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Infections > Bacteria Pt 2 > Flashcards

Bacteria Pt 2 Flashcards

1
Q

What are general characteristics of Staphylococci bugs?

A
  • Gram positive cocci
  • produce catalase
  • S aureus is coagulase positive, the rest of Staph are not
  • tend to appear in grape like clusters
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2
Q

What are tests that can be done to differentiate S aureus (3)? What color are the colonies of S. aureus?

A

Coagulase positive (S. epidermididis is coagulase negative)
produces clumping factor
contains protein A (an IgG binding protein)

S epidermidis is negative for these three

Gold

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3
Q

What are the characteristics of Staphylococcus epidermidis?

A

Classification: Coagulase -, Clumping F-, Protein A-, White colonies

Transmission: colonized on skin (part of skin flora)

Pathogenesis: produces exopolysaccharides (slime)

Defense: Antibacterial resistance (plasmid DNA contains resistance genes), Catalase, Slime makes adherance to foregin bodies easier

Clinical: UTI, Nosocomial Bacteremia, Endocarditis of native OR prosthetic valve, Osteomyelitis, Infections of prosthetic devices, bladder infections in sexual active women

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4
Q

How is S. aureus transmitted?

A

Encounter: 25% of normal healthy people are carriers

Transmission: Risk of Invasive disease increases in:

  1. Carriers
  2. Post-Influenza A
  3. Chemotactic defects in WBC, Phagocytic Cells
  4. Patients with other immune defects (complement deficiency- gamma globulin deficiency)

Colonization:
Anterior nares
Axilla, grown

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5
Q

How does S. aureus pathogenesis occur?

A

Virulence factors in cell wall include peptidoglycan, teichoic acids, protein A

Superantigens- activate up to 20% of immunity non-specifically (similar to Strep toxins)
- overwhelming inflammatory response including fever, shock, endothelial leakage, multiorgan failure, and sometimes death

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6
Q

What are some specific toxin causing diseases associated with S aureus?

A
  1. Epidermolytic Toxins- Staph scaled skin syndrome (SSSS) causing exfoliation, ET-A and ET-B responsible for manifestation
  2. Enterotoxin- Toxic Shock Syndrome- leads to desquamation, hypotension, and diarrhea
    - sustained release of inflammatory cytokines, non-specific T cell mitogens interact with Class II MHC, stimulate CD4 cells to produce IFN-gamma
    - other enterotoxins are major source of food born illness producing vomitting and diarrhea, these toxins are heat stable
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7
Q

What are defense mechanisms/virulence factors for S. aureus?

A

Catalase- inactivates bactericidal hydrogen peroxidase

Coagulase- converts fibrinogen to fibrin which decreases WBC accumulation by creating a barrier clot

B-lactamase- hydrolyses active binding site on penicillin (resistance)

Secreates hyaluronidases, DNAses, and Lipases

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8
Q

What is the clinical presentation of S aureus?

A

Localized infection: folliculitis, carbuncles, impetigo, cellulitis, wound infections
PUS PUS PUS

Deep infection:

  • abscesses (brain abscess, endopthalmitis, renal carbuncle, splenic abscess
  • bacteremia
  • infection (bursitis, myositis, osteomyelitis, pneumonia, septic arthritis)

Endocarditis (tx 4-6 weeks IV Abs)

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9
Q

How does S. aureus design it’s resistance? What can treat it?

A

Produce beta-lacatamase which hydrolyzes binding site of PCN

MRSA- alter the Penicillin Binding Protein 2 to PBP2a

Treat with vancomycin (recently S aureus has become resistant to this, received resistance to vancomycin from enterococcus)

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10
Q

How is S. epidimis treated?

A

Vancomycin plus rifampin (80% are methicillin resistant)

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11
Q

Name 3 factors that enable S aureus to damage host tissue and form pus?

A

Coagulase
Catalase
Hyaluronidase

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12
Q

What are two examples of toxin mediated disease in the Staph family?

