Plant disease Study Guide

📖 Core Concepts Plant disease: Illness in a plant caused by a pathogen (fungi, oomycetes, bacteria, viruses, etc.) or unfavorable environment. Plant pathology: Scientific study of plant diseases. Pathogen classes: Fungi (Ascomycetes, Basidiomycetes) – produce spores, can be biotrophic or necrotrophic. Oomycetes – fungus‑like stramenopiles; e.g., potato late blight. Bacteria – few are pathogenic; Agrobacterium induces galls by altering auxin. Mollicutes (phytoplasmas, spiroplasmas) – wall‑less, intracellular, transmitted by sap‑sucking insects. Viruses – mostly single‑stranded RNA; need a vector (often aphids) or mechanical damage to spread. Nematodes – microscopic worms that attack roots (root‑knot, cyst). Protozoa – produce long‑lived zoospores; can also vector viruses. Economic impact: 10 % yield loss in developed regions, >20 % in developing; ≈25 % of global crop loss. Control strategies: Border quarantine, chemical control, cultural practices (crop rotation), biological control agents. --- 📌 Must Remember Biotroph vs. Necrotroph: Biotrophs feed on living tissue; necrotrophs kill tissue first. Oomycete vs. True Fungus: Oomycetes are Stramenopiles, not true fungi, but use similar effectors. Agrobacterium: Causes crown‑gall disease by inserting T‑DNA that elevates auxin. Mollicute transmission: Always insect‑vectored (leafhoppers, psyllids). Major nematodes: Globodera spp. = cyst nematodes (host‑specific, major potato pest). Root‑knot nematodes = broad host range. Key control hierarchy: Prevention (quarantine) → Cultural (crop rotation) → Biological → Chemical (last resort). --- 🔄 Key Processes Fungal infection cycle Spore dispersal → germination on plant surface → penetration (appressorium or direct) → colonization (biotrophic or necrotrophic). Oomycete effector delivery Zoospore release → encystment on leaf → germ tube → secretion of effectors → suppression of host defenses. Agrobacterium tumor formation Wound entry → transfer of Ti plasmid → integration of T‑DNA → overproduction of auxin/cytokinin → gall growth. Mollicute spread Insect feeds → injects bacteria into phloem → systemic movement within plant → symptom development (e.g., yellowing). Nematode root infection J2 larvae hatch → chemotaxis to root → penetration → formation of feeding sites (giant cells for cyst nematodes, gall cells for root‑knot). --- 🔍 Key Comparisons Fungi vs. Oomycetes Cell wall: Chitin (fungi) vs. cellulose‑like glucans (oomycetes). Phylogeny: True fungi (Eukarya) vs. Stramenopiles. Biotrophic vs. Necrotrophic fungi Nutrition: Live cells vs. dead cells. Symptoms: Slow chlorosis/wilting vs. rapid tissue death/lesions. Cyst nematodes vs. Root‑knot nematodes Host range: Narrow (cyst) vs. broad (root‑knot). Feeding site: Specialized syncytium vs. giant cells forming galls. Chemical vs. Biological control Speed of action: Immediate (chemical) vs. slower, sustainable (biological). Side effects: Non‑target toxicity, resistance risk vs. ecosystem friendly, may need establishment time. --- ⚠️ Common Misunderstandings “All fungi are pathogens.” – Most fungi are saprotrophs; only a minority cause disease. “Oomycetes are fungi.” – They belong to a different kingdom; treatments effective on true fungi may fail. “Chemical control is always the best option.” – Overuse leads to resistance, non‑target damage, and loss of organic status. “All plant viruses need insect vectors.” – Some spread mechanically or via seed. --- 🧠 Mental Models / Intuition “Living vs. dead buffet”: Think of biotrophs as diners who need a fresh meal (living cells) and necrotrophs as scavengers that eat leftovers (dead tissue). “Pathogen toolbox”: Each pathogen class carries a distinct set of “tools” (spores, zoospores, plasmids, nematode stylets) that dictate how it enters and exploits the host. “Layered defense pyramid”: Start with the strongest layer (quarantine) and add successive layers (cultural → biological → chemical) only if needed. --- 🚩 Exceptions & Edge Cases Facultative saprotrophic fungi: Can live on dead matter but become pathogenic under favorable conditions. Virus‑like particles (viroids): Not covered in outline but can cause disease without encoding proteins. Protozoan zoospores: May persist for years in soil, unlike many fungal spores that lose viability faster. --- 📍 When to Use Which Quarantine: When a disease is not yet present in a region or when importing germplasm. Crop rotation: For soil‑borne pathogens (e.g., Fusarium, cyst nematodes) with limited host range. Biological agents: When chemical residues are undesirable (organic production) or resistance is emerging. Chemical fungicides/insecticides: For acute outbreaks where rapid disease suppression is critical and non‑target impact is acceptable. --- 👀 Patterns to Recognize Spore‑based spread → Look for aerial lesions, water splash, or soil movement. Vector‑linked symptoms → Sudden onset near insect activity, often with mosaic or stunting. Root galling → Indicates root‑knot nematodes or certain fungal infections. Localized tumor formation → Typical of Agrobacterium infection. --- 🗂️ Exam Traps Choosing “fungi” for oomycete questions – Remember they are not true fungi; answer should reflect oomycete classification. Assuming all bacterial plant pathogens manipulate hormones – Only Agrobacterium does; most are harmless saprotrophs. Selecting chemical control for an organic‑certified crop – This violates certification; the correct answer is biological or cultural control. Confusing cyst vs. root‑knot nematode host range – Cyst = narrow, root‑knot = broad; answer choices often swap these. ---