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This document provides a detailed overview of common parasitic infections, specifically focusing on amoebiasis and giardiasis. It includes learning objectives, clinical presentations, pathogenesis, and diagnostic methods. It appears to be a lecture or presentation.

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Common Parasitic Infections DR. LORINA BADGER-EMEKA. COM/KFU Learning Objectives Students should know; the difference between diarrhea and dysentery And the protozoa responsible them the pathogenesis of intestinal and extraintestinal amoebiasis. What is mean...

Common Parasitic Infections DR. LORINA BADGER-EMEKA. COM/KFU Learning Objectives Students should know; the difference between diarrhea and dysentery And the protozoa responsible them the pathogenesis of intestinal and extraintestinal amoebiasis. What is meant by the amoebic carrier and its management. The main clinical syndromes of intestinal giardiasis. Be able to describe mode of infection in human toxoplasmosis And the clinical presentation of toxoplasmosis in man. The reason Toxoplasma gondi is considered an opportunistic parasite Differences between diarrhea and dysentery and the causative protozoan Dysentery [Parasites in the Large Diarrhoea [Parasites in the small intestine] intestine] Defined as: Defined as: Painful frequent evacuation Increase in frequency, of small quantities of stool fluidity or containing mucus tinged with volume of bowel motions blood and tenesmus. Parasites in the Small intestine i.e., recurrent inclination to Giardia lamblia evacuate the bowels Cryptosporidium Parasites in large intestine. Cyclospora Entamoeba histolytica Balantidium coli Pathogenesis of intestinal and extraintestinal amoebiasis. Clinical outcome of infection could result in a carrier state, intestinal amebiasis, or extraintestinal amebiasis Pathogenesis of Amoebiasis Pathogenesis involves: ▪ Ingestion and passing of the cysts through the stomach. ▪ pathogenic trophozoite is release in the duodenum. ▪ trophozoites replication leads to extensive local necrosis in the large intestine. ▪ Tissue destruction is attributed to production of a cytotoxin Pathogenesis of Amoebiasis [adherence] Next is the attachment of E. histolytica trophozoites to host cells This is achieved using a galactose-inhibitable adherence protein for cytolysis and tissue necrosis to occur. There is lysis of colonic epithelial cells, human neutrophils, lymphocytes, and monocytes by trophozoites. Pathogenesis of Amoebiasis cont’d 2 [adherence] Attachment could lead to lethal alteration of host cell membrane permeability, The result? an irreversible increase in intracellular calcium levels. After lysis, release of toxic neutrophil constituents of neutrophils Will lead to the tissue destruction. There is ulcerations of the intestinal mucosa Presenting with inflammation, haemorrhage, and secondary bacterial infection. Pathogenesis of Amoebiasis [Invasion] Invasion into the deeper mucosa and Could extend to peritoneal cavity There is secondary involvement with organs, [the liver, the lungs, brain, and heart]. Extraintestinal amebiasis is associated with trophozoites. The pathogenic species, E. histolytica, and the non-pathogenic species [E. dispar and E. moshkovskii. Courtesy of Google images Amoebic pericarditis, Pericardial effusion, Amoebic brain Abscess Pathogenesis of Amoebiasis Intestinal Amoebiasis Extra-Intestinal Amoebiasis Flasked-shaped ulcer Trophozoites at boundary of necrotic and healthy tissue Amoebic Liver Abscess: Chocolate-coloured Trophozoites ingesting host cells. necrotic tissue (leucocytes & RBC). Dysentery (blood and mucus in faeces) Courtesy of Google images Question 1 Presence of ingested RBCs is a characteristic feature of which one of the following? (a) Entamoeba histolytica (b) Entamoeba coli (C) Dientamoeba fragilis What is meant by the amoebic carrier and its management Clinical Syndromes of Amoebiasis [Symptomatic] Intestinal Amoebiasis Extra-Intestinal Amoebiasis ▪ Fever, leukocytosis, rigors ▪ Abdominal pain, ▪ Abscess formation is common ▪ cramping, ▪ The right liver lobe is most ▪ And commonly involved. ▪ colitis with dysentery. ▪ Pain over the liver, with Severe disease is characterized hepatomegaly and by bloody stools ▪ elevation of the diaphragm, is observed Clinical Syndromes of Amoebiasis [Asymptomatic carrier] ▪ 80-90% of cases are asymptomatic Cyst Passers (Carriers) ▪ They must be detected and treated ▪ As infection can be transmitted ( e.g., food handlers). ▪ May develop complications later. ▪ They experience general abdominal discomfort. ▪ Distension of colon ▪ There is diarrhea alternating with constipation Management of Amoebic carrier (Diagnosis and treatment) For epidemiologic purposes carriers of E. histolytica should be detected Asymptomatic carriage could be eradicated By treatment with iodoquinol, diloxanide furoate, or paromomycin Luminal (intestinal): Iodoquinol 500mg tds/ 10 days. Tissue ( Systemic): Flagyl (Metronidazole): 750 mg tds/10 days. Tds [three times daily] The main clinical syndromes of intestinal giardiasis Giardia duodenalis (G. lamblia and G. intestinalis) Courtesy of Google images ▪ An inhabitant of the Small intestine ▪ attaches to intestinal villi with an adhesive disk Intestinal giardiasis ▪ Infection is by ingestion of contaminated food/drinks ▪ Or By person-to-person spread of infection. ▪ Risk factors: Poor sanitary conditions, travel to known endemic areas. Murray 8th Ed. ▪ Consumption of inadequately treated water. ▪ Infections may be in outbreak and endemic forms. Giardia duodenalis (G. lamblia and G. intestinalis) Pathogenesis of Giardiasis ▪ Trophozoites attach to villi by sucking disk. ▪ Villi appear flattened (atrophy) and ▪ inflammation of the mucosa ▪ NO frank tissue necrosis. ▪ Spread beyond GIT is very rare. Courtesy of Google images Giardia duodenalis (G. lamblia and G. intestinalis [Clinical syndromes] ▪ 50 % of infected individuals could be asymptomatic. ▪ Symptoms appear between 1 – 4 weeks ▪ There is Dyspepsia [a pain in mid or upper stomach] ▪ epigastric pain, nausea, flatulence, abdominal cramps. ▪ Sudden onset of explosive, watery, foul-smelling diarrhea. ▪ In severe case of infection, ▪ There is mmalabsorption of proteins, carbohydrates, fatty acids, vitamin B12 ▪ (perniciousanemia) Fatty diarrhoea (Steatorrhea). Giardia duodenalis (G. lamblia and G. intestinalis) Clinical syndromes 2 ▪ Spontaneous recovery could occur in 10 to 14 days. ▪ In more chronic disease there could be multiple relapses. ▪ This is common with Ig A deficiency patients. ▪ Laboratory Diagnosis: ▪ Stool examination: cyst, trophozoite, faecal antigen. ▪ Serology ▪ PCR Question 2 Which one of the structures of the following protozoan parasites has the shape of a tennis racket with a concave ventral surface and sucker? A. Entamoeba histolytica B. Giardia lamblia C. Isophora hominis Describe the mode of infection in human toxoplasmosis Toxoplasmosis ▪ Toxoplasma gondii is an intracellular parasite. ▪ Reservoir host are house cat (common), and felines [cat families]. ▪ Mode of infection in human is by the: ▪ Ingestion of improperly cooked meat. ▪ Ingestion of food/ drink handling cat excreta. ▪ Trans placental infection. ▪ Blood transfusion and organ transplantation. ▪ Contamination of mucous membrane & skin abrasion ▪ (in research workers & butchers). Courtesy of Google images ▪ Organisms develop in the intestinal cells of the cat, ▪ as well as during ▪ an extraintestinal cycle ▪ with passage to the tissues via the bloodstream ▪ Infective forms (trophozoites) of the oocyst ▪ develop as slender, crescentic types called