Microbio

Mycobacteria Tuberculosis (morphology)

Peptidoglycan similar to GP bacteria

Unique: waxy coat of mycolic acids and lipoarabinomannan (LAM) - hydrophobic

-       Limits nutrient entry (slow clumpy growth on plates)

-       Prevents gram staining

Confers acid-fast (AF) staining properties, resist acid decolorization

Mycobacteria Tuberculosis (reservoir)

Active human cases

Mycobacteria Tuberculosis (transmission)

Aerosol (low infectious dose)

 

Risk factors:

-       Prolonged exposure

-       Immunocompromised (extremes of age, AIDS, anti-TNF-alpha therapy)

 

Most cases from high burden countries

Mycobacteria Tuberculosis (clinical)

Primary TB (initial exposure)

-       Sometimes mild, asymptomatic

-       Can spontaneously heal

 

Latent TB (majority of cases)

-       Infection contained but not cleared

-       Asymptomatic, non-infectious

 

Secondary TB (5-10% latent cases)

-       Reactivation of latent TB into acute TB

 

Active infections (primary or secondary)

-       Cough, hemoptysis, fever, malaise, dyspnea

-       Cachexia (wasting)

-       Top 10 causes of death

 

Extrapulmonary spread (uncommon but greater risk if immunocompromised)

-       Spinal TB (Pott’s disease)

-       Miliary TB

 

Spinal TB (Pott’s disease)

-       Infection of 2 contiguous vertebrae

-       Nutrient supply to IVD lost

-       Microbial toxins leach into IVD

-       IVD degenerates

-       Leads to outward curvature of spine (kyphosis)

 

Miliary TB

-       Widely disseminated TB

-       Lung and tissues covered with white nodules (like millet seeds)

 

Pulmonary TB

-       Bacteria from infected person is inhaled

-       Lung macrophages phagocytose bacteria

-       Problem: bacteria has virulence factors that evade macrophage killing

-       Solution: wall it off in a granuloma

 

Outcome of granuloma formation: latent TB

-       Infection is contained

Problem: waning containment (granuloma collapses, bacteria released leading to secondary TB)

Mycobacteria Tuberculosis (virulence)

Host evasion: multiple virulence factors allow survival in macrophages (waxy coat protects bacteria, inhibits phagolysosome fusion and maturation)

 

Inhibits production of ROS

 

Secretes siderophores to compete for Fe

-       Macrophage attempts to starve for Fe using a pump in phagosome membrane

Bacteria secrete siderophores to get Fe

Mycobacteria Tuberculosis (diagnosis)

Clinical: cough, fever, weight loss, hemoptysis

 

Chest radiograph

 

Sputum: culture, acid fast stain (gram won’t work)

 

Tuberculin skin test: mantoux test or PPD

-       Mantoux: screening, bacteria proteins injected intradermally, mechanism: delayed-type hypersensitivity to bacteria antigens (delayed because it involves Th cells, not Abs)

-       If positive, additional tests to distinguish latent TB from active infection

 

Delayed-type hypersensitivity

-       Delayed kinetics (T-cell mediated rather than Ab)

-       Mechanism: memory Th cells activate local macrophages at injection site

 

Interferon gamma release assays

-       Blood test detects latent TB

Measures interferon gamma release from patient’s T. cells in response to bacteria antigens (not present in BCG vaccine)

Mycobacteria Tuberculosis (treatment/prevention)

Long-term treatment

-       Multiple drug combinations

-       MDR-TB emerging

 

Prevention:

-       SDOH (healthcare access)

BCG vaccine: attenuated strain, only used in countries with high prevalence (variable effectiveness, false + on TB skin test)

Mycobacteria leprae (morphology)

Similar waxy coat to Mycobacterium tuberculosis

 

Reduced genome: lacks genes for essential biosynthetic functions

Obligate intracellular pathogen

Mycobacteria leprae (reservoir)

Human cases

Mycobacteria leprae (transmission)

Skin breaks, respiratory

 

Low infectivity

 

Rare zoonotic outbreaks

Mycobacteria leprae (clinical)

Major signs are cutaneous

 

Tuberculoid leprosy

-       Bacteria contained in granulomas

-       Flat, anesthetic skin lesions

-       Neurovascular granulomas with rare acid fast bacilli

 

Lepromatous leprosy

-       Poor containment due to weak immune response

-       Widespread skin lesions

-       neurovascular granulomas with many acid fast bacilli visible

-       permanent damage to skin, nerves, limbs, eyes

common cause of crippled hands

Mycobacteria leprae (virulence)