A

Staph scaled skin syndrome

toxic shock syndrome

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13
Q

Why are S coagulase negative staphylocci able to survive and avoid host defenses in patients with prosthetic devices?

A

Production of exopolysaccharides or slime which helps adhere to foregin bodies and prevents binding of immune cells

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14
Q

What are general characteristics of spirochetes?

A

Dark field microscopy needed to visualize

Outer and Inner membrane like Gram-, but no LPS, dont gram stain well

Difficult/impossible to grow in vitro

HIGHLY MOTILE due to endoflagella

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15
Q

What are diseases caused by different spirochete bugs?

A

Syphilis- Treponema pallidum

Lyme disease- Borrelia burgdorferi

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16
Q

What are the general characteristics of Borrelia burgdorferi?

A

Classification: Highly motile, endoflagella between membranes increases risk for systemic infection

Encounter: Deer tick (ixodes) in NE and Great Lakes

Colonization: Arterial blood, vessels, CT, skin

Pathogenesis: Binds decorin protein on collagen to adhere to host cells

  • coats itself with host protease (plasminogen- just like Yersinia pestis) and may produce systemic infection
  • Few antigenic target: OspA- displayed when in tick, not once in human, OspC once in human, and prevents complement binding–> antigenic diversity (like Nisseriae)
  • Tissue damage is secondary to intense inflammatory response
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17
Q

What is the clinical presentation of Lyme Disease and what is the treatment?

A

Primary Local Spread

  • Days to weeks
  • expanding skin lesion, erythema migrans

Secondary Infection

  • weeks to months
  • 2nd erythema migrans, heart block, arthalgia, shooting pain, Bells palsy, meningitis, eye findings

Chronic Infection
- acrodermatitis atrophicans, chronic inflammatory arthritis with autoimmune etiology, difficulties with memory/concentration

Prevention/Treatment

  • protective clothing/insect repellant
  • antibiotics (early to prevent chronic infection)
  • OspA Vaccine
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18
Q

What are the characteristics of traponema pallidum?

A

Classification: Highly motile

Encounter: Human muccous membranes, small skin abrasions

Transmission: Sexual Contact, can cross placenta

Important points: Can cross placenta and cause multi-systemic infection, difficult to diagnose because organism cannot be cultured and serology is critical for diagnosis

Pathogenesis: Lipoproteins induce cytokines, Similar to B. burgdorderi, few antigenic targets, no known endo/exo toxins

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19
Q

What is the clinical presentation and treatment of Traponema pallidum?

A

Sexually Acquired Syphilis
Primary- Chancre- painless ulcer which heals in two to six weeks
Secondary- invasion and systemic illness, flu like Sx’s, lymphadenopathy
Tertiary- Great immitator, gummus, vasculitis, chronic inflammation of bone, CNS, sensory loss, personality changes

Congenitally Acquired Syphilis

  • prematurity, diminished growth
  • facial, tooth, bone deformities, deafness
  • arthritis

Prevention and Treatment
- PCN very effective, difficulty in reaching high risk communities, no vaccine 2nd to lack of antigenic targets

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20
Q

What are some similarities between Lyme and Syphilis?

A
  • Infections occur in stages
  • Periods of remission followed by relapse, with a variety of disease manifestations
  • Low bacterial load
  • Tissue destruction triggered in part by lipoproteins
  • Vigorous immune response is not able to clear organism
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21
Q

What host protease does Lyme disease spirochete coat itself with? What function might this serve in the mammalian host? What function might this serve in the tick vector?

A

Plasminogen

Promote systemic infection in both the mammal, and tick

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22
Q

What major pathogenic strategies contribute for Lyme disease and syphilis spirochetes to cause chronic infection?

A

motile
few antigenic targets
antigenic variation
major inflammatory response

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23
Q

How does Lyme and syphilis produce an inflammatory response?

A

Produce a cytokine leading to an inflammatory response, no toxin!

