Download Free Medical Schistosomiasis PowerPoint Presentation

Schistosomiasis PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Schistosomiasis".

This medical PowerPoint presentation talks about schistosomiasis, also known as bilharzia or snail fever. Schistosomiasis is a parasitic infection caused by several species of flatworms called Schistosoma. The disease is common in tropical and subtropical regions, especially in rural areas where there is poor sanitation and limited access to clean water.

The Schistosoma parasite is transmitted to humans when they come into contact with contaminated water, such as when swimming, bathing, or washing clothes. The parasite enters the skin, travels to the liver and then to the blood vessels where it lays eggs. These eggs can cause inflammation and damage to organs such as the liver, intestines, bladder, and reproductive organs.

Symptoms of schistosomiasis can include rash or itchy skin, fever, cough, diarrhea, abdominal pain, blood in urine, and genital sores. In the long term, chronic infection can lead to anemia, malnutrition, and increased susceptibility to other infections.

Treatment for schistosomiasis involves medications such as praziquantel, which can kill the parasites. Prevention measures include avoiding contact with contaminated water, improving sanitation and hygiene, and controlling snail populations, which are the intermediate host for the parasite.

Tags : Schistosomiasis, bilharzia, snail fever, parasitic infection, Schistosoma, Dermatology, Dermatology PowerPoint presentation

Published on : Apr 03, 2023 | Views : 2547 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Schistosomiasis
Slide 2-

Schistosomiasis (also known as bilharzia, bilharziosis or snail fever) is a chronic parasitic disease caused by several species of flatworm of the genus Schistosoma and can cause liver, intestinal and urinary damage. Schistosomiasis is known in many countries, after Theodor Bilharz, who first described the cause of urinary schistosomiasis in 1851. It is most commonly found in Asia, Africa, and South America, especially in areas with water that is contaminated with freshwater snails, which may carry the parasite.
Slide 3-

Types There are five species of flatworms that cause schistosomiasis. Schistosoma mansoni and Schistosoma intercalatum cause intestinal schistosomiasis Schistosoma haematobium causes urinary schistosomiasis Schistosoma japonicum and Schistosoma mekongi cause Asian intestinal schistosomiasis. Each causes a different clinical presentation of the disease.
Slide 4-

Epidemiology The definitive vertebrate host is man. The «intermediate» invertebrate host are the snails (usually of the Biomphalaria, Bulinus, or Oncomelania genus) that are the natural reservoirs of the Schistosoma pathogen. The mechanism of transfer is contact with contaminated water. The reservoir hosts for the S. japonicum are cattle, water buffalo, pigs, dogs, and rodents serve as major reservoirs; For the S. mansoni are possible but less important non-human primates and some rodents can sometimes act as reservoirs. Adult worms live for 3 to 7 years on average (in an endemic area up to 30 years previously), during which time the female worm produces eggs at the rate of 300 a day (S. mansoni) to 3000 a day (S. japonicum).
Slide 5-

Schistosoma mansoni - is cause of intestinal schistosomiasis Morphology The male is 10 to 12 mm long, and has gynaecophoric canal or schist in which may be tubercules or spikes. The shorter and flatter male envelopes the female in schist. The female is to 15 mm long. In a short uterus usually is on one egg. The eggs are ellipsoidal with a lateral spine. The size of eggs is 0,14 – 0,16 mm х 0,06 – 0,07 mm.
Slide 6-

Geographical distribution Schistosoma mansoni is found in parts of South America and the Caribbean, Africa, and the Middle East;
Slide 7-

Schistosoma haematobium causes urinary schistosomiasis Morphology The male is 10 to 15 mm long, and has gynaecophoric canal or schist in which may be tubercules or spikes. There are many papillars on the helminthes body. The female is more longer (to 20 mm) and thin than male worm. The uterus contains from 20 to 30 eggs. The eggs are large, colorless, fusiform and have a terminal spine. The size of eggs is 0,12 – 0,19 mm х 0,05 – 0,073 mm.
Slide 8-

Geographical distribution S. haematobium is found in Africa and the Middle East;
Slide 9-

Schistosoma japonicum causes intestinal schistosomiasis Morphology The male is 9,5 to 20 mm long, its schist is without papillars. The female is 15 to 20 mm long. The uterus contains many eggs. The eggs are more spherical form and have small knob nearly at one of poles. The size of eggs is 0,075 – 0,106 mm х 0,055 – 0,08 mm.
Slide 10-