Obligate intracellular pathogen

-       avoids intracellular killing

-       slow growth progressing over years

 

Preferentially infects Schwann cells

-       trigger neurovascular granulomas

nerves swell

Mycobacteria leprae (diagnosis)

Clinical: skin lesions with patchy anesthesia

 

Skin biopsy: acid fast rods, neurovascular granulomas

 

Unculturable

Mycobacteria leprae (treatment/prevention)

Curable with multidrug regimens

Non-tuberculous mycobacteria (reservoir)

Environmental

 

Opportunistic pathogens

Non-tuberculous mycobacteria (transmission)

Recent outbreak in tattoo parlors

E. coli (morphology)

GN Enteric bacteria

 

Reside in GI

E. coli (reservoir)

Lower GI commensals of animals/humans

 

Environment

-       Fecal coliforms (test used to screen aquatic environments)

 

UTIs: GI tract

 

Enterotoxigenic E. coli (ETEC)

-       Infected humans

 

STEC

-       Animals colonized by STEC

E. coli (transmission)

Fecal contamination

 

UTIs: ascending infections via urethra, hematogenous dissemination to kidney

 

Enterotoxigenic E. coli (ETEC)

-       Fecal-oral (high infectious dose)

 

STEC:

-       Food outbreaks

-       Low infectious dose

Serotype: O157:H7

E. coli (clinical)

UTIs

-       Infection of urinary track

-       Cystitis (lower UTI) - most cases (symptoms due to bladder infection)

-       Pyelonephritis (upper UTI) - symptoms due to kidney infection (risk of bacteremia)

-       Prevalence: reproductive years (50:1, female to male)

-       Elderly (2:1, female to male due)

 

Uncomplicated UTIs (uUTIs): confined to bladder

-       Toxin-mediated bladder damage and inflammation

-       Dysuria, hematuria, urgency, frequency, cloudy urine, suprapubic pain

 

Complicated UTIs

-       Additional signs/symptoms

-       Fever, chills, nausea, dropping bp, flank pain, CVA tenderness (pyelonephritis)

-       UTI associated with foreign bodies (catheters)

 

UTI risk factors:

-       Reduced urine flow (obstruction, neurogenic bladder, urologic surgery, pregnancy), chronic dehydration (nursing homes, voluntarily avoiding bathroom visits)

-       Females

-       Aging (both sexes)

-       Immunocompromise

-       Obesity

-       Sexual activity

-       Urinary catheters (biofilms)

 

Urinary tract defenses:

-       Mechanical flushing

-       Uromodulin (Tamm-Horsfall protein): most abundant protein in normal urine, from epithelium of thick ascending limb, decoy receptor for E. coli pili (blocks adhesion, allows flow to clear)

 

Neonatal meningitis

-       Second most common cause

-       Exposure to pathogenic strain during delivery

-       Rare in adults

 

Diarrhea

-       Non-infectious: inflammation mediated

-       Infectious: inflammation and toxin-mediated

 

Infectious diarrhea:

-       Secretory diarrhea: toxins and inflammation drive epithelial hypersecretion

-       Bloody diarrhea: secretory component, damage component (loss of epithelial barrier, damage to underlying vessels)

 

Diarrhea causing E. coli

-       Enterotoxigenic E. coli (ETEC)

-       Shiga toxin-producing E. coli (STEC)

 

Enterotoxigenic diarrhea E. coli (ETEC)

-       Most frequent cause of traveler’s diarrhea (secretory diarrhea)

 

STEC: hemolytic uremic syndrome (HUS)

-       Systemic toxin damages ECs in kidney triggering microthrombi

-       Thrombocytopenia, hemolytic anemia

-       Renal damage: fluid/electrolyte imbalance, uremia, hematuria

Common cause of acute renal failure in children

E. coli (virulence)

Uropathogenic virulence:

-       Adhesion/colonization: nearby rectal flora colonize perineum, if dislodged: adhere to urethra (pili) through intercourse, catheters, post-partum

-       Motility (flagella, pili)

-       Exotoxin release (damage to epithelium - inflammation)

 

ETEC

-       Adhesion

-       Enterotoxin secretion (hypersecretion of GI epithelium  watery diarrhea)

 

STEC

-       Adhesion

-       T3SS injects VFs into cell (creates permissive niche)

-       Exotoxin secretion (damages tissue)