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24
Q

What is the syphilitic equivalent to erythema migrans? Are both lyme and syphilis potentially spread congenitally?

A

painless ulcer

no, only syphilis

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25
Q

What are characteristics of Vibrio, Campylobacter, and Helicobacter species? How do they differ?

A

curved, microaerophilic, gram negative associated with human disease

differ in their environmental niches and disease manifestations

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26
Q

What are key concepts of Vibrio species?

A
  1. environmental organisms
  2. toxin mediated diarrheal disease
  3. wound infections
  4. systemic infections- compromised host
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27
Q

What are key concepts of Campylobacter species?

A
  1. Zoonotic infections
  2. Diarrheal disease
  3. Systemic infections- compromised host
28
Q

What are the key concepts of helicobacter pylori?

A
  1. Pathogen/commensal of human stomach
  2. chronic gastritis
  3. Peptic ulcer disease
  4. Gastric cancer
29
Q

What are characteristics of genital mycoplasms?

A

Encounter: Asymptomatic vaginal carriers (60%), sexual contact
Pathogenesis: Mycoplasma hominus, Ureaplasma urealyticum
- gliding motility to spread
- resistant to exfoliation of urinary tract epithelium
Associations:
- Endometritis
- Male non-gonoccal urethritis (20%)
- PID (

30
Q

What are the classifications and encounter of Mycoplasm pneumoniae?

A

Growth: 6 hr doubling, Fried egg appearance after 5-20 days, No murein cell wall, Osmotically fragile, small genome
Lab isolation: cell free media, Nutrient requirements: cholesterol, AA, nucleic acid precursors

Encounter: Respiratory Droplets (moderately contagious) and colonized on respiratory epithelium

31
Q

What is the pathogensis of Mycoplasma pneumoniae?

A

4-8 year cycles, HERD IMMUNITY
Mini epidemics in closed populations
- attachment to epithelium via terminal attachment structure with an adhesive protein (P1) that binds to sialylated glycoprotein on the hose cell
- slow growing with incubation period of 2-3 weeks vs 1-3 days for most viruses
- some infections localized as URI
— R epithelium only, no alveolar involvement, elicits mononuclear infiltrate surrounding bronchi or bronchioles (not a lobar process)
- spread to other hosts by blocking ciliary clearance, mucosal irritation, cough

32
Q

What is the clinical presentation, diagnosis, and treatment of Mycoplasma pneumoniae?

A

5-10% of cases progress to tracheobronchitis or pneumonia

Walking (Atypical) Pnemonia

  • headache and cough
  • no cervical adenopathy
  • CXR- non lobar patchy interstitial pattern
  • Non-responsive to sulfonamides or penicillins
  • No causal agent by gram stain or routine culture

Diagnosis: usually not specifically diagnosed because it is self limiting and difficult to culture (slow growing)

Not effected by cell wall antibiotics

Use Tetracycline, Erythromycin, Azithromycin

33
Q

What is the classification and transmission patterns of Mycobacterium tuburculosis?

A

Classification: no gram stain, aerobe, slow growing rod, waxy coat, acid fast stain
Encounter: brief encounters pose little risk, need close contact with infected individuals for infection
Transmission: Inhalation (droplets) and fairly contagious
Colonization: alveolar macrophages

34
Q

What is the pathogenesis of Mycobacterium tuburculosis?

A

Initial Spread: from initial point, spreads elsewhere in macrophages via blood and lymph, no symptoms within first few weeks

Containment of Infection:

  • cell mediated immunity (CD4)
  • granuloma contains infection
  • if unstable containment, get active Tb diseases with caseous necrosis (normal host) and hematogeous spread (extra-pulmonary disease and miliary Tb)

Primary vs Secondary Tb

  • 90%: primary infection contained, scar forms indiciating old disease
  • 10%: reactivation of disease given following conditions:
    • illness, malnutrition, stress, immunocompromise (AIDS)
35
Q

What is the clinical presentation, diagnosis, and treatment of Mycoplasma Tb?