Geographical distribution S. japonicum is found in the Far East
Slide 11-

Life cycle The life cycles of all human schistosomes are broadly similar: parasite eggs are released into the environment from infected individuals, hatching on contact with fresh water to release the free-swimming miracidium. Miracidia infect fresh-water snails by penetrating the snail's foot. After infection, close to the site of penetration, the miracidium transforms at first into a primary (mother) sporocyst and then into secondary (daughter) sporocysts, which migrate to the snail's hepatopancreas. Once at the hepatopancreas the secondary sporocyst begin to divide again and producing thousands of new parasites, known as cercariae, which are the larvae capable of infecting mammals.
Slide 12-

Life cycle
Slide 13-

Life cycle During 2 days after penetration schistosomulum may remain in the skin before locating a post-capillary venule; Then it travels to the lungs where it changes to next form and migrates to the liver sinusoids (8-10 days after penetration). Juvenile S. mansoni and S. japonicum worms develop an oral sucker after arriving at the liver, and it begins to feed on red blood cells. Worm pairs of S. mansoni and S. japonicum relocate to the mesenteric or rectal veins. S. haematobium schistosomula migrate from the liver to the perivesical venous plexus of the bladder, ureters, and kidneys through the hemorrhoidal plexus. Parasites reach maturity in six to eight weeks, at which time they begin to produce eggs. Many of the eggs pass through the walls of the blood vessels, and through the intestinal wall, to be passed out of the body in faeces. S. haematobium eggs pass through the ureteral or bladder wall and into the urine. Up to half the eggs released by the worm pairs become trapped in the mesenteric veins, or will be washed back into the liver, where they will become lodged. Worm pairs can live in the body for an average of four and a half years, but may persist up to 20 years.
Slide 14-

Clinical features Above all, schistosomiasis is a chronic disease. Many infections are subclinically symptomatic, with mild anemia and malnutrition being common in endemic areas. Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include: Abdominal pain Cough Diarrhea Eosinophilia - extremely high eosinophil granulocyte count. Fever Fatigue Hepatosplenomegaly - the enlargement of both the liver and the spleen.
Slide 15-

Clinical features There are 4 stages 1. STAGE OF INVASION: CERCARIAL DERMATITIS 2. STAGE OF MATURATION: ACUTE SCHISTOSOMIASIS 3. STAGE OF ESTABLISHED INFECTION 4. STAGE OF LATE INFECTION AND SEQUELAE
Slide 16-

STAGE OF INVASION: CERCARIAL DERMATITIS Penetration of the skin by cercariae, leads to occurrence of dermatitis (cercarial dermatitis or «swimmer's itch») and can be associated the death of cercariae in the skin. A transient immediate hypersensitivity reaction that occurs 10 to 15 min after exposure is followed by a more prolonged, delayed reaction, which develops after 12 to 24 h and may persist for up to 15 days. The lesion is characterized by a small, red, pruritic, macular rash, which progresses to papules, possibly accompanied by vesicle formation and oedema. Pustules may form if secondary infection occurs, and residual pigmentation may persist for months. The next symptoms develops a few days after exposure and can be associated with transient fever, cough and pulmonary infiltrates, as well as myalgia and abdominal pain.
Slide 17-

STAGE OF MATURATION: ACUTE SCHISTOSOMIASIS fever, rigors, sweating, headache, malaise, muscular aches, profound weakness, an unproductive, irritating cough, abdominal pain or swelling, nausea, vomiting, diarrhoea, and loss of weight. pyrexia (intermittent or remittent with evening peaks), oedema, a generalized soft lymphadenopathy, a tender enlarged liver, enlarged and soft spleen, stuporose, or show visual impairment or papilloedema. Severe central-nervous manifestations Eggs become detectable in the faeces about 6 weeks after exposure.
Slide 18-

ppt slide no 18 content not found
Slide 19-

STAGE OF ESTABLISHED INFECTION S. haematobium infection: hypogastric discomfort, suprapubic pain, dysuria, haematuria, proteinuria and pyuria. S. mansoni and S. japonicum infections is very frequently asymptomatic. Classical symptoms include: hypogastric pain, diarrhoea, and the passage of blood or mucus in the stool. the liver may be enlarged and tender; the spleen may also be enlarged, but is usually soft.
Slide 20-

STAGE OF LATE INFECTION AND SEQUELAE Urinary schistosomiasis, in the bladder: calcification, ulceration, papillomas, nocturia, precipitancy, retention of urine, dribbling, severe pain. The ureteric pathology is usually asymptomatic, but may lead to ureteric colic. uraemia. S. mansoni and S. japonicum infections, is associated with: intermittent diarrhoea, with or without the passage of blood or mucus; the colon may be tender. In between the episodes of diarrhoea, the stools are normal. bleeding from oesophageal varices haematemesis, melaena. Blood loss is frequently massive, and exsanguination is the usual cause of death rather than hepatic coma.
Slide 21-