 

Shiga toxin:

-       AB5 toxin acquired by HGT from shigella dysenteriae

MOA: GI epithelium endocytoses toxin  A subunit exits to cytoplasm, poisons ribosomes  epithelial cell dies, exposing underlying blood vessels (bloody diarrhea)

E. coli (diagnosis)

uUTIs

-       POC dipstick   leukocyte esterase (pyuria), nitrites (bacterial metabolites), protein (tissue damage), hematuria (tissue damage)

 

cUTIs

-       CVA tenderness

-       Vitals

Imaging

-       Urine culture

 

ETEC

-       Not tested (self limited)

 

STEC

Molecule testing (replace stool culture)

-       Specialized lab testing

E. coli (treatment/prevention)

uUTIs: empiric ABX, without urine culture (assume E. coli)

 

cUTIs: empiric ABX initially, ABX narrowed following urine culture/ID/susceptibility profile

 

Emerging: ABX cause GI microbiome dysbiosis

 

Prevention:

-       Frequent hydration/voiding

-       Catheter care

-       Vaccines: in development (target adhesion, siderophores, toxins)

 

ETEC:

-       Oral fluids

-       Prevention: well-cooked food, bottled water

 

STEC:

-       Oral rehydration

-       ABX not favored  evidence that they increase production of shiga toxin by bacteria

Prevention: hand washing, cook food to internal temp. in excess of 155 F

Shigella dysenteriae (reservoir)

Humans (infected or carriers)

Shigella dysenteriae (transmission)

Fecal-oral

 

Low infectious dose

 

Developed countries: pediatric disease

Developing countries: poor sanitation

Shigella dysenteriae (clinical)

Shigellosis:

-       Dysentery:

-       Fever, cramping, bloody diarrhea with mucus and inflammatory cells

-       Severe, but resolves within a week

-       HUS risk:

-       S.dysenteriae has the highest risk due to prevalence of Stx

Shigella dysenteriae (virulence)

Acid resistant

 

Facultative intracellular pathogen that tricks M cells into internalizing them

-       Bind to M cells in colon

-       Uses T3SS to inject VFs into the M cells (triggers endocytosis of bacteria)

 

Invasive spread within epithelium

-       Escapes endocytic vacuole

-       Actin polymerization promotes lateral spread

 

Shiga toxin

Destruction of epithelium and underlying tissue  bloody diarrhea

Shigella dysenteriae (diagnosis)

NAAT for Stx in stool

 

Stool culture - hektoen enteric agar (being replaced by molecular tests)

 

HUS suspected if classic triad of signs

-       Thrombocytopenia

-       Hemolytic anemia

-       Renal damage (clogged glomeruli)

Shigella dysenteriae (treatment/prevention)

Oral rehydration

 

ABX avoided except in severe cases

 

Prevention: sanitation, insect control (raw sewage)

Salmonella enterica serovar typhimurium (resorvoir)

Animals and humans

Salmonella enterica serovar typhimurium (transmission)

Outbreaks (from food and environment)

Salmonella enterica serovar typhimurium (clinical)

Acute gastroenteritis

-       Diarrhea, fever, abdominal cramps after a meal

-       Difficult to distinguish from other pathogens

-       Lasts about a week

Salmonella enterica serovar typhimurium (virulence)

Children <5 most at risk

-       Acid sensitive

-       T3SS like Shigella, tricks M cell endocytosis (but no lateral spread through comet tails), transcytosed all the way through to underlying tissue

Inhibits macrophage phagolysosome fusion (bacteria released, cause local damage and bloody diarrhea)

Salmonella enterica serovar typhimurium (diagnosis)

NAATs, stool culture (becoming rare)

Salmonella enterica serovar typhimurium (treatment/prevention)

Self limited

-       Fluid/electrolytes

-       ABX only in severe cases

 

Prevention: proper food handling, hand-washing

Salmonella enterica serovar typhi (reservoir)

Human specific (chronic carriers)

 

Healthy carriers

-       Gallbladder colonized by S. Typhi in chronic carriers

-       Forms gall stone biofilms and enter gall bladder epithelium, chronic shedding into GI

Salmonella enterica serovar typhi (transmission)

Fecal-oral

Salmonella enterica serovar typhi (clinical)

Typhoid fever

-       Severe systemic illness

-       Fever due to chronic bacteremia

-       Weakness, headache, loss of appetite, abdominal discomfort

-       Persistent bacteremia seeds to other organs

Chronic infection can lead to hemorrhage from intestinal perforations

Salmonella enterica serovar typhi (virulence)

