Gram Negative Bacteria

Joy N Bautista, RN, MPH, DRDM, MAN

Overview of Gram Negative Bacteria

Contains a cytoplasmic membrane. Thin peptidoglycan layer. Outer membrane containing the lipopolysaccharide layer. Porins act as pores in the outer membrane. Presence of the periplasmic space between the peptidoglycan layer and the secondary cell membrane. S-layer is directly attached to the outer membrane and not the peptidoglycan. Four flagella that support rings. Absence of teichoic acids and lipoteichoic acids. Lipoproteins are attached to the polysaccharide backbone, most of which contain Brauns lipoprotein that serve as a channel between the outer membrane and the peptidoglycan layer. Most do not produce spores.

Bacteroides
B fragilis opportunistic infections of the peritoneum, during GI surgery, and appendicitis Pathology: Opportunity to penetrate tissues Tissue necrosis and poor blood supply favor anaerobic bacterial growth Risk factors Vascular disease Cold, shock, trauma Cancer, edema, foreign bodies Gas production by bacteria

Bacteroides
B fragilis opportunistic infections of the peritoneum, during GI surgery, and appendicitis Pathology: Opportunity to penetrate tissues Tissue necrosis and poor blood supply favor anaerobic bacterial growth Risk factors Vascular disease Cold, shock, trauma Cancer, edema, foreign bodies Gas production by bacteria

Bordetella
B pertussis causative agent of pertussis Other species B parapertussis, B bronchiseptica, B avium, B hinzii Pertussis whooping cough Incubation period 1-2 weeks Catarrhal phase 1-2 weeks with low grade fever, rhinorrhea, progressive cough (highly infectious) Paroxysmal phase 2-4 weeks with severe spasmodic cough episodes, leukocytosis Convalescent phase 1-3 weeks with continuous improvement in coughing Complications bronchopneumonia, acute encephalopathy ( convulsions and death)

Bordetella
Pathology adherence to ciliated epithelium in nasopharynx Toxins Pertussis toxin reacts with T lymphocytes Heat-labile toxin dermonecrosis and vasoconstriction Adenylate-cyclase toxin penetrates host cell to increase cAMP that inhibit phagocytsis Tracheal cytotoxin Lipopolysaccharides (LPS) Agglutinogens bacterial agglutination with antibodies

Brucella
Very rare human infections; but usually via sexual intercourse or transplacental transmission Species B mellitensis goats and sheep B abortus cows B suis pigs B ovi sheep B pinnipedialis and B ceti marine mammals Infections flu-like symptoms Fever reaching 38-40OC with limb and back pains Sweating, fatigue, splenomegaly Symptoms continue for 2-4 weeks

Campylobacter
C jejuni main cause of bacterial food poisoning C coli and C fetus opportunistic infections Infections fecal-oral transmission Mild GI distress to fulminating or relapsing colitis Diarrhea, abdominal pain, fever, nausea, vomiting, bloody stools Massive watery-diarrhea like cholera Toxic megacolon, pseudomembranous colitis Complications Guillain Barre syndrome 2-3 weeks after diarrhea Pathology shedding (106-109 spp per gram of feces) with destruction of epithelial glands

Chlamydia
Obligate intracellular parasitic bacteria C trachomatis, C pneumoniae, C psittaci C trachomatis infections transmitted sexually or by contact with contaminated fingers, towels, fomites, and by passage through an infected birth canal Trachoma conjunctival infection Inclusion conjunctivitis STDs non-gonococcal urethritis, epididymitis, proctitis, acute salpingitis, cervicitis Neonatal acute conjunctivitis Lower RTI, pneumonia, bronchopneumonia Polyarthritis, lymphogranuloma venereum (with inguinal lymphadenopathy)

Chlamydia
C psittaci infections transmitted from infected birds or animals through the respiratory tract Fever, mild flu-like disease Toxic fulminating pneumonitis, pneumonia C pneumoniae infections spread via respiratory secretions Outbreaks of RTI Trachoma, inclusion conjunctivitis Lymphogranuloma venereum

