FUNDAMENTALS OF MEDICAL BIOLOGY - 2012

Representatives of the class Zoomastigophora (Animal Flagellates) as human parasites

Class="center">Phylum Sarcomastigophora.

Class Zoomastigophora (Animal Flagellates).

Species: Trypanosomes: Trypanosoma brucei gambiense, Trypanosoma brucei rhodesiense, Trypanosoma cruzi;

Leishmania: Leishmania tropica minor, Leishmania tropica major, Leishmania brasiliensis, Leishmania mexicana, Leishmania donovani, Leishmania infantum;

Giardia: Lamblia intestinalis;

Trichomonads: Trichomonas vaginalis, Trichomonas hominis, Trichomonas tenax.

The class Zoomastigophora includes Protozoans that possess locomotory Organelles known as flagella (one or more), which are thread-like cytoplasmic projections. The flagella are located at the anterior end of the animal's body. The Base of the flagellum is invariably connected to the kinetoplast—an organelle that performs energetic Functions and contains a high concentration of DNA. In addition to the outer membrane, the body of flagellates is covered by a pellicle, giving it a fixed shape. Sometimes, a undulating cytoplasmic membrane is formed between the flagellum and the pellicle. The latter performs undulating movements and serves as an additional locomotory organelle. A number of flagellates also possess a supporting organelle, the axostyle, in the form of a dense cord running through the interior of The Cell. Nutrition in plant-like flagellate forms is autotrophic (characterized by the presence of chlorophyll) via Photosynthesis, whereas animal forms feed heterotrophically. Reproduction occurs primarily asexually (longitudinal division); sexual reproduction is also found in the majority of species. Most species exist in a vegetative form, while some are capable of forming cysts. They are widespread in marine and freshwaters, and many have transitioned to a parasitic lifestyle.

Among the genus Trypanosoma, three species are pathogenic to humans: Trypanosoma brucei gambiense (Gambian trypanosome), Trypanosoma brucei rhodesiense (Rhodesian trypanosome), and Trypanosoma cruzi.

Trypanosoma brucei gambiense, Trypanosoma brucei rhodesiense - causative agents of African trypanosomiasis (sleeping sickness).

Geographical distribution: Trypanosoma brucei gambiense - Central and West Africa; Trypanosoma brucei rhodesiense - East and South Africa.

Localization: Brain, CEREBROSPINAL FLUID, Liver, Spleen, Kidneys, Heart, Lungs, Bone Marrow, Lymph Nodes, serous membranes. The brain is predominantly affected.

Morphology: Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense have a tortuous shape tapered at both ends. Length is 30-40 µm. The stages parasitizing humans possess a single flagellum, an undulating membrane, and a kinetoplast. Three forms are distinguished: the trypanosome form (the membrane terminates at the anterior end of the body, the flagellum projects forward forming a long free end), the critidial (epimastigote) form (the flagellum originates anterior to The Nucleus, is directed forward, and forms a short undulating membrane and a free end), and the metacyclic form (similar to the critidial form, but lacking a free flagellum). Trypanosome movement is active, facilitated by the flagellum, undulating membrane, and body flexion.

Life cycle. A parasite of humans and mammals. The transmission mechanism is vector-borne. The source of infection consists of infected humans and animals. Trypanosoma brucei gambiense more frequently infects humans, pigs, and dogs; Trypanosoma brucei rhodesiense infects wild animals such as antelopes and rhinoceroses. The specific vector is the Blood-sucking tsetse fly: for Trypanosoma brucei gambiense, it is Glossina palpalis, which most commonly lives near human settlements; for Trypanosoma brucei rhodesiense, it is Glossina morsitans, which inhabits open savannahs and savannah woodlands. Consequently, sleeping sickness caused by Trypanosoma brucei gambiense occurs in anthropogenic foci of cultural landscapes. Annually, 10,000 new infection cases are registered. East African trypanosomiasis is less widespread and occurs in natural foci. Hunters, tourists, and seasonal workers are primarily affected, with about 1,500 cases annually. Outside the tsetse fly habitat range, African trypanosomiasis does not occur. According to recent data, humans themselves serve as the primary reservoir of the pathogen.

Fig. 45. General structural plan of a trypanosome (A) and appearance of a trypanosome in a blood smear (B):

1 - Cytoplasm; 2 - periplast; 3 - nucleus; 4 - blepharoplast; 5 - rhizoplast; 6 - free margin of the membrane; 7 - free end of the flagellum; 8 - undulating membrane.