Exploits M cell transcytosis like S. typhimurium

-       Transported to lamina propria

 

Evasion of macrophage killing

-       Blocks phagolysosome fusion and oxidative burst

-       Infected macrophages don’t die, spread bacteria

Systemic infection

Salmonella enterica serovar typhi (diagnosis)

NAAT, blood/stool culture

 

Serology for public health monitoring

Salmonella enterica serovar typhi (treatment/prevention)

ABX

 

Prevention: hand-washing, vaccine (not 100% effective)

Vibrio cholerae (morphology)

GN, curved rods, motile (flagella)

Vibrio cholerae (reservoir)

Free-living bacteria in warm coastal brackish waters (reproduce slowly, not all are toxigenic)

Vibrio cholerae (transmission)

Environmental strains (shellfish, oysters)

 

Epidemic strains: obtained cholera toxin gene by HGT

 

Cause: present in environment, poor water/sewage treatment infrastructure

Vibrio cholerae (clinical)

Rapid onset (days)

 

Abdominal fullness/discomfort, vomiting

 

Rushes of peristalsis, voluminous stools (watery, almost odorless, mucous flecks)

 

Dehydration is life threatening (low bp, weakness, dizziness, confusion, electrolyte imbalance)

Vibrio cholerae (virulence)

Adhesion to GI epithelium

 

Motility (single polar flagellum, colonizes intestinal crypts)

 

Cholera toxin (AB5 toxin):

-       ADP ribosylates membrane-associated adenylate cyclase

-       Locks adenylate cyclase in “on” position

-       cAMP activates ion efflux channels

-       Ion buildup in GI draws water from tissues

-       Greatest effect is small intestine

 

Advantage of cholera toxin

-       Fitness  increases spread

-       Increases luminal concentrations of some nutrients that support bacterial growth

Flushes competing bacteria from the gut

Vibrio cholerae (diagnosis)

Clinical: signs and symptoms, appropriate epidemiologic setting

 

Laboratory: stool culture

Vibrio cholerae (treatment/prevention)

Oral rehydration therapy (self-limiting, resolves with hydration)

 

Severe cases: rehydration and ABX

 

Prevention: bottled water, peel fruits/vegetables, avoid raw shellfish

 

Vaccines: vaxchora (live, attenuated, deleted Ctx gene), dukoral (killed whole cell and B subunit)

Vibrio vulnificus (reservoir)

Warm, brackish water, coastal shellfish (oysters)

Vibrio vulnificus (transmission)

Food, skin breaks

Increased risk: coastal disasters

Vibrio vulnificus (clinical)

Blistering cellulitis/necrotizing fasciitis

Vibrio vulnificus (virulence)

Multiple toxins

Campylobacter jejuni (morphology)

Short corkscrew-shaped GNRs

 

Single polar flagellum

Campylobacter jejuni (reservoir)

GI tracts of animals

Campylobacter jejuni (transmission)

Contaminated food - most cases are chicken

 

Most common cause of diarrhea in U.S.

Campylobacter jejuni (clinical)

Abdominal discomfort a few days of exposure

 

Watery diarrhea that may become bloody

 

Usually resolves within a weak

 

Sequalae:

Post-infectious Guillain-Barre syndrome

-       Rare complication of campylobacteriosis

-       Demyelinating neuropathy (weakness/tingling in both legs, spreading to arms and upper body)

Similar mechanism to acute rheumatic fever

Campylobacter jejuni (virulence)

Adhesion

 

Invasion of GI epithelial lining cells

 

Toxins (secretory diarrhea, bloody diarrhea if cells are killed)

Campylobacter jejuni (diagnosis)

PCR/stool culture

Campylobacter jejuni (treatment)

Usually not treated unless severe

 

Prevention: cook chicken well, wash hands after handling meat

Helicobacter pylori (morphology)

GN curved rods, polar flagella

Helicobacter pylori (reservoir)

Humans (increases with age, life-long)

Helicobacter pylori (transmission)

Fecal-oral (contaminated food/water)

 

Mouth-to-mouth contact

Helicobacter pylori (clinical)

Infects stomach mucosa

 

Gastritis (nausea, vomiting, abdominal pain)

 

Gastritis can ulcerate lining (risk for bleeding)

Helicobacter pylori (virulence)