A
  • Organism may remain dormant for years
  • Tb pneumonia-primary
  • Rare- patients with lacking immunity get miliary Tb (millet seeds in lung)
  • If caseous lesions liquefy and dishcharge, Tb spreads to other sites (caviation)
    • growth of bacterial load (O2 access now), contagion (free in lung–> cough), spread to other sites in patient

Diganosis:

  • PPD- Tests T cell immunity, not disease
  • – False positive- BCG vaccination within 5 years, atypical mycobacterium, BCG treatment for bladder cancer
  • – False negative- immunocompromised patients who cant respond
  • IFN gamma release assays test for immune response using T cells from blood

Treatment:

  • multiple drug regimen to avoid resistant Tb, usually for 6-9 months
  • – Spontaneous resistance in 10^-6-10^-7
  • — Heterogeneity in bacterial population
  • – Multidrug resistant variants likely when more than 10^7 bacteria present, which is common in a granuloma
  • Isoniazid, rifampin, PZA, ethambutol- first line agents

Chemoprophylaxis (treatment for latent Tb)
- isoniazid and rifampin

36
Q

What are the characteristics of non-tuburculosis Mycobacteria?

A

No gram stain, aerobe, slow growing rods, slow growth (days to weeks), acid fast stain

Encounter: Ubiquitous in water
M marinum- fish
M fortuitum- complex nail infections

Transmission: no human to human transmission

Colonization: sputum, fish tanks, water containing items, surgical wounds

Pathogenesis: found in sputum and may invade areas of abnormal lung, infects tissues and spreads to lymph nodes, may cause skin and soft tissue infection

Clinical Presentation: pulmonary infections in elderly women and immunocompromised hosts
- disseminated infections in advanced HIV/AIDS

Prevention/Treatment: Direct probe to culture for some (MAC), grow repetedely on bronchoscopy or from tissue to prove infection
Treatment is often worse than disease, and need multiple drug regimen to avoid selecting resistance for 12-24 months

37
Q

What are the characteristics of Mycobacterium leprae?

A

No gram stain, not culturable in vitro, grows in 9 banded armadillo, acid fast stain

Encounter: found in endemic areas

Transmission: human to human, not easily transmitted

Pathogenesis: infects cool areas of the body, anesthetic hypopigmented macules, pathology depends on host

Clinical Presentation: Hansen’s disease

    • Lepromatous- multibacilliary, bad, poor T cell response, good humoral response
    • Tuburculoid- not as many bacteria, good T cell response, poor humoral response

Diagnosis: biopsy, clinical presentation in endemic area

Treatment: multi drug regimen 2-5 years

38
Q

What are the general characteristics and transmission patterns of Bacillus anthracis?

A
  • Gram + rod, aerobe, capsule forming (antiphagocytic)
  • invasive, non-motile, spore former

Encounter: spores in soil deposited by dead/dying animals
Transmission: damaged skin, inhalation, ingestion
Colonization: skin, pulmonary system, GI tract

39
Q

What is the pathogenesis of Bacillus anthracis?

A

Toxins: AB- share a B Moiety (protective antigen) which is encoded by plasmid
Edema Factor: AB- adenylate cyclase
Lethal Factor: AB- produces IL-1 and TNF production by Mphage, induces Mphage apoptosis
Capsule: Antiphagocytic PEPTIDE capsule (not polysaccharide)

40
Q

What is the clinical presentation of Bacillus anthracis?

A

Cutaneous anthrax (95%)

  • initial red papule–> ulcer
  • dark scab (Escher) forms surrounded by Edema
  • Minimal systemic symptoms
  • 5-20% mortality untreated

Pulmonary Anthrax:

  • Mild fever and malaise, non productive cough (1-4 d), respiratory distress (2-4 d), poor local inflammation response
  • edema of neck and chest (EF mediated)
  • hematogenous spread
  • septic shock
  • high mortality after acute phase

Gastrointestinal Anthrax
- high mortality due to toxemia and sepsis

Diagnosis: early diagnosis critical, readily cultured and identified for confirmation
Cutaneous Anthrax: Antibiotics
Pulmonary Anthrax: Antibiotics effective if given early
Control: Vaccine (animals and at-risk workers)

41
Q

What are the general characteristics, encounter, and transmission of Listeria monocytogenes?