The pathogen develops with a change of hosts. Upon entering the midgut of a tsetse fly with the blood of an infected human or animal, the trypanosomes (trypanosome form) begin to multiply intensively. After 15-20 days, the trypanosomes penetrate the Salivary Glands of the vector, where they gradually transform into the critidial and subsequently the metacyclic forms. Humans become infected when the saliva of an infected tsetse fly enters the wound during blood-sucking. Infective stage - metacyclic trypanosomes. Within 2-3 weeks, the pathogen spreads throughout all Organs and Tissues.

Pathogenic action: Trypanosomiasis is a vector-borne natural focal tropical disease accompanied by fever, Muscle weakness, exhaustion, fatigue, and lethargy. In the early stage, enlargement of lymph nodes (especially cervical ones) is observed. In the late stage, significant damage to the Central Nervous system occurs. The disease condition lasts for 7-10 years and, in the absence of Treatment, results in death. The clinical picture of Rhodesian trypanosomiasis is characterized by a more acute course. Without treatment, death occurs in approximately one year.

The parasitism of trypanosomes in mammals and humans is characterized by cyclic surges in infection intensity due to their multiplication, which is accompanied by Changes in the Structure and antigenic Properties of the parasite organisms. The Antigens they produce stimulate antibody formation in the host Organism. Under the action of Antibodies, most parasites perish, and the infection intensity decreases. The surviving trypanosomes shorten (trypanosome form) and begin to produce different antibodies. The trypanosome forms of the parasite that are infective to the tsetse fly acquire an elongated shape (metacyclic) again within its body, which is infective to humans. This alteration of body shape and modification of coat antigenic properties repeats numerous times. Thus, the parasite population within the host survives and evades the host's Immune Response.

The antigenic properties of the trypanosome surface depend on a single glycoprotein that completely covers the entire cell. The glycoprotein consists of 470 amino acid residues. Each wave of parasite multiplication represents a new population of trypanosomes possessing a novel surface antigen. These variations in antigenic properties help the parasite overcome the host's immunological response and make vaccination impossible for populations residing in natural foci of trypanosomiasis.

The modification of antigenic properties is ensured by changes in surface Glycoproteins encoded by different genes. A single clone of trypanosomes can alternately produce up to 100 different variant glycoproteins—this represents one of the parasite's adaptations to specific living conditions that enhances its survival.

Laboratory Diagnostics: Materials for laboratory diagnostics include BLOOD AND LYMPH node punctates in the early stage, and cerebrospinal fluid in the late stage; serological tests such as the Complement fixation test (CFT) and indirect hemagglutination assay (IHA) with diagnostic Reagents. Vegetative forms of trypanosomes are detected under a Microscope.

Prophylaxis: Personal prophylaxis involves protection against tsetse fly bites using repellents, nets, and prophylactic pharmacological agents to prevent infection. Public prophylaxis entails the eradication of tsetse flies using insecticides, alongside early detection and treatment of infected individuals.

Trypanosoma cruzi is the CAUSATIVE AGENT OF American trypanosomiasis, also known as Chagas disease.

Geographical distribution: Trypanosoma cruzi is found in Central and South America.

Localization: Cells of Internal Organs.

Morphology. In the blood, these trypanosomes reach up to 20 µm in length. The kinetoplast is large and rounded. A hallmark of the pathogen is its capacity for intracellular parasitism. The trypanosomes first invade macrophages of the Skin and mucous membranes, and subsequently infect Cells of the myocardium, neuroglia, and Muscles. Upon entry, they lose their flagella and undulating membranes, transforming into non-flagellated, or amastigote, forms. Multiplication of the parasites takes place here; these trypanosomes never divide in the bloodstream. Consequently, the infected cell becomes packed with amastigote trypanosomes and ruptures, releasing the parasites to invade neighboring cells. Some of these parasites transform back into flagellated forms and enter the bloodstream, from which they are taken up by the vector.

Life cycle. The vectors are triatomine bugs of the genera Triationa, Rhodnius, and Panstrongylus. Within these insects, the trypanosomes multiply and reach the infective stage, migrating to the hindgut. During blood-feeding, the bugs defecate onto the skin of a human or animal, and the trypanosomes enter the bloodstream through the wound. Definitive hosts, aside from humans, include armadillos, opossums, rats, monkeys, and domestic animals such as dogs, cats, and pigs. Infective stage: metacyclic trypanosomes.

Pathogenic effect. The disease predominantly affects young children, in whom it runs an acute course. In older individuals, the infection transitions into a chronic form.