Laboratory diagnosis Microscopic exam: detection the eggs in the feces or urine. Pelvic x-ray. Photomicrography of bladder in S. hematobium infection, showing clusters of the parasite eggs with intense eosinophilia
Slide 22-

Laboratory diagnosis Tissue biopsy (rectal biopsy and biopsy of the bladder) may demonstrate eggs when stool or urine examinations are negative. Serology test – Antibody detection.
Slide 23-

Treatment Praziquantel - is safe and highly effective in curing an infected patient, it does not prevent re-infection by cercariae and is thus not an optimum treatment for people living in endemic areas. Praziquantel is universally used. Antimony has been used in the past to treat the disease. In low doses, this toxic metalloid bonds to sulfur atoms in enzymes used by the parasite and kills it without harming the host. Oxamniquine has been used for treating Schistosoma mansoni. Niridazole, is active against all species of parasite. Metrifonate is an inexpensive organophosphorus compound that is active only against S. haematobium and that can be given orally(usually 7.5 mg/kg body weight, once every 2 weeks on up to three occasions each year).
Slide 24-

Preventation Individual protection against infection is achieved by avoiding contact with all potentially contaminated fresh water in endemic areas; for example, by wearing boots and other waterproof clothing. Such water should be boiled before drinking, or left to stand for at least 2 days before use for other purposes such as washing. Should contact with water occur, the skin should be immediately rubbed vigorously with a towel; the water should not be allowed to evaporate, as this aids cercarial penetration. Soap and alcohol also kill cercariae, and cercaricidal barrier creams can be used.
Slide 25-

ppt slide no 25 content not found
Slide 26-

Leishmaniasis is a parasitic disease caused by the protozoa belonging to the genus, Leishmania . Human leishmaniasis is not a disease, but a group of diseases. While several ways to classify leishmaniasis (eg, by geography or taxonomy) are available, clinically, it can present itself in various ways, and is more easily classified as cutaneous, mucocutaneous, and visceral leishmaniasis.
Slide 27-

Classification Eukaryota (organisms with nucleated cells), Kingdom Protista, Phylum Protozoa, Class Flagellates, Genus Leishmania.
Slide 28-

Species, Reservoirs, and Clinical Diseases
Slide 29-

Species, Reservoirs, and Clinical Diseases
Slide 30-

Species, Reservoirs, and Clinical Diseases
Slide 31-

During blood meal, infected sandflies inject the infective stage, the so-called promastigote parasite, into the human host. Injected promastigotes are first phagocytized by macrophages and transform into so-called amastigote parasites. These multiply in the infected cells and also affect different tissues, depending on the Leishmania species, which causes the corresponding clinical manifestation of the disease.
Slide 32-

When sandflies sandflies take blood meals from an infected host, they take up parasitized macrophages. In the vector fly's midgut, these parasites differentiate into the so-called promastigote form, which multiplies and finally migrates to the fly's proboscis.
Slide 33-

Clinical forms VISCERAL MUCOCUTANEOUS CUTANEOUS
Slide 34-

Visceral Leishmaniasis (Kala-azar) Etiology The L. donovani species complex includes several species: L. infantum and L. chagasi
Slide 35-

Epidemiology The species of visceral leishmaniasis are endemic in areas of India, China, Central and South America, East and West Africa, and the countries surrounding the Mediterranean. In India, no extrahuman reservoirs are known, but in other regions, infection may involve several mammalian species, including dogs, foxes, and wild rodents. Sandflies of the genus Phlebotomus are the insect vectors that spread L. donovani.
Slide 36-

Pathogenesis The flagellated promastigotes of L. donovani are introduced by an insect bite. After entering macrophages of the reticuloendothelial system, these forms change into amastigotes, which multiply in phagocytic cells. Released amastigotes disseminate hematogenously and invade reticuloendothelial cells in the spleen, liver, lymph nodes, bone marrow, and skin.
Slide 37-

Incubation and Clinical Symptoms Incubation period is 6-8 months. Symptoms: weakness, dizziness, weight loss, diarrhea, and constipation. Fever, may spike twice daily; chills and sweating. hepatosplenomegaly anemia and leukopenia. bleeding from the gingivae, nose, or GI tract, ecchymoses and petechiae on the skin.
Slide 38-

ppt slide no 38 content not found
Slide 39-

Cutaneous and Mucocutaneous Leishmaniasis Etiology and Epidemiology Old World cutaneous leishmaniasis is caused by three species of Leishmania that belong to the L. tropica complex: L. tropica is present in the Middle East and the Mediterranean littoral; L. major is found in the Middle East, Arabia, India, and sub-Saharan Africa; L. aethiopica is found principally in Ethiopia and Kenya. Phlebotomus sandflies are the principal vectors. Infections that are caused by Leishmania can be acquired by travelers, as well as by military and other personnel residing in endemic areas. Military personnel in the Middle East have acquired cutaneous leishmaniasis with L. major and viscerotropic infections with L. tropica.
Slide 40-

