Microsporidia

Microsporidium is a detachment of the simplest microorganisms belonging to the class of cnidosporidia. These are intracellular parasites that can not exist outside the host's body. There are almost 1,300 species of them, which are represented by almost 200 genera. This is only a fraction of the true diversity of mycorrhospiidae, which has already been described in the scientific world: the mass of possible infected hosts were not examined for the presence of these parasites in the body. The owner can be almost any animal - from the simplest to humans. The largest number and diversity are representatives of the microsporidia of crustaceans and insects.

A person can become infected with microspods of six genera - Encephalitozoon, Pleistophora, Nosema, Vittaforma, Enterocytozoon and Microsporidium. In spite of the fact that some parasites of this group, most likely, provoke the development of asymptomatic or fleeting intestinal infections, the mechanism of infection with microsporidiosis is not sufficiently studied.

Microsporidia have several unique features demonstrating their exceptional fitness for intracellular parasitism. In their disputes there is a set of organelles, peculiar only for them - the extrusion apparatus. With its help, a healthy cell is infected by piercing the envelope and isolating the spores directly into the cytoplasm. No other species of protozoa have such a mechanism for spreading their disputes.

[1], [2], [3], [4], [5],

Structure of microsporidia

The microsporidium genome is the smallest among all cells containing the nucleus. There are almost no introns in cells, and mitosis is represented in the form of closed intranuclear pleuromitis. The ribosomes of microsporidia are similar in structure to the ribosomes of cells with a non-nuclear structure. The cell does not have kinetosis, lysosomes, particles of reserve nutrients. Previously, it was believed that the microsporidia did not have mitochondria, but not so long ago they found small mitosomes, which served as a proof of their mitochondrial nature.

Spores usually have three layers of the shell: glycoprotein exospora, chitinous endospores and cytoplasmic membrane. The extrusion apparatus consists of a back vacuole, an anchor disk, a polaroplast and a polar tube. The posterior vacuole has a single chamber or multi-chamber structure. Sometimes the vacuole contains a poster. When the embryo is isolated into a healthy cell, it immediately increases, displacing the spore into a polar tube.
Polaroplast usually consists of membranes, compactly located in a kind of "packaging".

Sometimes a polaroplast contains vesicles and tubular structures. Polaroplast takes part in the formation of the necessary pressure, which is required to unscrew the polar tube, provides the membrane with a polar tube and a pathway inside it for sporoplasm. The polar tube is an elongated, double-edged formation, laid out by a spiral and extending from the anchor disk. Their appearance and development can be very different in microsporidia.

Life cycle of microsporidium

Sporoplasm is a single nucleus, which is surrounded by a small amount of cytoplasm containing ribosomes. The nucleus is located in the dispute. As soon as the spore penetrates into the inner environment of the host cell, sporoplasma forms its protective cytoplasmic envelope, of which little has been learned so far.

Then the sporoplasma rapidly grows. At this point, the cell has a minimum of organelles: posterosomes, ribosomes, smooth and rough endoplasmic reticulum.

With the beginning of the phase of sporogony - sporonta - another shell appears in the cell. In this phase, the nuclei actively divide, forming plasmodia.

Microsporidia can lay another additional shell - sporophorous vesicle, the species and sizes of which differ significantly in different species.

Sporoblast is an intermediate stage of development from sporogonal plasmodium to spore. During this period, all the shells are actively developing and the organelles are laid. Then the affected cell is destroyed, and the resulting spores attack neighboring healthy cells or are removed from the body in search of a new host.

Microsporidia are characterized by a variety of life cycles. This cycle includes only one host (monoxenous) with the formation of one species of spores, it is typical for 80% of known species. But it can differ greatly in different species: the features of sporogony, the number and types of divisions at all stages. For the remaining 20%, the life cycle can take place in two or more hosts, with the formation of different types of spores in the structure and functions assigned to them.

