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Plasmodium falciparum
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Pathogenesis
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Transmission occurs when an infected female Anopheles mosquito injects sporozoites into the human bloodstream during a blood meal
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Sporozoites invade hepatocytes and undergo exoerythrocytic schizogony, producing thousands of merozoites that are released into the circulation
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Merozoites invade red blood cells and develop through ring, trophozoite, and schizont stages, culminating in erythrocyte rupture and release of new infective forms
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Infected erythrocytes express PfEMP1, promoting cytoadherence to endothelial receptors and sequestration in microvasculature, leading to microvascular obstruction and local inflammation
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Pro‑inflammatory cytokines such as TNFα and IL‑1 are released, driving fever, endothelial activation, and systemic inflammatory response
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Pathological effects
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Periodic high‑grade fevers, rigors, and chills corresponding to synchronous schizont rupture
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Hemolytic anemia, jaundice, and splenomegaly due to massive destruction and clearance of parasitized erythrocytes
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Cerebral malaria characterized by seizures, altered consciousness, and high mortality from brain microcirculatory obstruction
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Acute kidney injury, metabolic acidosis, and hypoglycemia arising from microvascular dysfunction and high parasite biomass
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Diagnosis
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Thick and thin Giemsa‑stained blood smears remain the gold standard for detecting ring forms, trophozoites, schizonts, and gametocytes
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Rapid diagnostic tests targeting HRP2 antigen provide point‑of‑care detection with high sensitivity for P. falciparum
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PCR assays enable species‑specific identification and quantification of parasitemia in reference laboratories
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Prevention
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Insecticide‑treated bed nets and indoor residual spraying reduce mosquito‑human contact and transmission risk
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Chemoprophylaxis with atovaquone‑proguanil, doxycycline, or mefloquine is recommended for travelers to endemic regions
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RTS,S vaccine implementation in high‑burden areas has been shown to decrease clinical malaria incidence
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Candida albicans
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Pathogenesis
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Normally a commensal yeast on mucosal surfaces, it undergoes a morphological switch to pseudohyphae and true hyphae under immunocompromised or dysbiotic conditions, facilitating tissue invasion
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Adhesin proteins Als3 and invasin Ssa1 mediate tight binding to epithelial and endothelial cells, triggering endocytosis of the fungus
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Secretion of hydrolytic enzymes, including secreted aspartyl proteases (SAPs) and phospholipases, degrades host tissues and promotes deep invasion
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Biofilm formation on indwelling medical devices generates a protected environment resistant to antifungal therapy
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Pathological effects
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Oropharyngeal candidiasis presents as white adherent plaques on the tongue and buccal mucosa, often painful and bleeding on scraping
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Vulvovaginal candidiasis manifests with intense itching, erythema, and thick cottage‑cheese‑like discharge
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Invasive candidiasis in immunosuppressed patients can lead to candidemia, endocarditis, hepatosplenic microabscesses, and septic shock
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Diagnosis
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Microscopic examination of 10 % KOH wet mounts or Gram‑stained smears reveals budding yeast cells and pseudohyphae
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Germ tube test in human serum at 37 °C yields true germ tubes within 2 hours, confirming C. albicans
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Culture on Sabouraud dextrose agar produces creamy smooth colonies and green colonies on CHROMagar for presumptive identification
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1,3‑β‑D‑glucan assay and mannan antigen detection aid in early diagnosis of invasive disease
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Prevention
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Maintain good mucosal hygiene and manage predisposing factors such as uncontrolled diabetes and antibiotic overuse
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Employ strict aseptic technique and timely replacement of catheters and central lines to prevent device‑associated biofilm infections
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Consider prophylactic fluconazole or echinocandins in high‑risk neutropenic or transplant patients
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Aspergillus fumigatus
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Pathogenesis
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Small airborne conidia (2–3 μm) are inhaled and deposit in alveoli, where they are normally cleared by alveolar macrophages in immunocompetent hosts
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In immunocompromised individuals, conidia evade phagocytosis, germinate into hyphae, and penetrate pulmonary epithelium
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Hyphal angioinvasion damages vascular endothelium, induces tissue factor expression, thrombosis, and tissue infarction
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Secretion of gliotoxin impairs neutrophil and macrophage function, facilitating unchecked fungal proliferation
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Host airway epithelial cells release cytokines and chemokines that drive neutrophil recruitment and contribute to pulmonary inflammation
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Pathological effects
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Invasive pulmonary aspergillosis presents with fever, pleuritic chest pain, cough, and hemoptysis, often rapidly progressive
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Allergic bronchopulmonary aspergillosis occurs in atopic individuals, leading to bronchospasm, eosinophilia, and bronchiectasis
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Aspergilloma or fungus ball forms within preexisting lung cavities, causing chronic cough and hemoptysis
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Chronic pulmonary aspergillosis leads to weight loss, fatigue, productive cough, and progressive respiratory failure
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Diagnosis
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Chest CT imaging reveals the halo sign in early invasive disease and the air crescent sign during recovery
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Microscopy and culture of respiratory specimens show septate hyphae with acute angle (45°) branching
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Detection of galactomannan antigen in serum or bronchoalveolar lavage fluid enables early diagnosis
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Aspergillus‑specific PCR assays on blood or BAL fluid increase sensitivity, especially in neutropenic patients
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Prevention
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HEPA‑filtered air systems and protective isolation units reduce environmental spore exposure in high‑risk wards
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Limit patient exposure to construction, gardening, and compost during periods of profound immunosuppression
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Prophylactic antifungal therapy with voriconazole or posaconazole is recommended for hematopoietic stem cell transplant recipients and prolonged neutropenia
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Basic Microbiology 1 Views 1 Answers
Choose 1 species of protozoa and 2 species fungi/yeast/mold that you find interesting and DRAW its pathogenesis. Write its pathological effects, diagnosis and prevention
Choose 1 species of protozoa and 2 species fungi/yeast/mold that you find interesting and DRAW its pathogenesis. Write its pathological effects, diagnosis and prevention
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