GAMARRA ANDREA RODRIGUEZ ROSA SCHOOL OF MEDICINE UNIVERSITY OF CARTAGENA CARTAGE NA COLOMBIA PARASITES Any organism, including viruses

, bacteria, protozoa or helminths, which depend o n a host for survival. CLASSIFICATION OF PARASITES • Optional: you can live free or parasites. • Mandatory: are totally dependent o n the host. • Ectoparasites: living on the outside of the host (infestation) • e ndoparasites: living within the host (infection) • Monoxenos: inhabiting a singl e host. • heteroxenism: various hosts. • • • • Hosts The animal receives its definitive parasito.parasito: q is the host has to adult stage or in which reproduces sexually. Intermediate: q is the guest has th e parasite in larval or which reproduces asexually paratenic: or carrier, is the larval q has not developed. Reservoir: those containing parasites that can live and multiply in and be a source of infection to a susceptible host. Vector: art hropod or other invertebrate animal that transmits the parasite to the host. are just mechanical carriers of the parasites or biological when they are multiplie d in it • PARASITES OF Protista • PARASITES OF THE UNITED protists (protozoa) Morphology: - Unicellular. - Mobile. (Trophozoite) - Form of resistance. (Cyst) - Organelles : membrane, cytoplasm (ectoplasm and endoplasm), Food and excretion vacuoles, mi tochondria, single core. Physiology: - Food and phagocytosis by osmosis. - Anaer obic or aerobic respiration. Reproduction - Asexual: binary division multiple di vision. - Sexual by differentiation into gametes, F or M and other sexual mechan ism is the conjugation. Locomotion: - rhizopods: have pseudopods. - Flagellates: with flagella. - Ciliates: with cilia - Sporozoa: it has no organ of locomotion . • • • Amoebiasis (Entamoeba histolytica) • The mobile trophozoite emitted when a pseudopod through which it travels. • ka ryosome Nucleus with chromatin in the center and uniformly sized granules regula rly arranged. • How to transition or prequiste is round or oval, immobile, with a cystic membrane formation. • Thick rounded cyst with 1-4 cores inside. LIFE CYCLE grow and divide by binary fission Each core is surrounded by cytoplas m: 8 trophozoites Trophozoite in light of the colon, invading the intestinal wall. prequistes are immobilized and form. Acquisition of Housing and immature cysts. tetranucleadoa cysts.

with a nucleus. It is divided into two: metacyclic trophozoites, with 8 cores break into the sma ll intestine and trophozoites originating Ingestion of cysts Elimination in feces with the same # of cores that survive wk or months and are spread by water, hands, arthropods, food items Cyst carriers are the source of infection The oral cysts come E. HISTOLYTICA: LIFE CYCLE Cysts contaminate water, vegetables, hands, flies ... Intestinal amebiasis Extraintestinal amoebiasis Removing the stool Paracito The cysts are more resistant than trophozoites PATHOLOGY of amoebiasis Adhesion of lectins lithic to colonocytes Penetration through muscularis mucosa, submucosa, muscular *, serosa Dissemination extraintestinal amoebic Pleuropulmonary contiguity, peritoneal, skin, mucous Hematogenous spleen, kidney, brain, liver Amoebic colitis -Abdominal pain, diarrhea and tenesmus-Anorexia-Enflaquecimeinet or Principalmen you by E, dispar Acute: Great # of bowel movements, rectal and push ed Sputum Chronicle: "Abdominal pain, change in the rate of defecation. Asymptomatic amebiasis (75%) Parasites in light of colon Intestinal invasive amebiasis: Amebiasis CLINIC Ameboma: lesion in the colon tumor TO amoebic appendicitis treatment Metronidazole Etofamida dihydroemetine secnidazole Luminal Tissue Action Action DIAGNOSIS OF stool immunology intestinal amoebiasis