Periplasmic urease (hydrolyzes urea in gastric juice into ammonium, facilitates survival in low pH until they can swim down to where pH is higher)

 

Motility

 

Uses a T3SS to inject toxins into the cell

-       Damages epithelium

-       Some toxigenic strains linked to gastric cancer

 

Damages epithelium as it grows

Helicobacter pylori (diagnosis)

Urea breath tests (patient ingests capsule with 13C-labeled urea  if urea is in stomach, urea will be broken down, releasing 13C as part of Co2 in breath

 

Stool tests

Helicobacter pylori (treatment/prevention)

ABX for patients with evidence of ulcers

(not treated if no ulcers)

 

Proton pump inhibitor (raises pH to promote healing)

Mycoplasma pneumoniae (morphology)

Phylogenetically related to GP

-       No cell wall, just a membrane: pleomorphic (all kinds of shapes)

-       Smallest of free-living bacteria

In a separate class: mollicutes (soft skin)

Mycoplasma pneumoniae (reservoir)

Humans (especially children)

Mycoplasma pneumoniae (transmission)

Inhaling respiratory droplets

 

Dies quickly due to lack of cell wall  Rapid person-to-person spread

 

Any crowded place

 

Common tissue culture contaminant

Mycoplasma pneumoniae (clinical)

Walking pneumonia

-       Fever, cough, shortness of breath

-       Most are tracheobronchitis (not lungs), can progress to pneumonia

 

Smoldering infection

-       Incubation period can be weeks (vs. viral pneumonia)

Mycoplasma pneumoniae (virulence)

Adhesion: requires a specialized attachment organelle

 

Motility

-       Lack flagella, attachment organelle functions in gliding motility

-       Facilitates colonization of airway

-       Mechanism: inchworm or centipede-like (catch-release)

 

Host evasion

-       Surface antigenic variation

 

Damages mucociliary escalator

-       CARDS toxin (community acquired respiratory distress syndrome toxin)

Causes cough

Mycoplasma pneumoniae (diagnosis)

Overlaps with other respiratory infections

-       Slow onset is big clue

 

Sputum sample/throat swab

-       No gram stain

-       Slow growth in culture

NAA tests

Mycoplasma pneumoniae (treatment/prevention)

Most infections are mild/self-limited

 

ABX in severe situations

 

No vaccines

Rickettsia rickettsii (morphology)

GNR

 

Obligate intracellular bacterium

Rickettsia rickettsii (reservoir)

Ticks (vector)

 

Seasonal infection

Rickettsia rickettsii (clinical)

Within a week of tick bite

-       Fever, headache, vomiting, joint pain

-       Petechial rash (centripetal pattern, hands and feet spreading to trunk)

May progress to DIC (disseminated intravascular coagulation)

Rickettsia rickettsii (virulence)

Tick introduces bacteria into blood

 

Obligate intracellular bacterium

-       Endocytosed by cells

-       Escapes phagosome and grows in cytoplasm

 

Targets endothelial cells

-       Triggers vasculitis

-       Increased vascular permeability  (hypovolemia)

Hypercoagulopathy (petechiae)

Rickettsia rickettsii (diagnosis)

History of tick bite

 

Clinical signs/symptoms: spotted rash that expands centripetally

 

Serology/PCR

 

Unculturable on solid medium

Rickettsia rickettsii (treatment/prevention)

Treatment:

-       Mortality from vascular collapse if untreated

-       Vascular damage can be permanent, requiring amputation

 

Empiric ABX

 

Prevention:

-       Avoid ticks

-       Frequent de-ticking in infested areas

No vaccine

Rickettsia prowazeki (morphology)

GN coccobacillus

Rickettsia prowazeki (reservoir)

Humans (most cases)

 

Flying squirrels

Rickettsia prowazeki (transmission)

Vector-borne

-       Body lice acquire bacterium by biting an infected human and transmit to other humans

-       Contact with flying squirrels (rare)

 

World outbreaks: war, famine, poverty, aid workers

Rickettsia prowazeki (clinical)

Fever with neurological manifestations of stupor and confusion

 

Similar to RMSF (rocky mountain sided fever)

-       RMSF: tick-borne, rash on palms/soles spreads centripetally

-       Epidemic typhus: Louse-borne, centrifugal rash (trunk to extremities)

Both diseases may be fatal due to vascular collapse

Rickettsia prowazeki (virulence)

Obligate intracellular pathogen (infects ECs)

 

Lives in clothing and bedding, not body

 