Coliforms and Proteus

Coliforms Escherichia, Klebsiella, Serratia, Citrobacter, Proteus Produce opportunistic infections in the weakened patient Enteric infections infections of the GI Nosocomial infections infections in hospitalized patients Surgical, burn, high-risk nursery patients Sites: urinary tract, surgical sites, bloodstream, lower respiratory tract Others: catheterization, indwelling devices, invasive procedures

Coliforms and Proteus

Opportunistic infections Community-acquired infections UTI Proteus, Klebsiella, Enterobacter Bacteriuria P mirabilis Pneumonia Klebsiella Rhinoscleroma K rhinoscleromatis Nasal atrophy K ozaenae

Escherichia
Become pathogenic only when they acquire genetic elements that encode for virulence factors ETEC enterotoxigenic E coli Rapid onset watery, non-bloody diarrhea x 1-3 days Abdominal pain, malaise, nausea/vomiting EIEC enteroinvasive E coli; cause tissue destruction Bloody diarrhea with fever (hemorrhagic colitis) Abdominal pain with scanty stool containing blood and mucus (bacillary) EPEC enteropathogenic E coli; diarrhea outbreaks in nurseries; no toxins or invasion factors

Haemophilus
Infections meningitis, septicemia, pneumonia, bacterial endocarditis, chancroid, conjunctivitis, Brazilian purpuric fever Agents H influenzae, H parainfluenzae, H ducreyi, H aphrophilus, H aegyptius, H haemolyticus Pathology presence of type b polysaccharide capsule Penetration in the nasophrayngeal epithelium Invasion of capillaries leading to inflammation Meningitis, cellulitis, epiglottitis, respiratory diseases, otitis media, bronchopulmonary diseases, septic arthritis, neonatal sepsis

Helicobacter
Infections peptic ulcers, chronic gastritis, duodenitis, gastric cancer Agent H pylori Pathology production of urease that releases ammonia Present underneath the mucus layer Ammonia toxigenic to cells potentiate mucosal injury Inflammatory infiltration with PMNs, eosinophils, lymphocytes with lesion formation

Legionella
Infection Legionnaires disease, pneumonia, Pontiac fever, bacteremia transmitted by inhalation of mist droplets Pathology transmission with contaminated water Bacteria survives alveolar phagocytosis (macrophage) Inhibition of lysosomal fusion with phagosome Bacterial multiplication in he phagosome Macrophage is destroyed, releasing new generation of bacteria to infect other cells

Neisseria
Infections gonorrhea (N gonorrhea), acute bacterial meningitis (N meningitidis) Normal flora of the human mucosa N gonorrhea infections Vulvovaginitis, urethritis, endocervical infections Rectal infections, gonococcal proctitis, pharyngeal infections Ocular infections ophthalmia neonatorum, keratoconjunctivitis Dermatitis-arthritis syndrome fever, chills, skin lesions, arthralgias causes endocarditis, meningitis Endometritis, salpingitis, peritonitis

Neisseria
N meningitidis infections Acute meningococcemia chills, fever, malaise, h/a, vomiting, Kernigs, Brudzinskis Meningococcal meningitis no meningeal irritation, irritability, anorexia, vomiting, fever, seizures, motor tone problems, coma Fulminant meningococcemia (WaterhouseFriderichsen syndrome) high mortality rate; sudden high fever, chills, myalgias, weakness, n/v, h/a, apprehension, restlessness, delirium purpuric and ecchymotic lesions pulmonary insufficiency die within 24 hours Petechiae or purpura

Neisseria
Other agents Moraxella catarrhalis, M lacunata, M nonliquefaciens, M urethralis usually harmless; may cause pneumonia, meningitis, endocarditis, otitis media, sinusitis, conjunctivitis Kingella kingae, K dentrificans oral flora; infections of the bone, joints, tendons Eikenella corrodens Pathology N gonorrhea antigenic phase variation, enter epithelial cells, LOS action mucosal damage, production of TNF, resist bactericidal activity N meningitidis spread by respiratory droplets, LPS suppresses leukotriene synthesis decreased chemotaxis

