Gram Negative Bacteria New(1)

7/27/2019 Gram Negative Bacteria New(1)

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Gram

Negative

BacteriaJoy N Bautista, RN, MPH, DRDM, MAN


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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.


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Bacteroides

B fragilis opportunistic infections of theperitoneum, during GI surgery, and appendicitis

Pathology:

Opportunity to penetrate tissues

Tissue necrosis and poor blood supply favoranaerobic bacterial growth

Risk factors

Vascular disease

Cold, shock, trauma

Cancer, edema, foreign bodies

Gas production by bacteria


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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


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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 continuousimprovement in coughing

Complications bronchopneumonia, acute

encephalopathy ( convulsions and death)


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Bordetella

Pathology adherence to ciliated epithelium innasopharynx

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


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Brucella

Very rare human infections; but usually via sexualintercourse 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


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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


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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)


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Chlamydia

C psittaci infections transmitted from infected birds oranimals through the respiratory tract

Fever, mild flu-like disease

Toxic fulminating pneumonitis, pneumonia

C pneumoniae infections spread via respiratorysecretions

Outbreaks of RTI

Trachoma, inclusion conjunctivitis

Lymphogranuloma venereum


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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


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Coliforms and Proteus

Opportunistic infections Community-acquired infections

UTI Proteus, Klebsiella,

Enterobacter

Bacteriuria P mirabilis

Pneumonia Klebsiella

Rhinoscleroma K

rhinoscleromatis

Nasal atrophy K ozaenae


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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 containingblood and mucus (bacillary)

EPEC enteropathogenic E coli; diarrhea

outbreaks in nurseries; no toxins or invasion

factors


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Haemophilus

Infections meningitis, septicemia, pneumonia, bacterialendocarditis, 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, septicarthritis, neonatal sepsis


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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


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Legionella

InfectionLegionnaires 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 hephagosome

Macrophage is destroyed, releasing

new generation of bacteria to infect

other cells


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Neisseria

Infections gonorrhea (N gonorrhea), acute bacterialmeningitis (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, skinlesions, arthralgias causes endocarditis, meningitis

Endometritis, salpingitis, peritonitis


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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 (Waterhouse-

Friderichsen 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


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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


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Pasteurella

Infections swelling, cellulitis,bloody drainage, arthritis

Agents P multocida, P

hemolytica (hemorrhagic

pneumonia in horses and cattle)

Pathology nasopharyngealcolonization d/t cat or dog bites

Localized abscess of

extremities or face

Spread to draining lymph

nodes


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Pseudomonas

Opportunistic infections major threat to hospitalizedpatients, not to healthy ones

P aeruginosa UTI, cystic fibrosis, necrotizing

pneumonia, otitis media, meningitis, bacteremia, eye and

ear infections

P maltophilia pneumonia, endocarditis, UTI, woundinfections, septicemia, meningitis

P cepacia endocarditis, necrotizing vasculitis,

pneumonia, wound infections, UTI, chronic lung

infections

P mallei, P pseudomallei glanders, melioidosis


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Pseudomonas

Pathology secretion of exopolysaccharides and othersystems 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


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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 vasculardamage with thrombocytopenia d/t vascular plugging

Rickettsial pox fever, rash, cutaneous necrosis

Boutonneuse fever cutaneous necrosis


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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


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Salmonella

Infections typhoid fever, paratyphoid fever, other food-

borne 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


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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


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Vibrio

Infections cholera; life-threatening secretoryrice-

watery 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


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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 hemorrhagicblack buboes

Spread via bloodstream to liver, spleen, lungs

Severe bacterial pneumonia


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Gram Negative Bacteria New(1)

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