Biopsies of intestinal ulcers Serology BALANTIDIOSIS (Balantidium COLI) • • • • • • • • q larger Protozoa affect humans. Oval trophozoite. Surrounded by cilia. Ant cytosome mouth or feeding with long cilia. Food waste disposed of by the citopigio contractile vacuoles (some post). Binucleate, macronucleus and mi cronucleus. Reproduction by fission, budding and conjugation. MenB double thick cyst. It is the infectane. BALANTIDIOSIS (Balantidium COLI) LIFE CYCLE • trophozoites live in the large intestine in the light or in t he mucosa (ulceraciones. • Previous experience encysted in the intestinal lumen and out with the stool.€• After the membrane ingested each cyst ruptures and lea ves a trophozoite. Mucosal inflammation Asymptomatic Balantidiosis Parasites in lumen. Intestinal invasive balantidiosis: Mucosal ulceration, "irregular shape. -Hyperemia. Fund-necrotic. PATHOLOGY Intestinal perforation and invasion Appendix rare Balantidiosis genital pulmonsr hepatica. Few cases CLINICAL -More severe symptoms. -3 To 12 days. "Chronic diarrhea, Indigestion, Anorexia a nd fever. "Diarrhea. 5-10 times. "Excessive fluid loss. "The parasites disappear -malabsorption syndrome. , Between June 4th sem-pulmonary dissemination Fecal-oral infection. "Contamination of hands and vegetables, water. "Zoonoses c ommon. "Self-limiting diarrhea, does not require treatment unless the patient wi th immune deficiencies. Immunocompetent Patients Immunocompromised Patients EPIDEMIOLOGY TREATMENT • Trophozoite of pyriform shape. • In the ant has two cores q binds to each othe r in the middle. • It has a suction cup or cavity q occupies half of your body a nt with q fixed to the mucosa. • It has four flagella emerging from a central ba r or axostyle 2b. • The trophozoite is capable of translational motion, slow, vi bration and rotation. • The cyst is oval-shaped membrane 2b, 2-4 cores and aosti lo. Giardiasis (Giardia intestinalis) Giardia lamblia CYCLE

Trophozoite (set in duodenal mucosa) Division binary 4 Trophozoites x cyst (Int.delgado) Oral CYSTS (lumen) Trophozoite (lumen) Viable in moist soil or water for several months CYSTS (feces) Dogs Cats Ruminants ATOLOGIA OF GIARDOSIS SETTING trophozoite (intestinal mucosa) and duodenum and jejunum Principalment Mechanical action on mucous Mechanical barrier CATARRHAL INFLAMMATION Malabsorption syndrome "Villus atrophy, inflammation of the lamina propria or alterations in epithelial cells BENIGN whole picture TREATMENT OF THE GIARDOSIS quinacrine (USA) 5-nitro imidazole derivatives: metro nidazole Ornidazol secnidazole Tinidazole Albendazole LEVE: slight epigastric pain, defecation rhythm disturbance MODERATE : duodenitis, flatulence, diarrhea CLINICAL SEVERE: Duodenitis, steatorrhea, flatulence, diarrhea abundant and fetid DIAGNOSIS OF GIARDOSIS Serial stool Capsule Beal (Entero-test) Intestinal biopsy Blastocystosis (Blastocystis hominis) CLINICAL MORPHOLOGY NES-Diarrhea manifestations. -Abdominal pain. "Nausea. -Cram ps. -Anorexia. -Flatulence. -More pathogenic in immunosuppressed patients TREATM ENT -Form-A few spherical nuclei, are played by: .. .. sporogony fission, plasmotomi a .. .. endodiogonia. 5nitroimidazoles derivatives. Chilomastix mesnili • found in the colon of humans and animals without being pathogenic. • Trophozoi

te piriformis with limb post. Acute and curve. • Mobility given by four flagella . • round or pear-shaped cyst, 2b thick membrane and a nucleus. • The cysts are infectious when entering by mouth. • Only in immunocompromised patients can reac h serpatogeno. Trichomoniasis (Trichmonas vaginalis) • 4 Flagella, ovoid or pear-shaped, large nuclei. • It feeds on bacte ria and other particles. • Grows under anaerobic conditions. • Reproduction by b inary fission and has no cyst. • Sexually processed. PATHOLOGY OF Trichomonas vaginalis ADHESION OF RECEIVERS Predisposing factors of trichomoniasis (Lactoferrin) DESTRUCTION OF VAGINAL MUCOSA Increased vaginal pH Bacterial Flora (b. Doderlein) decreased estrogen deficienc y THE CLINIC IS Trichomonas (WOMEN) S OF VULVA, perineum and thighs SA CLINIC Trichomoniasis (MAN) Asymptomatic MORNING SECRETION Metronidazole Tinidazole Ornidazol secnidazole Trichomoniasis TREATMENT Treat partner CRYPTOSPORIDIOSIS parvum) (Cryptosporidium • It is an obligate parasite. Apicomplexa intracellular • You can only grow in a live host and multiply in the environment. • infects hu mans and animals like cattle and sheep and sometimes dogs, cats, rodents, birds, etc.. • It is commonly found in lakes, rivers, especially contaminated with sew age and animal wastes. LIFE CYCLE Infection of reservoirs or man Oral infection 5. Reproduction b.Ooquiste intestinal infectious. c. Desenquistación d.Esporozoi to. e. Merogony of 1 generation. f. Reinvación by merontes. g.Merogonias 2nd gen eration. h.Miccrogametocito. i. microgamete,. j. K. Mcrogameto Zygote l. oocyst VAGINAL FOAM FLOW, ABUNDANT, smelly REDNES Itching and burning red dots OF VAGINAL MUCO

