Parasitology Summary PDF

Studies the organisms (parasites) that live in or on other organisms Parasite: It is a living organism, which lives in or upon Endoparasite:...

Studies the organisms (parasites) that live in or on other organisms Parasite: It is a living organism, which lives in or upon Endoparasite: (hosts) and with the host-parasite relationship especially parasitism. Host: an organism, which harbours the parasite and provides Pasasitology @shatha Parasite: another organism (host) and derives nutrients directly from it, without giving any benefit to the host. Exoparasite: nourishment and shelter. - They live within the body of the host. They inhabit the surface of the body of the host. (ticks and mites) 2 V Protozoan Helminthic (Unicellular) (Multicellular) These are worm parasites. They are larger and more complex than protozoans. Sarcodina Mastigophora Sporozoa Ciliophora (Amoeba) (Flagellates) (Adult stage non-motile) (Cilliates) Nemathelminthes (Round worms) Intestinal pathogenic Amoeba Free-living Amoeba Giardia lamblia Tryponasoma burcei complex one of the most common parasitic # three subspecies: Entamoeba histolytica Naegleria fowleri diseases, causing intestinal T. brucei gambiense: causes West African sleeping sickness disease and diarrhea. T. brucei rhodesiense: causes of East African sleeping sickness “the brain-eating amoeba” > - trophozoitee T. brucei brucei: causes a disease affecting cattle in Africa site-procest found in warm fresh water, such as tropho ponds, lakes, rivers and hot springs. Strophozoite Gust , > cyst > - cyst Host: Single host. Infective form: Mature cyst. Mode of transmission: Ingestion of food and Host: Two hosts. Host: Single host human. water contaminated with mature cysts. -Vertebrate host is man and other animals. Infective form: Mature quadrinucleated cyst. Host: Single host human. -Invertebrate host is the tsetse fly (genus Glossina). Mode of transmission: Feco-oral route: By ingestion of Infective form: Amoeboid form is the invasive form & the Pathogenesis: -Both male and female flies bite man. contaminated food or water with mature quadrinucleated cysts usual infective form of the parasite. The spectrum varies from asymptomatic Infective form: The trypomastigote forms are found in carriage to severe diarrhea and malabsorption. salivary gland of tsetse fly. Mode of transmission: By the bite of tsetse fly, Platyhelminthes Life cycle: Mode of transmission: Nasal contamination during 2 Malabsorption of fat trypomastigote forms are transmitted to the punctured swimming in fresh hot water bodies like ponds, river, Foul smelling profuse frothy diarrhea wound. swimming pools or lakes. Symptoms: diarrhea, abdominal pain, Pathogenesis: primary amoebic meningoencephalitis (PAM) bloating, nausea, and vomiting. In chronic giardiasis the symptoms are Pathogenesis: African trypanosomiasis (Flat worms) Acute suppurative infection of CNS. Infection occurs in two stages: recurrent, and malabsorption and debilitation 1. First-stage disease (hemolymphatic): nonspecific This name is to differentiate it from the secondary may occur. signs and symptoms: invasions of CNS caused by E. histolytica. -Intermittent fever, pruritus and lymphadenopathy. Diagnosis: -Posterior triangle cervical lymphadenopathy, or Usually occurs in healthy children Stool examination—detects cysts and or young adults with recent history of swimming in fresh hot water. trophozoites (Winterbottom’s sign) is commonly seen in T. b. gambiense infections. Routes of Transmission of Parasites? Cestodes Antibody detection in serum—ELISA Clinical course is acute: Molecular method—PCR Winterbottom's Fecal-oral Route: The most common mode sign- Initial symptoms: of transmission of parasites. -Changes in the taste and smell (due to olfactory nerve involvement) -Headache Infection is transmitted orally by ingestion (Tapeworms) [ 2. Second-stage disease:invade the CNS variety of -Anorexia (‫شهية‬ّ ‫)فقدان ال‬ of food, water, or vegetables contaminated Trophozoites and immature cysts can be passed in stool of amoebic patients, but they can’t serve as infective form as they are disintegrated in the environment or by -Nausea Trichomonas vaginalis neuropsychiatric manifestations: -Sleep disorders “African sleeping sickness”. with the infective stages of the parasite. gastric juice when ingested. -Vomiting The most common parasitic cause of This is fatal without treatment. -High fever -Signs of meningeal involvement like stiff neck. sexually transmitted diseases (STDs). Secondary symptoms: Pathogenesis: The majority of infections - lumen of the intestine (luminal -Confusion -Hallucinations Leishmania donovani Direct Skin Contact: Some parasites can amebiasis) are asymptomatic. -Lack of attention -Seizures (‫)نوَبات‬ enter directly through the skin. Amebic colitis, or invasive intestinal amebiasis, occurs when the mucosa is invaded. > Obligat a ar Mortality rate (about 98%), (Death occurs within 7–14 form Symptoms: Amoebic dysentery days after exposure) ↳trophozoite Insect Bites. Diagnosis: Sexual Transmission: Some parasites like Microscopy CSF >extracellular form Molecular methods—PCR those causing trichomoniasis are sexually Imaging methods—CT and MRI Infective/Diagnostic stage: trophozoite transmitted. Trematodes Trophozoites divide by longitudinal binary fission to give daughter trophozoites in the urogenital tract. Host: Two hosts. Acanthamoeba species Pathogenesis: Trichomoniasis -Vertebrate host (human, dog, rodents, etc.) -Insect vector (female sandfly) (Flukes) Trophozoites secrete proteolytic enzymes that cause In women: symptomatic. Infective form: Promastigote. destruction of the tissue, producing flask shaped ulcers on the The prominent symptom: Mode of transmission: by the bite of infected female vaginitis with a purulent discharge. intestinal mucosa. trophozoiteest sandflies mainly during the late evening or the night > - Large numbers of trophozoites are liberated along with blood It can be accompanied by: time. and mucus in stool producing amoebic dysentery. -vulvar and cervical lesions -abdominal pain Pathogenesis: Complications of severe chronic infections: -dysuria Leishmaniasis caused by the obligatory intracellular (peritonitis, perforations, and the formation of amebic -strawberry cervix protozoa of the genus Leishmania. granulomas (ameboma)). Small bright red lesions caused by tiny Primarily affects reticuloendothelial system of the host. Host: Single host human. haemorrhages on the surface of the cervix. Produce widely varying group of clinical syndromes Extraintestinal amebiasis Mode of transmission: ranging from self-healing cutaneous ulcers to fatal 1. Amebic liver abscesses are the most common manifestation lnhalational route by aerosol contaminated with In men: asymptomatic but, urethritis & prostatitis visceral disease. 2. Pleuropulmonary abscess cyst or trophozoite. can occur. 3. Brain abscess Direct spread through broken skin or infected eye Visceral leishmaniasis “kala azar - black fever”: (rarely). Diagnosis: Caused by Lishmania donovani Diagnosis: Direct microscopy (wet saline mounting) Dogs, cats and rodents are the main reservoirs. 1. Intestinal amoebiasis: Pathogenesis: Antibody detection (ELISA) Stool microscopy by wet mount:detects cysts and trophozoites Molecular method (PCR) The hallmark of visceral leishmaniasis is a triad of Granulomatous amoebic encephalitis (GAE): Stool antigen detection ELISA -In immunocompromised patients like AIDS patients. (fever, hepatosplenomegaly and pancytopenia). Molecular diagnosis PCR -Has chronic onset and progressively worsens over a Also, hyperpigmentation and ascites and hematological span of weeks to months. abnormalities are present. 2. Amoebic liver abscess Signs and symptoms are typical of Fatal if not treated. Serology antigen and Antibody detection: ELISA meningoencephalitis and encephalitis. Molecular diagnosis PCR Life cycle: Ultrasonography Keratitis: In healthy individuals, occurs: Promastigotes extracellula is - trauma V - contact lens use Phagocytosis by Diagnosis: macrophages > - skin Direct microscopy (Wet mount examination of CSF or conrneal scrapping) a Antibody detection Amastigote Molecular methods: PCR CSF examination: lymphocytosis Replication within macrophage Infect other phagocytic cells NEXT PAGE  Sporozoa (Adult stage non-motile) @shatha I Plasmodium species Toxoplasma gondii Cryptosporidium parvum Malaria is one of the oldest documented diseases of mankind. An obligate intracellular parasite affecting a wide range of mammals and An intestinal parasite affecting humans and different animals. birds including humans. Human infection is mainly caused by five species: Host: completes its life cycle (both sexual and asexual stages) in single host - Plasmodium malariae: causes quartan malaria. periodicity of fever is once in 72 hours, it recurs every fourth day Morphology: (man or other animals). - Plasmodium ovale: tertian malaria. It exists in three morphological forms: periodicity of fever is once in 48 hours, it recurs every third day Tachyzoite: actively multiplying form (trophozoite), seen in acute infection. Morphology: - Plasmodium vivax: causes tertian malaria. (Crescent shaped) Oocyst (thin walled and thick walled) periodicity of fever is once in 48 hours, it recurs every third day Tissue cyst: resting stage of the parasite, seen in chronic infections Sporozoites - Plasmodium falciparum: causes malignant tertian malaria. Oocyst: found in cats and other felines Trophozoites severe malaria, periodicity of fever is once in 48 hours, recurs every third day Infective stage: Oocyst is the infective form of the parasite as well as the - Plasmodium knowlesi: causes quotidian malaria. diagnostic form excreted in the faeces. fever periodicity is once in 24 hours, it recurs every day Thick-walled oocyst is infectious to other persons. Thin-walled oocysts can cause autoinfection. Mode of Transmission: Plasmodium falciparum: Host: two hosts: Definitive hosts: cat and other felines; where sexual cycle takes place - Ingestion of food and water contaminated