Clinical picture and symptoms of microsporidiosis

Microsporidia is very common. The diseases caused by microsporidia, as well as the pathways of infection, have not been sufficiently studied. Microsporidia, which can live in cells of the human body, with the same success affect animals - both wild and domestic, but it is not yet clear whether people are infected with animals. People with depressed immunity can be carriers. Spores of microsporidia are present in water bodies, but no case of rapid spread of the disease has proved that contaminated water is to blame for this. In the external environment microsporidia are excreted from the host with feces, urine and sputum. It is assumed that people can get infected from each other, but there is no exact data. Most likely, intestinal microsporidiosis is infected when the parasite enters the oral cavity. Mostly, it is an infection caused by Enterocytozoon bieneusi, which affects the gastrointestinal tract.

Microsporidiosis of respiratory organs causes parasites that are almost never present in feces, therefore the most likely method of infection is airborne dust. The eyes are affected by the parasite's entry into the conjunctiva. Studies indicate that microsporidia can attack macrophagocytes and fibroblasts of their own plate of the mucosa.

Often there is intestinal microsporidiosis, but there are many variations of the disease: microsporidiosis of the bile ducts, eyes, sinuses of the nose, respiratory tract, muscle fibers, disseminated microsporidiosis, attacking the kidneys, liver, heart and nervous system.

Microsporidia during infection often provoke acute or chronic diarrhea. A greater likelihood of catching microsporidiosis is in those who underwent organ transplantation and the resulting immunodeficiency. Some cases of epilepsy are associated with the fact that the organism was attacked by microsporidia. Cases of keratitis and corneal ulcers caused by damage to Nosema ocularam, Vittaforma corneae and other microsporidia, which have not yet been classified, are described. Microsporidia was detected with inflammation of muscle fibers. Nosema connori is the cause of disseminated microsporidiosis. From a quarter to half of cases of prolonged diarrhea of unexplained etiology in patients with immunodeficiency are associated with microsporidia.

Usually, parasites attack young people whose lymphocytes are less than 100 μl, and microsoridiosis is found in children with severe immunodeficiency. Children, whose organs are affected by microsporidosis, may lag behind in development, periodically complain of pain in the abdomen and constant diarrhea.

Enterocytozoon bieneusi attacks the cells of the intestine, causing inflammation and damaging the villi, but almost never penetrates into the plate of the mucosa. Infection is limited to the gastrointestinal tract. Encephalitozoon intestinalis, on the contrary, often develops outside the gastrointestinal tract. Getting into the bile duct, it provokes their inflammation and non-calculous inflammation of the gallbladder. In HIV-infected parasites, they can attack the eyes, sinuses and lungs, and even develop into a disseminated form. Keratoconjunctivitis is characterized by reddening of the conjunctiva, unpleasant sensations from getting light on the eyes, problems with eyesight, a feeling that there is a foreign body in the eye. In addition, microsporidia can provoke the development of sinusitis with the release of mucus and pus from the nose. There are cases when the parasite enters the lower respiratory tract; then in the absence of signs of the disease can develop pneumonia or bronchitis. In some cases with immunodifitsitelnogo development of disseminated microsporidiosis. Which internal organs will suffer depends on the type of parasite. Encephalitozoon hellem attacks the eyes, urinary ducts, sinuses and respiratory organs. Encephalitozoon intestinalis develops within the gastrointestinal tract and bile ducts; there are cases when it attacks the kidneys, eyes, sinuses of the nose, lungs or bronchi. Encephalitozoon cuniculi is especially dangerous: it is capable of dissemination and can attack almost any organs.

[6], [7], [8], [9]

Diseases caused by microsporidia

Various forms of infections caused by microsporidia are characterized by specific signs.

1. Enterocytozoonosis (microsporidia of the species Enterocytozoon bieneusi). The causative agent affects the cells of the small intestine. Macroscopic studies of changes in the intestinal mucosa can not be identified. But under a microscope you can see a violation of the form of enterocytes, the defeat of microvilli, the growth of crypts, the growth of the number of lymphocytes.

Pathological cells gradually lose villi and die, and spores are released to settle in new healthy cells. Infection causes problems with digestion of food, worse absorbed carbohydrates and fats. Progression of diarrhea, which stretches for weeks and can cause dehydration. Lack of appetite causes weight loss.

Most often enterocytozoonosis occurs against the background of AIDS and develops in disseminated form, attacking the respiratory tract and causing fever.
Infection can be fecal-oral. Prevention of the disease is no different from preventing intestinal infections.