A

Gram + rod, Facultative aerobe, non-spore former, intracellular invasion
Cell-mediated immune response necessary to clear infection!
Encounter: water, soil, birds, mammals, fish, 1-5% are fecal carriers
Transmission: Foodborn (cheese, milk, under-cooked meat), transplacental at birth NOT in utero
Colonization: Intestinal epithelium, intestinal macrophages

42
Q

What is the pathogenesis of Listeria monocytogenes?

A

Lysteriolysin lyses the phagosome, replicates in the cytoplasm, and utilizes host cell actin for motility
– membrane collision results in projections towards a 2nd cell, projections pinch off to yield a vacuole with 2 membranes, vacuole lysed (PLC) in the new cell
Damage: Septicemia or meningitis, rare focal infections (3%)
- host-antibacterial response causes most pathogenesis (SEPSIS SYNDROME), NO SYSTEMIC TOXINS

43
Q

What is the clinical presentation/hallmarks/diagnosis and treatment of Listeria monocytogenes?

A

High Risk Groups- Pregnancy
– Mother: febrile bacteremia causing labor induction, meningitis
– Baby: granulomatosis, disseminated infection with abscesses, fatal
Neonates (3d), Immunosuppressed individuals
– Sepsis of unknown origin (fever, chills, hypotension), bactermemia, meningitis
– Meningitis and cerebritis is most common cause, patients have neoplastic disease, no neutropenia, occurs in previously healthy adults
- Low mortality

Diagnosis: Hx, Sx, Setting, Blood/CSF Culture, Direct Gram stain
Treatment: ampicillin, penicillin, TMP/sulfamethoxazole

44
Q

What are some characteristics of Bacteroides fragillis?

A

Encounter: Gram negative bacilli, anaerobic, part of normal flora in GI tract, female genital tract
Virulence: Produces beta lactamase
Pathogenesis: Abscess formation due to capsular polysaccharide with repeating units of +/- charged sugars, capsule induces protective cell-mediated immune response
If infection below the diaphragm, treat for bacteroides and clostridium

45
Q

Which organisms contribute to infections above the diaphragm, and which ones below the diaphragm?

A

Above- gram positive cocci, Fusobacterium

Below- Bacteroides fragilis and Clostridum species

46
Q

What are common bacteria at different sites of the normal flora?

A

Oral Cavity: Gram + (Peptococcus species, Peptostreptococcus species)
Gram - (Fusobacterium species)

GI Tract: Bacteroides fragilis (gram -)

Female Genital Tract: Clostridium (spore formers)

47
Q

What are features of Bartonella?

A

Gram negative
Cat scratch fever (axillary lymph nodes, immunocompetent people)
Bacillary angiomatosis- immunocompromised individuals
Treatment: doxycycline, macrolides

48
Q

What are Brucella sp. characateristics?

A

Pleomorphic gram negative rod
Produces Urease
Facultative Intracellular
Pathogens of cattle, pigs, sheep–> veterinary medicine
Produce Brucellosis- a granulomatous disease/undulent fever with fever, headache, anorexia
Can be followed by persistant infection, with potential for systemic symptoms

Encounter: unpastuerized dairy products or penetration of mucous membranes with exposure to infected animals

Spread: Acute phase: bateria move from site of infection to lymph nodes, predilection for RES, lives in macrophage, escapes phagolysosome fusion by generating a replicative vacuole
Chronic: months to years–> undulant fever with manifestations of arthritis, epididymitis and orchitis, host attempts to control infection by forminga granuloma

Diagnosis/Treatment: slow growing, involves multi-drug antibiotic treatment with one which can act in macrophage acidic environment (similar to Tb treatment)
Tetracycline and rifampin

49
Q

What are general characterisitcs of Campylobacter?

