Gram Negative enteric Bacilli

Gram Negative Enteric Bacilli

Mariam Kavtaria

Pneumonia

Urinary Tract Infections

• K. pneumoniae accounts 1–2% of UTI among healthy adults
• 5–17% of complicated UTI
• infections associated with urinary catheters.

Proteus

Proteus Infections

• pneumonia - in LTCF residents, hospitalized patients),
• nosocomial sinusitis,
• intraabdominal abscesses,
• biliary tract infection, surgical site infection, soft tissue infection (esp. decubitus and diabetic ulcers),
• osteomyelitis
• neonatal meningitis - umbilicus is the source;
• complicated by cerebral abscess.
• Bacteremia - from the urinary tract infection

Abdominal Infection

• K. pneumoniae causes small proportion of CAP

in hosts with underlying conditions - alcoholism, diabetes, or chronic lung disease

• Pulmonary infection is very common among residents of LTCFs and hospitalized patients
• Mechanical ventilation - important risk factor
• production of purulent sputum and airspace disease
• Pulmonary necrosis, pleural effusion, and empyema can occur with disease progression.

The new variant of K. pneumoniae (hvKP)

(1) Community-acquired hepatic abscess,

(2) in patients without a history of hepatobiliary disease

(3) metastatic spread to distant sites 11–80% of cases (eyes, central nervous system, lungs)

• Patients have diabetes mellitus and are of Asian extraction;
• Survivors suffer catastrophic morbidity, - loss of vision and neurologic sequelae.

Klebsiella:Other Infections

Klebsiella Infections

• P. mirabilis - 90% of Proteus infections,
• P. vulgaris and P. penneri - infections in LTCFs or hospitals.
• P. mirabilis colonizes healthy humans (prevalence, 50%)
• P. vulgaris and P. penneri - individuals with underlying disease.
• adhesins, flagella, IgA protease, and urease - principal virulence factors

The urinary tract - the most common site of Proteus infection,

Proteus: Diagnosis

• Proteus is isolated and identified in the laboratory.
• lactose negative,
• produce H2S,
• characteristic swarming motility on agar plates.
• P. mirabilis is indole negative,
• P. vulgaris and P. penneri are indole positive.

• K. pneumoniae is the most important pathogen
• causes community-acquired and nosocomial infections.
• Klebsiella species colonize mucosal surfaces
• Person-to-person spread
• In hospitals and Long Term Care Facilities (LTCF).
• nosocomial outbreaks in ICUs and neonatal nurseries.

pneumonia, UTI, abdominal infection, intravascular device infection, surgical site infection, soft tissue infection, and subsequent bacteremia

• cKP (classic k.Pneumoniae) - severe community-acquired pneumonia, primarily in alcoholics;

subspecies rhinoscleromatis is the causative agent of rhinoscleroma, upper respiratory infection, progresses slowly (over months or years) and causes necrosis of the nasal passages

• K. pneumoniae subspecies ozaenae - chronic atrophic rhinitis
• These two subspecies are usually isolated in tropical climates

• Klebsiella cellulitis
• soft tissue infection
• Decubitus and diabetic ulcers, burn sites
• surgical site infection,
• hematogenously derived Endophthalmitis (esp. in association with hepatic abscess),
• nosocomial sinusitis
• osteomyelitis
• meningitis after neurosurgery

Treatment: Proteus Infections

Proteus: UTI

Bacteremia

• P. mirabilis is susceptible to most antimicrobial agents

resistant to: tetracycline, nitrofurantoin, polymyxin B, and tigecycline.

• Resistance to ampicillin and cephalosporins I in 10–50% of strains.
• 10–15% - resistant to fluoroquinolones;
• P. vulgaris and P. penneri are Resistant to ampicillin and cephalosporins I
• 30–40% - resistant to fluoroquinolones.
• Imipenem, cephalosporins IV (cefepime), amikacin, and TMP-SMX excellent activity against Proteus (90–100% - susceptible).

• P. mirabilis - 1–2% of cases of UTI in healthy women,
• 5% of cases of hospital-acquired UTI
• 10–15% of cases of complicated UTI - associated with catheterization;

In chronically catheterized patients, the prevalence of Proteus is 20–45%.

Diagnosis

Treatment: Klebsiella Infections

Infections of the urinary tract, respiratory tract, and abdomen (especially hepatic abscess) account for :

• 15–30% of episodes of Klebsiella bacteremia.
• Intravascular device–related infections - 5–15%
• Surgical site infections account for the rest
• Klebsiella is a cause of sepsis in neonates

• resistant to ampicillin, ticarcillin,
• Partially resistant to fluoroquinolones, aminoglycosides
• nitrofurantoin is only poorly active against them.