with faeces containing thick- Intermediate hosts: man and other mammals (goat, sheep, pig, cattle and walled oocysts certain birds); where asexual cycle takes place. - By autoinfection: Thin-walled oocyst can infect the same host 1. Definitive host: Female Anopheles mosquito where sexual cycle takes place. Pathogenesis and clinical features: Humans can become infected by any of several routes: 2 2. Intermediate host: Man Anopheles mosquito where asexual cycle takes Four slender crescent Eating undercooked meat of animals harbouring tissue cysts. place. Consuming food or water contaminated with cat faeces or by contaminated shaped sporozoites are Benign malaria released from each cyst Benign malaria is milder in nature. environmental samples (such as faecal-contaminated soil or changing the - Infective form: The sporozoites are the infective form. litter box of a pet cat). Sporozoites invade the brush It is characterized by a triad of febrile paroxysm, anaemia and splenomegaly. border epithelium of the small Mode of transmission: Humans are infected by the bite of female Anopheles Blood transfusion or organ transplantation. intestine within which all the mosquito. Transplacental from mother to fetus. stages of development take place. Falciparum malaria (malignant Tertian malaria) Plasmodium falciparum possesses a number of virulence factors and its Life cycle: Life cycle : pathogenesis is different from other species. The disease is more acute and severe with more complications than the benign malaria. - In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. n b we a tsee can Febrile paroxysm is it under microscope Fever comes intermittently depending on the species. It occurs every fourth day (72 hour cycle for P. malariae) and every third day (48 Pathogenesis: hour cycle for other three species) Infection with Cryptosporidium spp. and genotypes results in a wide range Paroxysm corresponds to the release of merozoites into the bloodstream of signs and symptoms. Each paroxysm of fever is comprised of three stages: (1) cold stage Immunocompetent patients: (2) hot stage asymptomatic (3) sweating stage develops self-limiting watery non-bloody diarrhea Falciparum malaria (Malignant Tertian malaria) Cryptosporidiosis in Immunocompromised Hosts: High level of parasitemia Disease is more severe data Sequestration: An important feature of the pathogenesis of P. falciparum. chronic, persistent profuse diarrhea, leading to significant fluid and This leads to blockade of the blood vessels of deep visceral organs like brain, ② electrolyte loss. kidney, etc. Autoinfection by thin-walled oocyst is key factor for the chronic diarrhea Plasmodium falciparum possesses different virulence factors, and its pathogenesis · which maintains the infection. Immunocompromised patients may have more severe complications, such asexual is different from other species. as life-threatening malabsorption and wasting. alegametotset The disease is more acute and severe with more complications than the benign Extraintestinal cryptosporidiosis has been reported. ma malaria. snamite Complications of Falciparum malaria Cerebral malaria Occurs due to plugging of brain capillaries leading to Pathogenesis: In immunocompetent persons: vascular occlusion and cerebral anoxia an asymptomatic infection. Pulmonary edema and adult respiratory distress syndrome (sometimes flu-like symptoms or cervical lymphadenopathy) 2 ring stage Renal failure Severe jaundice Ocular toxoplasmosis: an important cause of chorioretinitis (acquired or reactivation) Laboratory diagnosis In congenital infection, patients are often asymptomatic until the second or Microscopic tests: third decade of life, when lesions develop in the eye. - Peripheral blood smear—Gold standard - Thick smear—more sensitive In immunodeficient patients: - Thin smear—species detection (due to newly acquired or reactivated latent infection) Non-microscopic tests: Toxoplasmic encephalitis , and pneumonitis or other systemic diseases. Antigen detection tests and Antibody detection—ELISA Molecular diagnosis—PCR Congenital toxoplasmosis: The incidence and severity of congenital toxoplasmosis vary with the Treatment: trimester during which infection was acquired. (Most severe in the first Chloroquine in uncomplicated Benign malaria. trimester). Control: Congenital infections cause abortion and encephalitis mina Vector control Classic triad of congenital toxoplasmosis: Treatment of patients chorioretinitis, intracranial calcifications, and hydrocephalus. Chemoprophylaxis Recently the WHO announced the availability of a malaria vaccine (in April Some infants with subclinical infection at birth will subsequently develop 2023), it was approved in Ghana, (a subunit vaccine) signs or symptoms of congenital toxoplasmosis later in life. Laboratory diagnosis: Direct microscopy: Detection of tachyzoites in blood and tissue cyst in tissue biopsy Diagnosis is usually achieved by serology detection of antibodies Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR microgameto -