The pathogenicity manifests as damage to the organs housing the proliferating parasites, typically resulting in myocarditis, meningeal Hemorrhage, and meningoencephalitis. Occasionally, the infection is mild and resolves spontaneously.

Laboratory Diagnosis — in the acute stage, trypanosomes can be observed in blood smears. Microscopy of lymph node punctates and cerebrospinal fluid is also performed. In chronic cases, patient blood is inoculated into guinea pigs, where large numbers of trypanosomes can be detected in the blood as early as 14 days post-inoculation. Immunodiagnostic Methods are additionally employed.

Prevention. Personal: protection against bug bites. Public: detection and treatment of infected individuals, and vector control using insecticides.

Trypanosomes are of profound scientific interest not only because they can cause severe, fatal human diseases.

Their exceptional ecological plasticity enables them to parasitize the host effectively for years in the face of continuous immune responses, allowing these parasites to successfully colonize new hosts.

Leishmania species are intracellular parasites and the causative agents of leishmaniasis. Several species are pathogenic to humans.

Dermatotropic (cutaneous) leishmaniasis. Causative agents: Leishmania tropica minor, which causes anthroponotic (urban) cutaneous leishmaniasis; Leishmania tropica major, the agent of zoonotic (desert) cutaneous leishmaniasis; Leishmania brasiliensis, responsible for mucocutaneous (American) leishmaniasis; and Leishmania mexicana, which causes cutaneous leishmaniasis.

Geographical distribution: Leishmania tropica minor is found in Central and Western India; Leishmania tropica major in Central Asia, Northern Afghanistan, Iraq, Iran, and Central Africa; Leishmania brasiliensis and Leishmania mexicana in South America.

Localization: Intracellular (monocytes, macrophages) within skin cells;

Morphology. Very small (2–4 µm, occasionally up to 8 µm) intracellular parasites. Their life cycle comprises two stages: 1) the non-flagellated (amastigote, or leishmanial) stage, which is rounded, 2–6 µm in diameter, with a spherical nucleus occupying up to 1/3 of the cell, and a kinetoplast, found in humans and other vertebrates; and 2) the flagellated (promastigote, or leptomonad) stage, which is elongated and spindle-shaped, up to 10–20 µm in length, motile, with a flagellum of 15–20 µm, found in the vector insects (Fig.). Flagellated forms also develop in culture media.

Life cycle. Leishmaniases belong to the group of vector-borne infections. The natural reservoir for L. tropica minor is humans, whereas for L. tropica major it is rodents (gerbils, gophers, hamsters, etc.), which in nature may exhibit infection rates up to 70%. The sources of infection are infected animals and humans. Transmission is mediated by blood-sucking dipteran insects—sandflies of the genus Phlebotomus (specific vectors). Sandflies become infected when feeding on the blood of sick humans or animals. Within the first 24 hours, the ingested non-flagellated parasites transform into motile flagellated forms, begin to multiply, and accumulate in the Pharynx of the sandfly within 6–8 days. Transmission occurs via sandfly bites. When an infected sandfly bites a human or animal, motile leishmaniasis parasites from its pharynx enter the wound and subsequently invade skin cells, where they transform into amastigote forms. Infective stage: the flagellated leptomonad form of Leishmania.

Pathogenic effect. Painful, slow-healing ulcers (persisting for about a year) develop at the site of the bite (on exposed areas of the body, primarily the face), leaving scars upon healing. Individuals who recover develop lifelong Immunity. In animals, the disease similarly manifests as skin ulcers.

In mucocutaneous (American) leishmaniasis, caused by L. brasiliensis, a small ulcer forms at the bite site and heals, leaving a characteristic scar. Several weeks or months later, multiple metastatic ulcers appear on the mucous membranes of the Nasal cavity, Mouth, pharynx, and Larynx. These ulcers enlarge and progressively destroy not only soft tissues but also Cartilage (such as the Nose). Without treatment, the condition persists for years and ultimately proves fatal due to secondary bacterial infections.

Fig. 46. Leishmania species:

a) leptomonad (flagellated) form; b) leishmanial (non-flagellated) form; 1 - flagellum; 2 - nucleus; 3 - nucleus of a tissue cell infected with Leishmania

Laboratory diagnosis — detection of Leishmania under a microscope in smears of scrapings from skin ulcers. In mucocutaneous leishmaniasis — identification of Leishmania in biopsy material or ulcer exudate smears.

Prevention. Personal: protection against sandfly bites, and prophylactic vaccination using strains of cutaneous leishmaniasis from animals applied to covered areas of the skin. Public: vector control targeting sandflies and the eradication of natural reservoirs (rodents) in areas adjacent to human settlements.