Cutaneous and Mucocutaneous Leishmaniasis New World cutaneous leishmaniasis arises from infection with parasites belonging to the L. mexicana group or the L. braziliensis (Viannia subgenus) group. The patterns of illness vary with the nature of the infecting leishmanial organisms, which are found in different regions of North, Central, and South America. Infections with strains of L. viannia, which are endemic in various areas of South America, cause cutaneous leishmaniasis and, in a small percentage of those infected, result in the later development of mucocutaneous leishmaniasis. Such mucocutaneous disease (espundia) involves the nasal or oropharyngeal mucosa, or both, and may prove fatal. All of these New World leishmanial parasites are transmitted principally by sandfly vectors, although direct human contact may also bring about infection. Various mammals are naturally infected reservoirs of the organisms.
Slide 41-

Pathogenesis Both Old World and New World forms of leishmaniasis are initiated when the bite of an infected sandfly injects promastigotes into the human host. The organisms enter tissue macrophages and capillary endothelial cells, become amastigotes, and multiply. A granulomatous inflammatory response develops at the bite site. With local ischemia, the lesion ulcerates; a bacterial infection of the necrotic area may extend the ulceration.
Slide 42-

Incubation and Clinical Symptoms Incubation period is from 2-8 months to 1,5 years and more. In Old World symptoms of cutaneous leishmaniasis: a papule (at the inoculation site). papule ulcerates and a shallow circular lesion appears that is several centimeters in diameter and has a raised margin. lymphadenopathy. Healing of the lesions is slow, sometimes requiring more than a year.
Slide 43-

Clinical Symptoms of New World leishmaniasis L. mexicana single lesion or a few lesions on exposed surfaces of the body such as the face and ear, which heals spontaneously over 6 months. extensive destruction of the pinna. L. viannia lesions on the skin or mucous membranes. progressive ulcerations of lymphatic nodes and mucous membranes. the infection metastasizes to the nasal or oral mucosa. Metastatic lesions can erode the nasal septum or the hard palate or soft palate. Some patients die of malnutrition or bacterial infection. Incubation period is 2-3 weeks to 1-3 mounths.
Slide 44-

ppt slide no 44 content not found
Slide 45-

ppt slide no 45 content not found
Slide 46-

Immunity In visceral leishmaniasis (Kala-Azar) cellular immunity is responsible for resolving mild disease. High levels of antibodies are found. In cutaneous and mucocutaneous leishmaniasis host defense relies on cell-mediated immunity; antibody titers are low. The response ranges from a local granuloma with few parasites to a histiocytoma with many parasites.
Slide 47-

Laboratory Diagnostics of visceral leishmaniasis Demonstration of the organism in host tissues cultured on a Novy-MacNeal-Nicolle (NNN) or other medium or detection of Leishman-Donovan bodies (amastigotes) in stained tissue samples. PCR can be performed using genus- or species-specific oligonucleotides. Established by examining bone marrow aspirates. Splenic aspirates have the highest yields but may be risky. Liver biopsy or aspiration of enlarged lymph nodes can also provide diagnostic material.
Slide 48-

Laboratory Diagnostics of cutaneous and mucocutaneous leishmaniasis Demonstrating amastigotes on stained smears of a biopsy or of scrapings from the border of an ulcer. Culturing amastigotes on NNN medium inoculated with lesion material. PCR targeting parasite kinetoplast DNA has allowed detection of organisms that might be missed on histologic section or culturing.
Slide 49-

Laboratory Diagnostics of cutaneous and mucocutaneous leishmaniasis Except in diffuse cutaneous leishmaniasis, the leishmanin skin test is usually positive.
Slide 50-

Treatment There are two common therapies containing antimony, meglumine antimoniate (Glucantim®) and sodium stibogluconate (Pentostam®). Unfortunately, in many parts of the world, the parasite has become resistant to antimony and for visceral or mucocutaneous leishmaniasis, amphotericin is now the treatment of choice. Miltefosine (Impavido®), is a new drug for visceral, mucocutaneous and cutaneous leishmaniasis. Drug-resistant leishmaniasis may respond to immunotherapy (inoculation with parasite antigens plus an adjuvant) which aims to stimulate the body's own immune system to kill the parasite.
Slide 51-

Prevention: Preventing sandfly bites is the most immediate form of protection. Insect repellent, appropriate clothing, screening of windows, and fine mesh netting around the bed (in endemic areas) will reduce exposure. Public health measures to reduce the sandfly population and animal reservoirs are important. There are no preventive vaccines or drugs for leishmaniasis.