Louse feces laden with this bacteria —> person scratches infected excrement into skin

 

RMSF vs. typhus

-       RMSF: tick is the reservoir, transmitted by bite

Epidemic typhus: humans are reservoir, louse is vector (acquires bacterium from infected humans)

Rickettsia prowazeki (diagnosis)

Serology

ABX

Louse control

Pseudomonas aeruginosa (morphology)

GN rods

 

Prolific biofilm producer

Pseudomonas aeruginosa (reservoir)

Widespread  humid environmental bacterium

Pseudomonas aeruginosa (transmission)

Airborne droplets

Contact with contaminated surfaces (biofilms)

Pseudomonas aeruginosa (clinical)

Potent opportunistic pathogen:

-       Lung infections

-       Skin infections

-       Eye infections

Many tissues affected

-       Urinary tract

-       CNS

-       GI tract

-       Ears

-       Bones and joints

-       Heart

 

Lung infections (pneumonia)

-       Life threatening

-       At risk: CF patients, immunocompromised, patients on ventilators (biofilms)

 

Skin infections:

-       Mild: hot tub rash (pseudomonas folliculitis)  thrives in hot-tub temperatures, transmission: contact with contaminated water, treatment not necessary

-       Green snail syndrome (more prevalent in cooks and dishwashers, treatment: topical ABX)

-       Severe: Problem in burn units

 

Eye infections:

Pseudomonas keratitis: most common cause of corneal infection associated with contact lenses  contaminated solutions, eye trauma caused by lens insertion/removal or debris

Pseudomonas aeruginosa (virulence)

-       Forms in response to host environment to protect bacteria

-       Overproduces biofilm rich in alginate (polysaccharide)

 

Neutrophil defenses against Pa

-       H202: causes oxidative damage to bacteria

-       LL-37: antimicrobial protein (AMP), damages bacterial membranes

 

Biofilms contain a mix of two variants

-       Mucoid variants (make alginate): block entry of LL-37, but not H202, unable to make catalase

-       Nonmucoid variants (don’t make alginate): produces catalase to neutralize H202

-       Protected from LL-37 by alginate

 

Toxin production

-       Pyocyanin: oxidative damage to human cells

-       Tissue damaging enzymes: proteases, elastase

-       T3SS inject toxins that impair phagocytosis

 

Fe acquisition

-       Secretes pyoverdine (siderophore)

 

 

Motility

-       Flagellum (swimming in liquid) - gets it to a surface

Twitching motility: crawling on surfaces (mucosa and biofilms)  catch pull release mechanism involving type IV villi

Pseudomonas aeruginosa (diagnosis)

Culture

Pseudomonas aeruginosa (treatment/prevention)

ABX

-       Notorious for acquiring resistance by mutations

-       ABX selection pressure can drive LOF mutations in MutS (involved in DNA damage/repair, creates a hypermutator phenotype: allows massive mutations)

 

Prevention:

-       Reduced hospital stays

-       Sanitation of surfaces, hot tubs, contact lenses

No vaccine

Legionella pneumophila (morphology)

GN rods (some longer filaments)

 

Motile

Facultative intracellular pathogen

Legionella pneumophila (reservoir)

Biofilms in aquatic environments

Legionella pneumophila (transmission)

Inhalation of aerosols (mists)

-       Contain bacteria released from biofilms

 

No evidence of PtP

 

Incidence is increasing

-       Aging infrastructure (older plumbing and cooling)

-       Climate change

-       Vulnerable population

Legionella pneumophila (clinical)

Severe

-       Legionnaires’ disease (legionellosis)

-       Severe pneumonia: headache, fever, chills, dry cough, chest pain

Mild

-       Pontiac fever

Resolve without treatment

Legionella pneumophila (virulence)

Biofilm formation in wet environments

 

Evades macrophage killing

-       Inhibits phagolysosome fusion and maturation

-       Recruits ER membrane to pathogen-containing vacuole (PCV)  resembles an organelle

Multiplies in phagosome

Legionella pneumophila (diagnosis)

Clinical manifestations are non-specific

-       Requires lab testing

 

Urinary antigen test

 

PCR on sputum

 

Culture requires specialized media

Legionella pneumophila (treatment/prevention)

Treatment:

-       ABX with high intracellular potential

-       No vaccine

 

Prevention

-       Sanitation and hyperchlorination of water systems

-       Superheating of stagnant water

-       Copper - silver disinfection of pipes