Visceral leishmaniasis. Causative agents: Leishmania donovani, the agent of visceral leishmaniasis (Indian kala-azar); Leishmania infantum, the agent of visceral (Mediterranean) leishmaniasis.

Geographical distribution: Leishmania donovani — India, Pakistan, Northeastern China, Nepal, Bangladesh; Leishmania infantum — Mediterranean basin, Middle East, Central and South America.

Localization: cells of the liver, spleen, Cytology/practical/86.html">Red bone marrow, and lymph nodes (Mediterranean leishmaniasis).

Morphology. In terms of morphology and life cycle, they are almost indistinguishable from dermatotropic leishmanias. They exist in leishmanial and leptomonad forms.

Life cycle. The vectors are sandflies of the genus Phlebotomus, which become infected from humans and dogs suffering from leishmaniasis, and in the wild, from jackals, gerbils, porcupines, and other animals belonging to the dog and rodent families. When a human or animal is bitten by an infected sandfly, motile leishmanias emerge from its pharynx into the wound and subsequently invade the cells of internal organs. The infective stage is the leptomonad form of leishmania.

Pathogenic effect. Visceral leishmaniasis (Mediterranean) predominantly affects children due to their weaker immune systems. Following an incubation period ranging from several weeks to several months, patients develop a fever, lethargy, adynamia, pallor, and loss of appetite. The lymph nodes, spleen, and liver enlarge, resulting in a markedly protruding abdomen. Anemia and severe weight loss develop. The disease lasts for several months and, in the absence of specific treatment, is fatal.

Laboratory diagnostics. The definitive diagnosis of visceral leishmaniasis is established by detecting leishmania via microscopy of bone marrow smears. In the preparation, leishmanias may be found in clusters or singly, either intracellularly or extracellularly. In some cases, bone marrow material is cultured on a nutrient medium prepared from Agar supplemented with defibrinated rabbit blood. In positive cases, flagellated forms of leishmania appear in the culture on days 2–10.

Prevention. Personal: individual protection against sandfly bites. Public: detection and treatment of infected individuals, vector control, treatment (or elimination) of infected dogs, and health education.

To prevent all types of leishmaniasis, control measures against sandflies are implemented, along with precautions to protect people from sandfly bites.

Lamblia. Lamblia intestinalis is the causative agent of giardiasis. The parasite was first described by the Russian scientist D.F. Lambl (1859).

Geographical distribution: worldwide.

Localization: duodenum; may also penetrate the biliary tract.

Morphology. Giardia exist in a vegetative form (trophozoite) and are capable of forming cysts. The vegetative form is active, motile, and resembles a longitudinally sliced pear; the anterior end is broad and rounded, while the posterior end is narrow and pointed. A characteristic feature is bilateral Symmetry of the body. All organelles are paired. There are four pairs of flagella. Two supporting filaments, the axostyles, run through the center of the body, with two nuclei located symmetrically on either side of them.

Fig. 47. Giardia (Lamblia intestinalis):

a) ventral view: 1 — two nuclei; 2 — flagella; 3 — two axostyles; 4 — adhesive disc; b) lateral view (On the surface of an epithelial cell); c) cyst.

On the ventral surface of the body, There is a depression—the adhesive disc—by which the parasite attaches to the intestinal mucosa. The anterior end of the body is rounded, and the posterior end is pointed. The length is 9–18 µm. They reproduce by longitudinal fission. They feed osmotically on substances that accumulate in the zone of membrane Digestion. In the lower PARTS OF THE intestine, they form cysts, which are non-motile, oval, tetranucleate (4-nucleated) forms. A characteristic feature of the cyst is a thick wall, often detached from the cytoplasm. Cysts are resistant to environmental conditions and can remain viable for up to a month.

Life cycle. Infection with giardiasis occurs through the ingestion of cysts. The main factors of transmission are unwashed hands, toys, vegetables and fruits contaminated with cysts, and Water. The infective stage is the tetranucleate cyst. Once ingested into the intestine, the cysts transform into vegetative forms. Each cyst gives rise to two vegetative forms. Giardia parasitize the upper sections of the Small Intestine, attaching to its villi using the adhesive disc. Giardia do not inhabit the Gallbladder. They are frequently found during duodenal intubation because they enter the Contents of the duodenal walls. Vegetative forms are not excreted in feces (although they may occasionally be observed in freshly passed stool during diarrhea). Upon reaching the lower intestine, Giardia encyst and are excreted into the external environment with feces.

