method

Since the pathogenic examination of Toxoplasma gondii is difficult and the positive rate is not high, serological examination is an important auxiliary diagnostic method that is widely used at present.

Dyeing test

indirect hemagglutination test

indirect immunofluorescence test

Enzyme-linked immunosorbent assay

immunoenzyme staining test

modified agglutination test

It is distributed worldwide and widely exists in a variety of mammals, and infection in humans is also common.

Source of infection

way for spreading

Susceptible groups

The ectoplasm is transparent and gel-like, and has functions such as movement, feeding, nutrition, excretion and protection;

The endoplasm is sol-like, containing organelles, contents and nuclei. It is the main place for cell metabolism and nutrient storage.

The nuclear membrane is a two-layer unit membrane with micropores connecting the inside and outside of the nucleus. 3 The nucleolus is rich in RNA, and the chromatin contains protein, DNA and a small amount of RNA. Most of the parasitic protozoa have vesicular nuclei, with few and granular chromatin distributed in the nucleoplasm or the inner edge of the nuclear membrane, and containing only one nucleolus. A few ciliates have compact nuclei, which are large and irregular, with rich chromatin and often with more than one nucleolus.

Some protozoa have only one developmental stage in their entire life cycle, that is, the trophozoite, which is usually transmitted through direct contact. For example, Trichomonas vaginalis is transmitted through sexual contact;

Some protozoa have two stages in their life history: trophozoite and cyst. The former has the functions of movement and feeding, and is the growth, development, reproduction and pathogenic stage of the protozoa. The latter is in a quiescent state and is the transmission and infection stage of the protozoa. It is generally transmitted through drinking water or food. For example, the life cycle of Entamoeba histolytica and Giardia lamblia is of this type.

Including binary fission, polyfission and budding reproduction.

Sexual reproduction of protozoa includes conjugation and ga-metogony.

Anaerobic sugar metabolism is the main pathway of energy metabolism in protozoa.

Most protozoa carry out facultative anaerobic metabolism, especially the parasitic protozoa in the intestines. The parasitic protozoa in the blood can use an appropriate amount of oxygen to perform aerobic metabolism.

Protozoa can use various enzymes to break down the proteins they ingest into free amino acids.

These include limitations of host tissue cells on parasite invasion or growth, such as resistance to Plasmodium falciparum in individuals with heterozygous or homozygous sickle cell hemoglobin.

Although nonspecific factors play an important role in host resistance, often they act in conjunction with the host's immune system.

After the protozoa that invade the human body proliferate to a certain number, they may show obvious damage or appear corresponding clinical symptoms.

The secretions (including various enzymes), excretions and decomposition products of dead parasites of parasitic protozoa have toxic effects on the host. The above toxic substances can damage host cells, tissues and organs through different pathways.

Individuals with normal immune function have no obvious clinical manifestations after being infected with certain protozoa and are in a state of latent infection.

However, when the body's resistance decreases or the immune function is insufficient (such as AIDS patients, long-term immunosuppressant treatment, or patients with advanced tumors), the reproductive capacity and pathogenicity of these protozoa are significantly enhanced, causing patients to develop obvious clinical symptoms and signs. Even life-threatening.