Pasteurella
Infections swelling, cellulitis, bloody drainage, arthritis Agents P multocida, P hemolytica (hemorrhagic pneumonia in horses and cattle) Pathology nasopharyngeal colonization d/t cat or dog bites Localized abscess of extremities or face Spread to draining lymph nodes

Pseudomonas
Opportunistic infections major threat to hospitalized patients, not to healthy ones P aeruginosa UTI, cystic fibrosis, necrotizing pneumonia, otitis media, meningitis, bacteremia, eye and ear infections P maltophilia pneumonia, endocarditis, UTI, wound infections, septicemia, meningitis P cepacia endocarditis, necrotizing vasculitis, pneumonia, wound infections, UTI, chronic lung infections P mallei, P pseudomallei glanders, melioidosis

Pseudomonas
Pathology secretion of exopolysaccharides and other systems that export proteins Escape from phagocytosis with hemolysis Produce thermolabile protein (leukocidin) which destroy WBCs Production of large amounts of extracellular polysaccharides that impair phagocytosis Extracellular protease digests casein and elastin and induce formation of hemorrhagic lesions necrosis Toxin A inhibits cell synthesis Exoenzyme S

Rickettsia
Obligate intracellular parasites carried by ticks, fleas, lice 3 classifications: Spotted fever R rickettsii, R akari, R conorii, R sibirica, R australis, R jaonica, R africae, R hoogstraalii Typhus R prowazeckii, R typhii Scrub typhus R tsutsugmushi (Orientia tsutsugmushi) Infections Rocky Mountain spotted fever severe vascular damage with thrombocytopenia d/t vascular plugging Rickettsial pox fever, rash, cutaneous necrosis Boutonneuse fever cutaneous necrosis

Rickettsia
Infections North Asian tick typhus, Queensland tick typhus, Oriental spotted fever Epidemic typhus and Brill-Zissner disease d/ unsanitary and crowded conditions Murine typhus in seaports Pathology transmission by vector bites and by feces of infected lice and fleas Induction of phagocytosis with escape into cytosol Rickettsial division in cell leading to cell lysis Release of microbes to infect other cells

Salmonella
Infections typhoid fever, paratyphoid fever, other foodborne infections Agents found in chicken, turkeys, pigs, cows Enteric fevers (typhoid fever) S typhi, S paratyphii, S schottmuelleri Gastroenteritis S typhimurium, S enteritidis Septicemia S choleraesuis Pathology ingestions of contaminated food Release of virulence factors Invasions and replication in the intestinal lumen Colonization, invasion, and proliferation in colonic epithelium and lymphoid follicles Inflammatory response ulceration

Shigella
Infections - bacillary dysentery (severe scant diarrhea containing mucus and/or blood and inflammatory cells) Species S dysenteriae complication: bacteremia S flexneri and S sonnei complications: convulsions, neurologic symptoms S flexneri complication: reactive arthritis S/Sx watery diarrhea, vomiting, mild dehydration, bloody mucoid stools, tenesmus, cramps Daily loss of 200-300 mL of serum protein in feces Depletion of nitrogen stores malnutrition Pathology release of cytikine IL-1 that initiate PMN infiltration

Vibrio
Infections cholera; life-threatening secretory ricewatery profuse diarrhea Agents V cholerae Trasmission eating undercooked or raw seafood S/Sx associated with fluid and electrolyte loss Watery diarrhea up to >1L in the initial hour Several liters of fluid within hours leading to hypovolemic shock Death d/t hypovolemic shock, metabolic acidosis, uremia from ATN Pathology expression of adherence factors and cholera enterotoxins

Yersinia
Infections bubonic plague; transmitted through blood or by ingestion of food contaminated with infected urine or feces Species Y pestis, Y enterocolitica Pathology development in tissue macrophages Re-encapsulation prior to release into tissues Spread to lymph nodes which become hot, swollen, tender, and hemorrhagic black buboes Spread via bloodstream to liver, spleen, lungs Severe bacterial pneumonia