1 4 5 3 Oocyst in stool output. 2 Invasion of the small intestine Microvellosidade s atrophy PATHOLOGY Enlarged crypt Mononuclear cell infiltrate in mucosa and lamina propria Increased intestinal infection in the jejunum. SIGNS AND SYMPTOMS • • • • • In immunocompetent persons, the time between onset of symptoms and the elimination of oocyst in the faeces is 18 days. The duration of symptoms is one to three weeks. Symptoms include watery diarrhea, nausea, vomiting, headache, f atigue, anorexia and / or intestinal cramps. The infection can occur in children and newborns and if there is dehydration, death ensues. Malnutrition accompanie d by infection, the favors or the cause. DIAGNOSIS Microscopic observation of oocyst in feces Other A. Inmunofluorescenci Staining Kinyoun stain ZiehlNeelsen Most used ELISA TREATMENT latex agglutination. Self-limiting in immunocompetent In immunosuppressed no effective drug Cyclosporiasis (Cicloespora cayetanensis) • alcohol acid resistant oocyst. • in each oocyst has 2 sporocysts, each with tw o sporozoites. • The diff of cryptosporidium which has four loose inside the ooc yst sporozoites. • The diff from other coccidia that have 4mesporozoito within e ach oocyst • Reproduction by fusion of gametes or merge multiple. Life cycle of Cyclospora Multiple fission

4 sporozoites Ingestion I MERONTES 8-12 merozoites . MERONTES II 4 merozoites Microgametocytes Sporulated oocyst Sporulation 7 - 12 days Multiple fission Macrogameto Microgametes Lee Oooquiste not sporulated PATHOLOGY DUODENAL PARASITE CLINICAL Immunocompetence AIDS diarrhea, anorexia, weakness absorption deficiency, flatulenci to symptomat ology logy is more intense and prolonged Villous atrophy and crypt hyperplasia DIAGNOSIS Ziehl-Neelsen staining of oocysts in feces TREATMENT Ol TrimetoprimSulfametoxaz ISOSPOROSIS (Isospora belli) • oval oocyst helisoidal. - Immature oocyst: a kernel will not infectnates. - Ma ture oocyst: two nuclei of the infection. • It is easy to see the cysts without coloring. • Man is the only definitive host. • It is found in small intestine. • sexual and asexual reproduction. • When released in the form of oocyst. Maturation in immature oocyst environment Ingestion of oocysts mature. Desenquistació n in duodenum Release of sporozoites Union and zygote formation

Invasion of enterocytes Step by micro and macro Dif gametes to male and female gametocytes Asexual reproduction: formation of merontes Rupture of merontes: release of merozoites CLINICAL PATHOLOGY mucosal flattening and necrosis. Chronic diarrhea Destruction of enterocytes. Asymptomatic eosinophilia-inflammatory reaction. -Self-limiting . -Watery diarrhea. -High eosinophilia. "Commitment of lamina propria and Immuno competent lifaticos Omet immunocompromised DIAGNOSIS TREATMENT ZiehlNeelsen staining of oocysts Ol TrimetoprimSulfametoxaz Microsporidiosis (Microsporidium) • opportunistic intracellular pathogens. • Stationary. • Stay in the gut can pas s into the blood by macrophages. • susceptible to attack by the immune system in immunocompetent patients. • proplasma Injection System. LIFE CYCLE Pathology • granulomatous lesion. • Cell Infiltration Mo, L and plasma around a necrotic c enter. I immunosuppressed patients • Atrophy • Flattening of villi enterocytes. Granulomas are produced and cell destruction. Ion Diseminaci Myocardial Kidney Liver Lung CNS Cornea Clinical It depends on the parasite and location Co diagnosed Identification of spores in secretions. • Giemsa stain. • Hematoxylin-eosin stain Ziehl-Neelsen • • • Fluorescence Trocr omica amended. NO DRUG EFFECTIVE MALARIA (Plasmodium falciparum, vivax. Malariae and ovale) • Via contagion anopheles mos quito. • The two main humans are affecting p. falciparum and P. Vivax. • In Apri l circulating blood parasite forms: trophozoites, ezquizontes, merozoites, gamet ocytes PATHOLOGY OF MALARIA Loss of elasticity ERYTHROCYTE cytoadherence Decrease Fragility transp.