A

Commensal of GI or animals (cattle, sheep, goats etc.)
- bile salt resistant, microaerophilic, motile, non-spore former, slow growth, prolonged incubation for lab growth needing selective media

50
Q

What are characteristics of Campylobacter jejuni?

A

Curved, gram negative rod
Encounter: animal exposure, contaminated food, grows at 42, oxidase positive

Virulence: cytotoxins, Enterotoxins, Flagellae

GI Disease: Local infection with 12-24 fever, myalgia, malaise, abdominal cramps, diarrhea
Can be invasive causing bacteremia, reactive arthritis
Post Infectious Sequelae: Guillain-Barre syndrome (peripheral polyneuropathies- ascending paralysis

Treatment: antbiotics

51
Q

What are the general characteristics of E. coli?

A

Gram - rod, facultative anaerobe, encapsulated, lactose fermenter, catalase positive
Serotyping- H Ag (flagellar protein), O Ag (LPS polysaccharide- sepsis), K Ag (capsular polysaccharide)
Encounter: colonized on intestinal epithelium
Pathogenesis: Gene exchange (plasmids) causing frequent Ab resistance
Virulence: plasmids, pathogenicity islands

Clinical Presentation- Colitis/diarrhea
Neonatal meningitis- 1st month
–via maternal transmission, associated with K1 capsule (identical to Group B meningococci), bacteremia
Opportunistic Infection
– pneumonia and bacteremia
– complement resistant siderophore, with increased risk if impaired immunity, intestinal trauma, or foreign body
Most common cauase of G negative sepsis

UTI- E. Coli is most frequent cause!

  • urethritis, cystitis, pyelonephritis, sepsis
  • pili formation (P type)
  • associated with hemosylin production, siderophore production, complement resistance
52
Q

What are characteristics of EHEC

A

Entero-hemorrhagic
Most common serotype:O157-H7

Encounter: person-person, contaminated meat, water

Transmission: fecal-oral route with very low infectious dose (like Shigella)
Colonizes: intestinal epithelium
Damage: Thinning of enterocytes, loss of microvilli, pedestal formation (intimin), Shiga-like toxin (tagets 60s subunit of ribosomes)

Clinical: Mild diarrhea, bloody
Hemorrhagic Colitis (afebrile, abdominal pain, blood diarrhea)
Hemolytic Uremic Syndrome
– hemolytic anemia, renal failure, thrombocytopenia, caused by Shiga Like Toxin

53
Q

EIEC

A

Enteroinvasive
Rare in US
Like less-virulent Shigella, self limiting, No Shiga Like Toxin
Clinical Presentation is Diarrhea, Fever, Dysentary (inflammation of intestine)

54
Q

EPEC

A 
Enteropathogenic 
Colonizes intestinal epithelium
Similar to EHEC, No Shiga Like Toxin 
Diarrhea with mucous but little or no blood
Malaise, vomitting, fever
Childhood Diarrhea
55
Q

ETEC

A

Enterotoxigenic
Rare in US
Colonizes intestinal epithelium via pili via CFA
Produces Toxins– Causing Diarrhea
– Heat Labile Toxin, and Heat Stabile Toxin
Clinical Presentation: Afebrile watery diarrhea, infant diarrhea, travelers diarrhea

56
Q

EAEC

A

Enteroaggregative
Colonizes intestinal epithelium
Pathogenesis: Aggregative adherance fimbraie (AAF) encoded on pAA plasmid, stack brick pattern of adherance

Many stains encoded on plasmids and chromosomes, Shiga like toxin in some strains
Clinical Presentation: Travelers diarrhea and diarrhea in HIV pts, inflammatory watery diarrhea, vomiting, nausea, fever, growth impairment in children

57
Q

What are characteristics of Francisella tularensis?