Pathogenic effect. The parasites disrupt membrane DIGESTION AND ABSORPTION, particularly of fats and Fat-soluble Vitamins, contributing to The Development of vitamin deficiency. The course of giardiasis can be acute, chronic, or frequently asymptomatic. Patients experience nausea, eructation, epigastric pain, flatulence, and diarrhea. The source of infection is an infected person or a cyst carrier.

Laboratory diagnostics. Detection of cysts in feces or vegetative forms in the duodenal contents obtained via intubation.

Prevention. Personal: thoroughly washing vegetables and fruits consumed raw; thermal Processing of food and drinking water; control of flies and cockroaches, which disseminate cysts; washing hands before meals. Public: detection and treatment of patients, Sanitary supervision of water supply sources and public catering establishments, and health education.

Trichomonads. There are three species of trichomonads in The Human Body: Trichomonas hominis (intestinal trichomonad), Trichomonas vaginalis (urogenital/vaginal trichomonad), and Trichomonas tenax (oral trichomonad).

Urogenital (vaginal) trichomonad (Trichomonas vaginalis) is the causative agent of urogenital Trichomoniasis.

Geographical distribution: worldwide.

Localization: in women—the Vagina, greater vestibular (Bartholin's) glands, Ureters, and Urinary Bladder; in men—the Urethra, Seminal Vesicles, and prostate.

Morphology. It parasitizes exclusively in the human body and has no free-living stages. The body shape is oval, pear-shaped, or spindle-shaped, reaching a length of 15–20 µm. The nucleus is spherical and located at the anterior, broadened end of the body. Anterior to the nucleus emerge four free flagella and an undulating membrane. An axostyle runs along the axis of the trichomonad, protruding at the posterior end of the body like a spike. The trichomonad feeds on Bacteria and leukocytes. It reproduces by binary fission. It exists solely in the vegetative form (trophozoite) and does not form cysts.

Life cycle. The source of infection is an infected person. The infection rate increases with the onset of Puberty. Transmission occurs sexually, as well as through shared undergarments and personal hygiene items. Infection is also possible during gynecological examinations via insufficiently sterilized instruments and gloves. Transmission can originate from symptomatic individuals with pronounced clinical signs as well as from asymptomatic carriers. The invasive stage is the trophozoite.

Pathogenic effect. It induces inflammatory processes in the reproductive tract. In women, acute cases are typically characterized by excessive, watery, seropurulent discharge, along with itching and burning in the vulvovaginal region. In men, the disease is predominantly asymptomatic.

Laboratory diagnosis: identification of vegetative forms in native and stained smears from the vagina, urethra, and cervix, and less frequently in urine sediment. Both male and female carriers are typically asymptomatic with no signs of urogenital inflammation; however, laboratory analysis reveals the presence of vaginal trichomonads.

Prevention. Personal: avoiding casual sexual encounters and using condoms. Public: treatment of infected individuals and sterilization of gynecological and urological instruments.

Intestinal trichomonad (Trichomonas hominis) — the causative agent of intestinal trichomoniasis.

Geographical distribution — ubiquitous.

Localization — Large Intestine.

Morphology. Measures 5-15 micon in size, oval-shaped with a pointed projection at the posterior end. Three to four free flagella extend from the anterior end, directed forward, while another flagellum is directed backward and connected to the undulating membrane. A supportive rod (axostyle) runs through the middle of the body, with its tip protruding at the posterior end. There is a single nucleus (fig.). It feeds on bacteria engulfed through the cytostome (cell mouth) and absorbs liquid nutrients osmotically. Reproduction occurs via longitudinal fission. Cyst formation has not been established. Infection occurs through food and water contaminated with vegetative forms of trichomonads.

Pathogenic effect. Pathogenicity has not been established. It is found in both healthy individuals and those with gastrointestinal disorders.

Laboratory diagnosis. The sample for analysis is feces. Vegetative forms are identified microscopically in fecal smears.

Prevention — identical to that of amebiasis.

Fig. 48. Trichomonads: a) Trichomonas hominis; б) T.vaginalis:

1 - nucleus; 2 - flagellum; 3 - undulating membrane; 4 - axostyle.

Oral trichomonad (Trichomonas tenax) — structurally similar to the intestinal trichomonad. It does not form cysts. Its pathogenic significance has not been proven. They can be observed in the sputum of patients with pulmonary disorders, as well as in individuals with oral conditions (gingivitis, periodontitis, dental caries).