Release of O2 tox. and Ag Spleen, liver, bone marrow, brain ANEMIA Chill REST FOOT CLINIC OF MALARIA sweats Leukopenia BENIGN quartan fever (P. malariae) FEVER benign tertian (vivax and ovale: 5-15) Less common than benign tertian Recrudescence tendency to chronicity Incubation: 4 weeks Relapses in vivax by hypnozoites SEVERE Malignant tertian (falciparum, 15 days) (Not complicated) ACUTE Cerebral Insuf. emia Hyponatremia Severe Renal Anemia Edema Pulmo. Jaundice Hypoglyc dark pigmentation Tissue damage

Thick DIAGNOSIS OF MALARIA Extended Probes, PCR Immunology (Epidemiology) CHEMOTHERAPY antimalarial quinacrine Species oroquine Primaquine Quinine Tetracycline Sulfonamides TREATMENT OF MALARIA Stage Susceptibility Toxoplasmosis (Toxoplasma gondii • Morphology of a crescent. • tachyzoites: flagellates, are multiplying rapidly. • In chronically infected cysts predominate. • bradyzoites (from hundreds of cy sts). Multiply slowly. Without flagellum Cycle of Toxoplasma gondii Female Ingestion Of Tachyzoites S bradyzoite cyst Bloodstream via the lymphatic Ep. int.delgado Ooq. mature 2 days Nal extraintestinal Chl

Schizogony Lee Oocyst Macrogametocytes Macrogameto Merozoites schizonts 25 days Microgametes microgametocytes Cysts in humans Retina Chorioretinitis-ant-granulomatous uveitis Esqulético Muscle Brain "Focus of necrosis. Reaction-inflammatory glial nodules Myocardial -Cell destruction Asymptomatic TOXOPLASMOSIS ACUTE TOXOPLASMOSIS "Fever of septic. -Sore throat, cough, expectoration. - Gastrointestinal disorde rs (severe) CLINICAL Lymphnode toxoplasmosis + Common-clinical form. -Poly septic fever of nodes. -Node size, hard and painfu l. "Anemia, leukopenia, linfomoocitocis. OCULAR TOXOPLASMOSIS "For prenatal infection. -Chorioretinitis. - Severe cases of retinal detachment. CONGENITAL TOXOPLASMOSIS rimestre 1 º º Trimestre3 quarter2 Irreversible consequences Acute Encephalitis Generalized infection DIAGNOSIS • Diagnostic parasitology • Inoculations • Title • antibody • ELISA • IFI indire ct hemagglutination (CSF, lymph, bone marrow) sulfadiazine primetamina spiramycin CONGENITAL PREGNANCY TREATMENT

GENERAL • Proof of Sabin and Feldman • Complement Fixation • Toxoplasmina sulfa pyrimethamine clindamycin Trypanosomosis CHAGAS DISEASE Transmitted by insects of the Reduviidae family Trypanosoma cruzi Trypomastigote (Circulating) -Flagellate. -Elongated, fusiform-pleomorphism. Amastigote (intracellular Nests) -Rounded or oval. Binary-Division. "Without scourge. LIFE CYCLE OF TRYPANOSOMA CRUZI Sting 2 0 d i a s Epimastigotes Esferomastigotes metacyclic Infective Amastigotes Other cells CHINCH Circulating trypomastigote amastigotes 7-14 days WASTE VERTEBRATE CHRONIC FORM "Heart damage, digestive or neurological. "Myocarditis, viseromegalia. "Chronic myocarditis. -Meningoencephalitis. ACUTE FORM (8-10 wk) -Chagoma inoculation. -Inflammatory nodule. Roman-Linfoadepatia sign. "Febrile s yndrome. Disemnacion lymphatic-spleen, liver, and MO CONGENITAL FORM CLINIC "Uncommon. "It may be asymptomatic. Hepato-and splenomegaly without fever. -Meni ngoencephalitis. Cutaneous and cardiovascular-deletions Indeterminate -O latent phase. -Asymptomatic. "Months or years Traditionally difficult TREATMENT OF CHAGAS

