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Neisseria
Gram-negative diplococci
Pathogenic species
N. meningitidis, N. gonorrhoeae
Gram-negative
Present
Bean-shaped diplococci
Present
Capsule
Present
Pili
Present
Flagella
Absent
Spores
Absent
Strict parasite
Poor survival outside host
Aerobic
Present
Oxidative metabolism
Present
Catalase production
Present
Oxidase production
Present
Requires enriched complex media
Present
Requires CO₂ for optimal growth
Present
Size
0.8 × 0.6 µm
Media
Blood Agar, Chocolate Agar
Growth Enhancement
Blood or Serum
CO₂ Requirement
2–8% CO₂ improves growth
Temperature
36–39 °C
pH
6–8
Colony Appearance
1–2 mm diameter, convex, grey, transparent
Hemolysis on Blood Agar
Absent
Oxidase
Positive
Catalase
Positive
Mannitol Fermentation
Fermented
Maltose Fermentation
Fermented
β-lactamase production
None
Polysaccharide Capsule
Antiphagocytic
Endotoxin (LPS)
Causes septic shock, induces cytokine release
IgA protease
Cleaves IgA antibodies in respiratory mucosa
Natural host
Humans
Transmission
Airborne droplets
Colonization
Nasopharynx
Pathogenesis
Enter bloodstream, spread to meninges, multiply in CSF
Most common disease
Meningitis in persons 2–18 years old
Outbreak seasons
Winter, early spring
High-risk environments
Close contact
Main diseases
Meningitis, Meningococcemia
Specimens for diagnosis
Blood, CSF
Diagnostic methods
Gram Staining, Culture, Oxidase Test, Fermentation Tests, Latex Agglutination Test
Gram staining result
Gram-negative bean-shaped capsulated diplococci
Oxidase test
Detects cytochrome oxidase enzyme, positive = purple within 10 seconds
Latex agglutination test
Detects capsular polysaccharide antigen in CSF
Treatment
Penicillin G, Sulphonamides
Alternative drugs
Chloramphenicol, Cefotaxime, Ceftriaxone
Prevention
Meningococcal Vaccine containing capsular polysaccharide antigens
Escherichia
Gram-negative short rods
Family
Enterobacteriaceae
Spores
Absent
Capsules
Present
Slime Layer
Present
Motility
With peritrichous flagella
Fimbriae (Pili)
Present
Oxygen Requirement
Facultatively anaerobic
Glucose Fermentation
With acid production
Nitrate Reduction
NO₃ → NO₂
Oxidase
Negative
Catalase
Positive
Nutritional Requirements
Simple (except Shigella and Klebsiella are non-motile)
K antigen
Capsular polysaccharide (heavy in Klebsiella)
H antigen
Flagellar protein of motile genera or species
O antigen
Somatic antigen, O-specific polysaccharide of LPS
F antigen
Fimbrial antigen
Vi antigen
Capsule of Salmonella
Lactose Fermenters
Citrobacter, Escherichia, Enterobacter, Klebsiella
Non-Lactose Fermenters
Shigella, Yersinia, Proteus, Salmonella
Other Genera
Morganella morganii, Providencia spp., Serratia spp., Erwinia
Opportunistic Enterobacteriaceae
Citrobacter, Enterobacter, Serratia, Morganella morganii, Edwardsiella
E. coli Host Location
Lower intestines of warm-blooded animals
Intestines of fish and cold-blooded animals
Absent
Carnivores
Present
Omnivores
Present
Stomach
Absent
Anterior bowel
Absent
Normal Flora Role
Produces Vitamin K, prevents colonization of pathogenic bacteria
Pathogenic Importance
Food poisoning, urinary tract infections (UTI)
Transmission
Fecal to oral route
Discoverer
Theodore Escherich, 1885
Model Organism
Most widely studied prokaryotic model organism
Toxin-producing strains
O157:H7
O Antigen
Somatic antigen
K Antigen
Capsule
H Antigen
Flagellar antigen
F Antigen
Adhesive fimbrial antigen (best known: K88/F4)
Heat-Labile Enterotoxin (LT)
Plasmid encoded, 1 A subunit, 5 B subunits, increases intracellular cAMP, causes diarrhea
Heat-Stable Enterotoxin (STa)
Activates guanylate cyclase, inhibits Na⁺ and Cl⁻ absorption, active in suckling mice
Heat-Stable Enterotoxin (STb)
Insoluble, no activity in suckling mice, causes fluid secretion in pig intestine
Edema Disease Toxin
Thermolabile protein, related to Shiga-like toxin 2, causes paralysis and vascular damage
Shiga-Like Toxin (SLT)
Inhibits protein synthesis, lethal to mice, enterotoxic in rabbits, destroys intestinal microvilli
Pathogenesis
Intestinal disease, septicemia of newborns, respiratory disease in poultry, opportunistic infections in udder, uterus, other tissues
ETEC
Enterotoxigenic E. coli, produces LT and ST toxins, non-invasive
EPEC
Enteropathogenic E. coli, uses intimin adhesin, causes attachment and effacement
EIEC
Enteroinvasive E. coli, invades intestinal mucosa, shigellosis-like disease
AEEC
Attaching and Effacing E. coli, produces Shiga-like toxin, destroys microvilli
EHEC
Enterohemorrhagic E. coli, e.g., O157:H7, bloody diarrhea, HUS
EAEC
Enteroaggregative E. coli, aggregates cells, watery diarrhea
AIEC
Adherent Invasive E. coli, invades epithelial cells, replicates intracellularly
Diseases in Swine
Enteric colibacillosis, neonatal enteritis, weanling enteritis, edema disease
Neonatal Enteritis
Adhesion → colonization → toxin production, watery diarrhea, fatal dehydration, up to 90% mortality