tachyzoites. ▪ multiply rapidly and are responsible for initiating infection and tissue damage ▪ The shorter forms are slow growing, called bradyzoites develop and form cysts in chronic infections. ▪ Humans become infected from two sources: (1) ingestion of improperly cooked meat from animals that serve as intermediate hosts And (2) ingestion of infective oocysts from contaminated cat faeces. The clinical presentation of toxoplasmosis in Man [Pathogenesis Clinical Syndromes] Most T. gondii infections are benign and asymptomatic, Symptoms occur with parasite movement from the blood to tissues. They become intracellular parasite. Symptoms appear, with infection is characterized by cell destruction. Multiplication of the parasite leads to more organisms, and eventual formation of cyst. The clinical presentation of toxoplasmosis in Man [Pathogenesis Clinical Syndromes] cont’d Many tissues could be affected; however, the organism has a predilection for cells of the lung, heart, lymphoid organs, and CNS, including the eye. Symptoms of acute disease include chills, fever, headaches, myalgia, lymphadenitis, and fatigue; In chronic cases, signs and symptoms include lymphadenitis, occasionally a rash, evidence of hepatitis, encephalomyelitis, and myocarditis In some of the cases, there is chorioretinitis and could lead to blindness. Pathogenesis Clinical Syndromes Toxoplasmosis is considered an opportunistic infection. Congenital infection: Congenital toxoplasmosis [occurs in infants born to mothers infected during pregnancy] Clinical Manifestations would depend the stage of the pregnancy Acquired infection: Acquired toxoplasmosis Recrudescence: Toxoplasmosis in immunocompromised patients Reactivation of latent toxoplasmosis is a special problem for these people Courtesy of Google images Why is Toxoplasma gondii considered an opportunistic parasite? Toxoplasmosis in the immunocompromised Reactivation of latent toxoplasmosis. Opportunistic Parasite Usually neurologic manifestations: Encephalopathy, meningoencephalitis, or cerebral mass lesions. Symptoms are related to the location of the lesions. Hemiparesis, seizures, visual impairment, confusion, and lethargy Diagnosis of Toxoplasmosis Clinical: Laboratory diagnosis: Serology: Detection of IgM in patient’s blood indicates active infection. Detection of IgG (two folds rising titer) indicates active infection. Molecular techniques: PCR Laboratory Diagnosis of Congenital Toxoplasmosis: Detection of IgM in baby’s blood indicates fetal infection. Maternal IgM does not cross the placenta Detection of parasite DNA in infant’s urine or amniotic fluid by PCR. Treatment and prevention of Toxoplasmosis Pyrimethamine + Trisulphapyrimidine Spiramycinto infected pregnant women. Prevention of congenital infection: 1. Routine ELISA for pregnant women in early pregnancy for detection and treatment 2. Avoid consumption and handling of raw or undercooked meat. 3. Avoid exposure to cat feces. Question 3 In Toxoplasmosis infection the only known hosts of this organism are domestic cats and their relatives. Which of the following is the most common mode of with T. gondii infection in humans? A. Blood transfusion B. Ingestion of oocysts C. Ingestion of tissue cysts D. Transplacental transmission Summary Lecture looked at: Differences between dysentery and diarrhea Their causative organisms and clinical presentation Also discussed is who amoebic carriers are And how they could be managed Giardiasis, clinical syndromes of intestinal giardiasis as well as Toxoplasmosis, the mode of infection in human toxoplasmosis And the reasons why Toxoplasma gondii is considered an opportunistic parasite References MEDICAL MICROBIOLOGY, Murray, et al., 8thedition, Chapter, 73 (717: 721) & 74 (737:739) Other images are google images

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