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Leishmania donovani

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  Leishmania donovani: Life Cycle, Pathogenesis, Treatment Prevention and Diagnosis   Leishmania donovani: The Causative Agent of Kalaazar (Visceral Leishmaniasis) Lifecycle   Reservoir Hosts: Various mammals (e.g., dogs, foxes, rodents).   Vector: Female sandflies.    Require blood meals for egg maturation.    Ingest macrophages containing amastigotes when feeding on an infected host. Inside the Sandfly: 1. Amastigotes transform into promastigotes in the gut. 2. Promastigotes multiply and migrate to the pharynx and proboscis. 3. This process takes about 10 days. Transmission to Humans: 1. Sandfly bites human, injecting promastigotes. 2. Promastigotes are engulfed by macrophages. 3. Inside macrophages, promastigotes transform back into amastigotes. Within the Human Host: 1. Amastigotes evade destruction by preventing vacuolelysosome fusion. 2. Infect other macrophages and reticuloendothelial cells. Cycle Completion:   Another sandfly ingests

Leishmania donovani: Life Cycle, Pathogenesis, Treatment Prevention and Diagnosis

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    Leishmania donovani: The Causative Agent of Kalaazar (Visceral Leishmaniasis) Lifecycle Leishmania donovani's life cycle, relies on sandflies as vectors and various mammals, including dogs, foxes, and rodents, as reservoirs. Female sandflies, requiring blood meals for egg maturation, ingest macrophages containing amastigotes when feeding on an infected host Inside the sandfly, the amastigotes transform into promastigotes in the gut, multiply, and migrate to the pharynx and proboscis, ready to be transmitted during the next bite. This sandfly phase takes about 10 days. Upon biting a human, the sandfly injects promastigotes, which are engulfed by macrophages and transform back into amastigotes (Figure 1). Amastigotes evade destruction by preventing the fusion of the vacuole with lysosomes, leading to the infection of other macrophages and reticuloendothelial cells. The cycle completes when another sandfly ingests macrophages containing amastigotes.                  

"Unveiling Thrombotic and Thrombocytopenic Purpura: Pathogenesis, Clinical Features, and Treatment Strategies"

  Thrombotic and Thrombocytopenic Purpura Definition: TTP occurs in familial or acquired forms. Pathogenesis: Deficiency of ADAMTS13 metalloprotease leads to ULVWF multimers. Causes: Familial forms involve ADAMTS13 mutations; Acquired forms result from inhibitory IgG autoantibodies. Clinical Features: Pentad of symptoms: thrombocytopenia, microangiopathic hemolytic anemia, neurological abnormalities, renal failure, fever. Treatment: Plasma exchange with FFP or cry supernatant, rituximab, alacizumab, and immunosuppressive therapies. TTP is type of Thrombocytopenia mean platelets count decrease its normal count. TTP is rare blood disorder characterized by clotting in small blood vessels (Thromboses) but unnecessary clot   resulting in a low platelet count . Normally clotting present in tissue & vessels injury . In TTP, Patient have defect in   (ADAMTS13) enzyme. ( For clearing the VWF multimers) Normally Gene to code for different protein. ADAMTS13

Understanding Trypanosoma: Life Cycle, Causes, Symptoms, Diagnosis, and Treatment

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  Trypanosoma Cruzi Chagas disease is caused by the parasite Trypanosoma Cruzi (also known as American Trypanosomiasis). Life Cycle Clinical Findings: ·          Acute: Fever, Swollen lymph nodes, Facial edema, Hepato-splenomegaly ·          Chronic: Myocarditis, Heart failure, enlarged esophagus, enlarged colon, Nerve damage        Symptoms         Fever,  Fatigue,  Body aches, Headaches. Rash. Loss of appetite. Diarrhea. Vomiting.   Diagnosis   ·          Wet preparation for motile trypanosomes ·          Thick and thin smear ·          Bone marrow staining ·          Muscle biopsy   Treatment   ·          Nifurtimox ·          Benznidazole Trypanosoma Gambiense and Rhodesiense These organisms cause sleeping sickness (African Trypanosomiasis), transmitted by the tsetse fly .   Life Cycle   Symptoms: Headache, Malaise, Weakness, Fatigue, Pruritus, Arthralgia   Diagnosis   Microscopy of lymph node aspirate, blood, or CSF.   Treatment   ·   

Decoding Malaria: Causes, Life Cycle, Symptoms, Diagnosis and Treatment

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  Malaria  is caused by a parasite that destroys red blood cells and is transmitted by female Anopheles mosquitoes , Usually, mosquito’s bites late in the evening or at night. The primary causative agent of malaria is the protozoan Plasmodium , which includes several species such as 1.        Plasmodium vivax 2.        P. malariae 3.        P. falciparum 4.        P. ovale 5.        P. knowlesi Life Cycle: 1. The Plasmodium parasite initially infects female Anopheles mosquitoes . 2. Infected mosquitoes then transmit saliva containing sporozoites into the human bloodstream during a bite. 3. Sporozoites travel to the liver, reproduce asexually, and emerge as merozoites. 4. Merozoites invade red blood cells (RBCs) and form trophozoites , initiating a cycle of asexual reproduction. 5. Trophozoites develop into merozoites , causing RBCs to burst and release more parasites. 6. Some trophozoites develop into gametocytes, which are ingested by non-infected mosq

Understanding Giardiasis: Definition Mode of Transmission,Life cycle, Causes, Symptoms, Diagnosis, and Treatment

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  Giardiasis caused by Giardia lamblia, results in infection in the colon. Mode of Transmission: ·           Fecal-oral route ·           Ingestion of contaminated food or water Life Cycle Symptoms: ·           Abdominal pain ·           Cramps ·           Diarrhea ·           Nausea ·           Weight loss ·           Release of gases ·           Bloating ·           Fatigue Diagnosis: Stool for routine  examination:Cysts Treatment: 1.         Metronidazole 2.         Tinidazole               Nitroimidazole  

First Short Notes of Clinical Parasitology (Amoebiasis Definition , Mode of Transmation, Life Cycle, Symptoms, Diagnosis and Treatment)

  Amoebiasis is a disease caused by Entamoeba histolytica , leading to ulcers in the large intestine. Mode of Transmission: The disease spreads through the fecal-oral route , primarily via contaminated water, food, flies , or through contact with contaminated hands. Life Cycle: Entamoeba cysts are present in the environment and then enter the body through ingestion. 1. Cysts undergo nuclear duplication. 2. The nucleus quadruplicates . 3. Multiplication begins through division. 4. The fourth stage involves the transformation into trophozoites . 5. Trophozoites undergo binary division . 6. The pre-cyst stage precedes cyst formation . Symptoms: Symptoms typically manifest 1-4 weeks after infection, including: ·          Diarrhea ·          Presence of blood in stool ·          Abdominal cramps and pain Diagnosis: - Trophozoites observed in a Stool Examination . - Cysts are identifiable in Sting Test of Stool . Treatment: Common treatments inc