A

Gram negative, coccobaccili, facultative intracellular pathogen, highly infectious, causative agent of tularemia (rabbit fever), very low infectious dose (chemical warfare)

Encounter: natural pathogen of animals, contact with mucous membranes is enough for infection

Transmission: aerosol, man with infected animal (skinning a rabbit), bite of infected tick/fly, can survive and growth within macrophages

Clinical Presentation: Acute onset of fever/chills, ulcer at cutaneous infection site and lymph nodes inflamed/painful, sepsis can develop if severe
Treatment: Streptomycin (aminoglycosides)

58
Q

What are some characteristics of Helicobacter pylori?

A

Gram -, curved, microaerophilic, slow growth, tightly coiled, motile with flagellae, urease positive, oxidase positive
Encounter: oral-oral contact, vomit
Transmission: fecal-oral, Gastric-oral
Colonization: gastric mucosa

Pathogenesis: Infection with multiple strains, infected for long time (at least decades) and exhibit low grade gastric inflammation with neutrophil invastion
Virulence: Adhesins (RBC agglutination)
CagA Virulence Island
LPS
Urease- local CO2 production allows survival in acidic environment

Clinical Presentation: Chronic Gastritis (antral)
Gastric Cancer (aenocarcinoma- CagA+ H pylori)
Primary gastric non-hodgkins lymphoma
low grade MALT lymphoma
GERD- CagA+ stains protect from GERD
Non-ulcer dyspepsia
Peptic Ulcer Disease- 2 hit hypothesis of acid production and gastric inflammation, duodenal ulcer

Diagnosis: Upper GI endoscopy, serology, breath test, stool antigen
Treatment: Triple Therapy- PPI, Amoxicillin, Clarithromycin

59
Q

What are the general characteristics of Legionella pneumophila? (Classiciation, encounter, transmission, colonization)

A

Gram -, needs silver stain to visualize, aerobe, fastidious growth, intracellular pathogen, charcoal-containing media, among 3 most common causes of community acquired pneumonia, oxidase positive
Encounter: aerosol from contaminated water system
Transmission: NOT PERSON TO PERSON
Colonization: Alveolar macrophage

60
Q

What is the pathogenesis of Legionella pneumophila?

A

2-10 d incubation period, and then establishes infectious niche

  • bacterium killed by PMN, no macrophages
  • macrophages phagosome infected, and L pneuomphila modifies the phagosome
  • – smooth vesicles bud from phagosome, removing macrophage proteins which would allow for proper phagosome function
  • – pores formed in cells to transfer effector molecules
  • – DOT- defect in organelle trafficking
  • – phagosome associates with RER, and bacteria replicate in this phagosome

Bacterial Differentiation

  • Exponential phase- non-virulent
  • Post-exponential phase- virulent
  • switch from replicating, avirulent phenotype to post-exponential, virulent phenotype induced by amino acid starvation

Damage

  • vigorous immune response
  • cytokines signal monocytes, neutrophils
  • Microabscesses: PMN, macrophage, fibrin, RBC, debris
  • LPS and hydrolytic enzymes contribute to inflammation
61
Q

What is the clinical presentation, diagnosis, and treatment of Legionella pneuophila?

A

Pneumonia
- fever, malaise, non-productive cough, pleuritic chest pain, rales early in course, mortality as high as 50%, Pneumonia with headaches and diarrhea

Control of Infection

  • cell-mediated immunity, IFN gamma activation of macrophage
  • down-regulation of transferrin receptor, suppressing growth by limiting iron
  • antibodies may serve auxillary role promoting uptake b neutrophils

Risk Factors
- age, chronic lung disease, immunosupression, smoking

Diagnosis: CXR, Sputum, culture (days), serology (4-12 weeks), urine antigen test

Treatment: treat upon suspicion with tetracycline, ezytrhomycin, azithromycin, fluroquinolones

62
Q

What are characteristics of Neisseria gonorrhoeae?