Benznidazole Nifurtimox Leishmaniasis (Leshmania) • Atropozoonosis by infected insects. • amastigotes: rounded, without flagella w ithin macrophages of vertebrates. • promastigotes: within the spineless, elongat ed, flagellated. LIFE CYCLE Leishmania Rupture Macrophages amastigotes viscera Phlebotomus sandfly Lutzomyia 10 days VERTEBRATE Skin or mucous Infective promastigotes Cutaneous leishmaniasis CLINIC Boiling PRINGADURA BUTTER Chronic vegetating Very chronic ulcer of the chicle Spontaneous Healing macule Papules or pustules ULCER Mucous membrane Fuzzy L. Tropica (East Button dry type) L. Urbana: antropnótica L. Aethiopica (Middle Button, diffuse) mucocutaneous THE OLD WORLD CUTANEOUS LEISHMANIASIS L. Major Middle Button or wet type l. Rural Skin (zoonotic) CLINICA DE LA LEISHMANIASIS VISCERAL DEATH BITES NEWS FLASH LIGHT SKIN Skin Asymptomatic INVASION OF SRE Spontaneous Healing DIAGNOSIS of leishmaniasis • LIVE REVIEW: ULCERS • Biopsy • CULTURE • intradermal MONTENEGRO • PCR • ELISA Sales glucantime pentavalent antimony, Pentostam) Amphotericin B

Helminths: Nematodes and flatworms • Morphology: - multicellularity. - Nematodes: Body cylindrical hollow body and di gestive tract full. - Platyhelminthes: flattened body without gut body cavity an d rudimentary - Organs of fixation with hooks or suckers. - Some have a cuticle resistant to digestive juices of the host. - Pseudocele (fluid-filled cavity whe re are the bodies). - Glands with lytic secretions to pass through the tissues. - Hermaphroditic breeding system. - Oviparous. - Excretory system of collecting ducts q simple flow abroad. - Rudimentary nervous system. Source movements and s timuli.€- Facultative anaerobic respiration. Helminths: Nematodes and flatworms (R. animalia, SR. Metazoans) • Physiology: ANIMALIA (United) METAZOA (Subkingdom) Nematodes (phylum) Platyhelminthes (phylum) VIA ACQUIRED BY INTESTINAL NEMATODES DIGESTIVE Enterobius vermicularis (threadworm) Trichuria Trichuris (whipworm) Ascaris lumbricoides (Ascaris) INTESTINAL NEMATODES ACQUIRED DERMAL Ancylostoma duodenale Necator americanus (hookworm) Strongyloides stercoralis Ascariasis (Ascaris lumbricoides) • largest intestinal nematodes. • The sexes differ in the rear area. (Female: st raight, male-curve. • Adults are not setting bodies and live in the intestinal l umen to the wall sustained muscle. • Average life of one year. Spontaneous Heali ng. • fertile eggs from females are fertilized and Round 3 member. The infertile females produced fertilized were elongated with protrusions. • The presence of eggs in the stool is of diagnostic importance. Life cycle of Ascaris lumbricoides Egg Egg Stool embryonic adult DELGADO I. Larva. HEART PHARYNX Sist. Venous or ly mphatic hatching (Int.delgado) LARYNX LUNGS Pathology LUNG -Rupture of capillaries and alveolar wall. -Hemorrhage and inflammation. In mass -produces Loeffler's syndrome. (Multiple alveolar injury)

INTESTINE -Irritation of the mucosa. "In abundance are intertwined and create obtruccion. Biliary Tract "Biliary obstruction. -Cholangitis. When they lay eggs that reach the liver pare nchyma produce foreign body granulomas. Or peritoneal Step-by the parasite through intestinal perforations. CLINICAL Respiratory "A simple cold. -Cough, expectoration fever. -Eosinophilia, allergic manifestati on. -Grave: Loeffler's syndrome OTHER BODIES L INTESTINE "Diffuse abdominal pain. -Diarrhea, nausea, vomiting. Abdominal swelling. Abdomi nal mass obstruction. S NUTRITION -Anorexia. Items consumed by the parasites. Brain, eye Various neurological signs such as seizures. Chemotherapeutic treatment against Ascaris Pyrantel pamoate Piperazine (Flubendazole Albendazole, mebendazole, levamisole) Benzimidazoles ARTHROPODS ARTHROPODS • Morphology and Physiology - Invertebrates. - Chitinous exoskeleton. - Body bil aterally symmetrical articulated. - Circulatory system: hemolymph-filled hemocoe l - nodal rudimentary nervous system. - Digestive and well-developed senses. - G ender separated with complete or incomplete metamorphosis. Rating: - Insecta: mo st important in medicine. Three pairs of legs. - Arachnida: spiders, scorpions, ticks and mites. Four pairs of legs. - Crustacea: very little medical importance . Cyclops. •