G (-ve) Cocci B. Nomanpour
Neisseriaceae Neisseria Kingella Eikenella Simonsiella Alysiella
Neisseriaceae Neisseria- cocci Moraxella, Acinetobacter- rods Subgenus Branhamella- cocci Acinetobacter- rods Kingella- rods
Characteristics Aerobic Gram-negative cocci : arranged in pairs (diplococci) like coffe beans Oxidase positive Most catalase positive Nonmotile Acid from oxidation of carbohydrates
Pathogenic Species Neisseria gonorrhoeae(plasmid+) Neisseria meningitidis (capsule +)
Infectious Diseases (Ophthalmia neonatorum)
Saprophytic Species Neisseria lactamica N. polysaccharea N. cinera N. flavescens N. subflava N. sicca N. mucosa
Neisseria gonorrhoeae (gonococcus)
Gonorrhea STD Only in humans Asymptomatic carriage is major reservoir Antigenic diversity of strains Higher risk of disseminated disease in patients with late complement deficiencies C5,6,7&C8 Urethritis; Epididymitis
Women Infection Cervicitis Vaginitis Pelvic Inflammatory Disease (PID) Disseminated Gonococcal Infection (DGI) Scarring of fallopian tubes : infertility or ectopic pregnancy
Disseminated Gonococcal Infection (DGI) Gonococcal bacteremia Skin lesions Petechiae (small, purplish, hemorrhagic spots),Pustules on extremities Arthralgias (pain in joints) Tenosynovitis Septic arthritis Occasional Hepatitis; Rarely endocarditis or meningitis Fitz-hugh-Curtis Syndrome
Gonococcal ophthalmia neonatorum corneal epithelium causing microbial keratitis, ulceration and perforation
Pathogenicity Pili- (human columnar epithelial cells) inhibit phagocytosis. Protein I (Por) a porin is important for intracellular survival. Protein II (Opa): 11-12 genes Heparin-related compounds and CD66 or carcinoembryonic antigen Rmp (Protein III) a reduction-modifiable protein the formation of pores Blocks host serum bacteriocidal (IgG) action
Pathogenicity Lipooligosaccharide: LOS (blebs) Causes ciliary loss and mucosal cell death Molecular mimicry Suppression of leukotreine B4 synthesis→ inhibits PMN activation Activates alternative complement pathway Activates TNF → inflammation Lip (H8) is a surface exposed is heat modifiable like Opa.
Pathogenicity Tbp 1 & Tbp 2 (transferrin-binding proteins) Fbp (ferric-binding protein) IgA1 protease Tbp 1 & Tbp 2 (transferrin-binding proteins) Lbp (lactoferrin binding protein) Hbp (hemoglobin-binding protein) Plasmid-encoded beta-lactamase Chromosomally-mediated :penicillins, tetracycline, erythromycin,aminoglycosides
Induced uptake
Prevention & Treatment Ceftriaxone , cefixime or fluoroquinolone Combined with doxycycline or azithromycin for dual infections with Chlamydia Chemoprophylaxis of newborns against opthalmia neonatorum with 1% silver nitrate, 1% tetracycline, or 0.5% erythromycin eye ointments Treatment of newborns with opthalmia neonatorum with ceftriaxone
Neisseria meningitidis (meningococci)
N.meningitidis Second most common CA meningitis Capsule Younger 20 years Capsule 13 capsular serogroups (A, B, C, Y, and W135) with 90% of meningococcal disease due to serogroups A, B, and C Pili-mediated, receptor-specific colonization of nonciliated cells of nasopharynx Toxic effects by hyperproduction of LOS
Infectious Disease Meningitis Septicemia (meningococcemia) with or without meningitis Meningoencephalitis Pneumonia Arthritis Urethritis
Infectious Disease N. meningitidis : rapidly progressive meningitis School-aged children, adolescents, and young adults with a mortality of 7-13% N. meningitidis bacteremia (mortality of 19-70%) Waterhouse-Friderichsen syndrome Petechiae Purpura Adrenal hemorrhage Disseminated intravascular coagulation (DIC) Shock
Waterhouse-Friderichsen syndrome
Pathogenesis GD1 ganglioside :receptor Internalizing into phagocytic vacuoles Replicate intracellularly and migrate to subepithelial space LOS: blebbing L2,L3,L7,L9 Thrombosis (clotting), disseminated intravascular coagulation (DIC) Autolysin(amidase)
Diagnosis
Modified Thayer-Martin Agar Colistin: Inhibits gram-negative flora (N. gonorrhoeae and N. meningitidis resistant to colistin, most saprophyic species of Neisseria susceptible) Vancomycin: Inhibits gram-positive flora Nystatin: Inhibits yeast flora Trimethoprim: Inhibits swarming Proteus
Findings in CSF Clear , colorless 0-5 lymphocytes Sterile Normal CSF: Clear , colorless 0-5 lymphocytes Sterile 150-450 mg /l protein 2.8-3.9mmol/l glucose
Neisseria and Related Organisms N. gonorrhoeae
Identification On chocolate agar :White Acid from glucose but not maltose, sucrose, fructose, or lactose Positive superoxol test (Catalase with 30% H2O2) Colistin resistance (growth on Modified Thayer-Martin medium)
Neisseria and Related Organisms N. meningitidis
Biochemical Reactions
Antimicrobial Therapy Neisseria and Related Organisms Antimicrobial Therapy Pen-resist Cefinase test (cephalosporin) CMRNG (chromosome mediated resistant N.gonorrhoeae). Tetracycline and Spectinomycin chromosomal mediated resistance strains also occur. Ceftriaxone, a third generation cephalosporin, is recommended N. meningitidis :Penicillin
N. meningitidis - Vaccines Tetravalent capsular polysaccharide vaccine (Menomune-A,C,Y,W-135) (Sanofi Pasteur, Inc.) against four (A, C, Y, and W-135) of the five pathogen serogroups. Highly effective in adults but not in infants and children less than two years of age; immunity ~3 years. No vaccines available against serogroup B N. meningitidis (MenB) disease, is responsible for 32% of meningococcal disease in the U.S. and 45% to >80% in Europe.
N. meningitidis - Vaccines The MenB capsular polysaccharide is identical to a widely distributed human carbohydrate (a self-antigen). The immunity to N. meningitidis group B must develop naturally after exposure to cross-reacting antigens. Vaccination with Menomune - to control an outbreak of disease with a serogroup present in the vaccine, for travelers to hyperendemic areas, or for individuals at increased risk (patients with complement deficiency).
In January 2005, a quadrivalent meningococcal polysaccharide-diphtheria toxoid conjugate vaccine [MCV4] Menactra (Aventis Sanofi Pasteur, Inc.) was licensed for use among persons aged 11-55 years. CDC recommends routine vaccination of young adolescents (at aged 11-12 years) with MCV4 at the preadolescent health-care visit (at age 11-12 years). By 2008, the goal will be routine vaccination with MCV4 off all adolescents beginning at age 11.
Acinetobacter