A

Gram negative diplococci, non-maltose fermenter, and lacks a capsule. This bacteria lives in humans and is transmitted sexually (more frequenty male to female), or perinatally during delivery

In women, it moves its way up the fallopian tubes and uses Pili and Opa proteins to form tight adhesions to mucosal cells (can make micro-colonies)

These bugs survive in host due to its ability to acquire iron (has receptors for human transferrin), resisting phagocytosis, and bind Human factor H, which inhibits complement

N. gonorrhoeae attaches to human cells and use Opa to facilitate their endocytosis and invasion. Also uses a LPS-like molecule, Lipooligosaccharide (LOS) that is cytotoxic to ciliated Fallopian tube epithelial cells. Will also take advantage of antigenic/phase variation

In women, causes Cervicitis, pelvic inflammatory disease, infertility, ectopic pregancy. In men, causes purulent urethral discharge and epididymitis. Disseminated Gonococal Infection leads to arthritis, rarely causing endocarditis and meningitis

Treat with ceftriaxone and azithromycin or doxycycline to treat possible chlamydial coinfection

63
Q

What are the characteristics of neisseria meningitidis?

A

Gram negative diplococci possessing a capsule and is a maltose fermenter. Transmitted by respiratory and oral secretions. Generally asymptomatic respiratory carriers but colonization can be caused by smoking or by an earlier virl infection. Found on the non-ciliated columnar epithelium of the nasopharynx.

Spreads locally first and then to bloodstream, but minimal local inflammation. Will spread to the CNS (crosses BBB) and causes meningitis 50% of the time. Its damage is mediated by release of high doses of lipooligosaccharide (LOS) which leads to endotoxic shock and vascular shock

Virulence is dictated similarly to N. gonorrhoaea with Pili/Opa aiding adherence and entrance into host cells, iron acquisition, will avoid phagocytosis because of the capsule, has LOS, and has antigenic and phase variation.

Is preventable with vaccine (type B vaccine not widely available), and treated with ceftriaxone or penicillin G

64
Q

What are the characteristics of pseudamonas auerginosa?

A

Gram negative rod, motile, non-lactose fermenting, oxidase positive strict aerobe. Has many means of avoiding treatment (efflux pumps, effective porins), so are sometimes difficult to treat. Most effective treatment is synergistic (piperacillin/tazobactam, cephalosporins, carbapenems)

Transmission is through “moist” sources as they are frequently found in water. Uses pili and polar flagella to colonize

Nasty bug because it has membrane degrading toxins (leukocidin which forms pores in cells and PLC which causes cell lysis). Has exotoxin A which inactivates EF-2, pyocyanin (generates reactive oxygen species), and delivers Exotoxins S, T, and U via Type III Sec system. Proteases to spread through infected tissue, LPS as well

Has capsule to avoid phagocytosis

Causes: pneumonia, sepsis, ecthyma gangrenosum (rapidly progressive necrotic cutaneous lesion typically seen in IC patients), UTIs, osteomyaelities, otitis externa, and general skin infections

65
Q

What are the characteristics of Salmonella enterica, serovars Typhi and Typhimurium?

A

Gram negative rods that can disseminate hematogenously and have flagella

Typhi: Colonizes human macrophages and remain in phagosomes (prevent lysosomal fusion) and add bacterial proteins into the vacuole membrane that permits the acquisition of nutrients. Can also colonize gall bladder with a long-live asymptomatic carrier state. Is the cause of enteric fever (Typoid) which is a systemic infection with fever, abdominal symptoms, rose spots. Can cause intestinal hemorrage and perforation as well as focal infections (pericarditis, liver abscess, spleen abscess)

Typhimurium: Transmitted person to person but first encountered in contaminated food, colonizes the intestinal epithelium. Once in host, will deliver proteins via type III secretion. Will cause gastroenteritis, nausea, vomiting, fever, chills, headache, loose stools lacking blood/mucous, and an inflammatory cell response (dealt with by PMNs)

Infections (6 decks)

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