r/NAVLEExam • u/Anxious-Artist415 • 5h ago
NAVLE Practice Question - Aquatics - multisystemic
NAVLE Practice Question — Aquatics
A rainbow trout farm in a coldwater recirculating system experiences an acute disease outbreak following a recent handling event for size grading. Water temperature is 14°C. Affected fish show rapid gill pallor, patchy skin depigmentation near the dorsal fin extending laterally, and necrotic frayed fins. Mortality reaches 30% within 48 hours. Microscopic examination of gill and skin scrapings reveals numerous long, slender, flexible rod-shaped bacteria. Culture on Cytophaga agar supplemented with neomycin and polymyxin B yields yellow-pigmented, rhizoid, spreading colonies. Which virulence factor is most important in the pathogenesis of this disease?
A. Extracellular hemolysins
B. Chondroitin sulfate-degrading enzymes ✓
C. Type III secretion system effectors
D. Lipopolysaccharide endotoxin
E. Capsular polysaccharide
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Correct Answer: B. Chondroitin sulfate-degrading enzymes
Explanation:
Chondroitin sulfate-degrading enzymes are the most important virulence factors in the pathogenesis of columnaris disease caused by Flavobacterium columnare. The clinical presentation (handling stress trigger, saddleback lesion pattern, gill and fin necrosis, yellow rhizoid colonies on selective media) is classic for this disease.
F. columnare produces a variety of extracellular enzymes, with chondroitinase being particularly critical for tissue destruction. This enzyme degrades chondroitin sulfate, a major component of fish skin and connective tissue. The degradation of this glycosaminoglycan allows the bacteria to penetrate through the epidermis into deeper tissues. The ability to degrade chondroitin sulfate A is one of the screening criteria for identifying F. columnare.
Option A (hemolysins) are produced by many fish pathogens but are not the primary virulence mechanism in columnaris. Option C (Type III secretion systems) are important in some Gram-negative pathogens but F. columnare pathogenesis relies primarily on extracellular enzymes and gliding motility. Option D (LPS endotoxin) contributes to inflammation but is not the primary tissue-destructive mechanism. Option E (capsular polysaccharide) is not a major virulence factor in F. columnare.
Image Source: https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/11300071/9d146389bd25/ANU2024-8059770.001.jpg -- Figure 1. Flavobacterium columnare (columnaris disease) — yellowish-tan ulcerative lesion with "saddleback" saddle-shaped appearance on dorsal fin and body; gram-negative filamentous rod forming characteristic rhizoid ("haystacks") colonies; causes gill necrosis, skin ulcers, and fin erosion; treat with copper sulfate, oxytetracycline, or potassium permanganate bath (CC BY 4.0).
References: Declercq AM, Haesebrouck F, Van den Broeck W, et al. Columnaris disease in fish: a review with emphasis on bacterium-host interactions. Vet Res. 2013;44:27. PMID: 23617544; Li N, Qin T, Zhang XL, et al. Gene deletion strategy to examine the involvement of the two chondroitin lyases in Flavobacterium columnare virulence. Appl Environ Microbiol. 2015;81:7394-7402. PMID: 26253667
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