2. Encephalitozoonoses (microsporidia of the species Encephalitozoon cuniculi and Encephalitozoon hellem). E. Cunculi attack macrophagocytes, blood and lymph vessels of brain cells, liver, kidneys and other organs. When cells die as a result of infection, spores are released into the blood and lymph. The onset of encephalitozoonoses is acute, with concomitant heat and dysfunction of the affected internal organs. If the infection has attacked the brain, patients report severe headaches, the meninges are irritated or even meningitis occurs. If the liver is damaged, there are signs of hepatitis, if the kidneys are signs of jade.

The greatest risk is for people with AIDS. The source of encephalitozoonoses is animals. To avoid infection, it is necessary to carry out the deratization in time and adhere to the rules of personal hygiene.

Encephalitozoon hellem in people with immunodeficiency is the culprit of keratoconjunctivitis, inflammation of the kidneys and the development of renal failure. This parasite also develops in the respiratory system, which is accompanied by fever, coughing, shortness of breath, signs of interstitial pneumonia. Several systems of internal organs are often affected simultaneously. Infection comes from a sick person through the respiratory system, the oral cavity or on the conjunctiva.

3. Invasion (microsporidia of the species Trachipleistophora hominis). It affects muscle fibers, is accompanied by weakness in muscles, fever, keratoconjunctivitis. People and monkeys can get infected by infection by contact method.
4. Septaptosis (microsporidia of the species Septata intestinalis). Microsporidia first attack the cells of the intestinal mucosa and macrophagocytes. In the foci of infection ulcers and necrosis develop. Then the pathogen can develop in other organs. The main sign of infection is chronic diarrhea. It can provoke inflammation of the gallbladder and bile ducts. You can get infected from a sick person through food or water.
5. Nosematosis (microsporidia of the species Nosema connori). This is disseminated invasion. The main symptoms are nausea, vomiting, severe diarrhea, impaired breathing. Studies will show the presence of Nosema connori in the muscle tissues of the heart, diaphragm, stomach and small intestine, as well as in the walls of the blood vessels of many organs, in the kidneys, liver and lungs. Infection occurs through food.
6. Nosematosis (microsporidia of the species Nosema ocularum) is a common disease. The parasite lives in the cornea and provokes the development of a combined inflammation of the cornea and the vascular membrane of the eyeball and even the corneal ulcer.
7. Invasion (microsporidia of the species Vittaforma corneum) also affects the eyes.
8. Invasion (microsporidia of the species Bruchiola vesicularum) attacks muscles, develops in people with immunodeficiency.

[10], [11]

How to detect microsporidiosis?

Microsporidia are stained with some reagents, give a positive PAS response, but they are often not recognized: an extremely small (1-2 μm) size and no signs of an inflammatory process in neighboring tissues prevent it from doing so. Microsporidiosis is best diagnosed with an electron microscope. A qualitative diagnosis is provided by a modified tri-color coloration and PCR.

Microsporidiosis can be suspected if the patient complains of chronic diarrhea, conjunctivitis, impaired breathing, kidney and liver, if the cause of these complaints has not been clarified earlier, and the tests have not shown the presence of viruses, bacteria and other protozoa.

To verify the diagnosis for analysis, a fecal swab is taken. If there is reason to suspect disseminated microsporidiosis, flushes from the cornea, a urine sediment, biopsies of the mucosa of the bladder and duodenum are taken for analysis. The smears are stained, and then it is possible to detect the spores of the pathogen that are getting under. The action of the reagent is a reddish color, while most of the bacteria turn green - in the color of the background.

In tissues, the presence of the parasite will detect an electron microscope: spores with a characteristic polar tube are found in the cells.

Treatment

Treatment of microsporidiosis with proven effectiveness does not exist. E. Intestinalis neutralizes the drug albendazole. The tests also showed the effectiveness of fumagiline. Atovaquone and nitazoxanide relieve symptoms, but there was no research into their effectiveness in fighting the disease. In HIV-infected manifestations of microsporidiosis decrease with antiretroviral therapy.

Is microsporidiosis dangerous? Microsporidia is often found in the tissues of the body, without any manifestation or disturbance. Most often, only with progression of immunodeficiency in HIV-infected or in recipients of organ transplants, infection becomes dangerous. But a person with normal immunity in most cases has nothing to worry about.