24% of K. pneumoniae device-associated infections were due to strains resistant to cephalosporins III in 2006–2007

The optimal choice for therapy is unclear

• Tigecycline, polymyxin B, and polymyxin E (colistin) are the most active agents in vitro - used most frequently - resistance to these agents is already emerging
• strains of Klebsiella resistant to all known antimicrobial agents have been described in the United States

• Isolated and identified in the laboratory.
• ferment lactose,
• The new hypervirulent clinical variant has capsular serotype K1 or K2 and
• possesses a hypermucoviscous phenotype

• Urease, hydrolyzes urea to ammonia and results in alkalization of the urine.
• Alkaline urine causes precipitation of organic and inorganic compounds
• formation of struvite and carbonate-apatite crystals,
• Frank calculi
• Staghorn calculi may form - obstruction and renal failure.
• formation of biofilms on catheters,
• Proteus can be eradicated only by removal of the stones or the catheter.

unexplained alkaline urine should be cultured for Proteus - prevention of stones

bacteremia in neutropenic patients

Citrobacter Infections

Edwardsiella Infections

Serratia Infections

Morganella and Providencia Infections

Enterobacter Infections

• Pneumonia,
• UTI (catheter-related),
• intravascular device–related infection,
• surgical site infection, and abdominal infection
• Nosocomial sinusitis, meningitis related to neurosurgical procedures
• osteomyelitis, and endophthalmitis after eye surgery
• E. (C.) sakazakii - neonatal meningitis/sepsis (in premature infants);

contaminated formula has been found as a source of this infection

• E. cloacae - 65-75%
• E. aerogenes - 15-25 %
• E. sakazakii, E. gergoviae are less common

hospital-acquired and other health care–related infections.

• prevalent in foods, environmental sources (equipment at health care facilities), and a variety of animals.
• colonization,
• direct introduction via IV lines
• Extensive antibiotic resistance

Individuals who have previously received antibiotic treatment, comorbid disease, treated in ICUs are at greatest risk for infection

C. freundii and C. koseri - clinically similar to Enterobacter infections.

• commonly present in water, food, soil, and certain animals.
• Citrobacter - normal fecal flora in a minority of healthy humans,

colonization rates increase in LTCFs and hospitals

• Citrobacter species - 1–2% of nosocomial infections.

Immunocompromised or debilitated patients

most common sites of Serratia infection and sources of Serratia bacteremia:

• The respiratory tract,
• genitourinary tract,
• intravascular devices,
• surgical wounds.

Diagnosis

• cultured and identified by the laboratory
• lactose and indole negative.
• S. marcescens strains and S. rubidaea are red-pigmented

Treatment:

>80% resistant to ampicillin, cephalosporins I, nitrofurantoin, and polymyxin B.

>90% susceptible to other antibiotics appropriate for use against GNB.

• The urinary tract infections 40–50%

diseases of biliary tree, the respiratory tract, surgical sites, soft tissue, the peritoneum, and intravascular devices.

• Osteomyelitis
• neurosurgery-related infection
• C. koseri causes neonatal meningitis - brain abscess in 50–80% of cases.
• Bacteremia is most often due to UTI, biliary or abdominal infection, or intravascular device infection.
• occasionally causes bacteremia in neutropenic patients.

Diagnosis: isolation

35–50% of isolates are lactose positive, 100% are oxidase negative

Treatment: Citrobacter Infections

• Ampicillin and the cephalosporins I and II - poor activity.
• Carbapenems, amikacin, cefepime, tigecycline, fosfomycin, polymyxins - are most active; >90% of strains susceptible.
• agents of last resort because of potential toxicities

M. morganii, P. stuartii, P. rettgeri

largely similar to Proteus species;

• Morganella and Providencia - more commonly in LTCF residents
• UTIs in long-term (>30-day) catheterization.
• biofilm formation - can cause catheter obstruction
• struvite bladder or renal stones
• surgical site infection, soft tissue infection burn site infection, pneumonia intravascular device infection, and intraabdominal infection.

Diagnosis: isolation and identification

Treatment:

• Most are resistant to ampicillin, cephalosporins I, nitrofurantoin, fosfomycin, tigecycline, and polymyxin B;
• 40% are resistant to quinolones.
• beta -lactamase inhibitor tazobactam increases effectiveness of beta lactam drugs
• Imipenem, amikacin, and cefepime - most active agents (>90% susceptible)
• Removal of a colonized catheter or stone is critical for eradication of UTI

• S. marcescens >90% of infections;

S. liquefaciens, S. rubidaea, S. fonticola, and S. odorifera- in the environment (including health care institutions)

• In LTCFs or hospitals - hands and fingernails of health care personnel, food, milk, sinks, respiratory equipment, pressure monitors, IV solutions or parenteral medications, blood products, hand soaps and lotions, irrigation solutions, and even disinfectants.

E. tarda - found predominantly in freshwater and marine environments

• Human infection - interaction with these reservoirs.
• Gastroenteritis - 50–80% of infections
• Self-limiting watery diarrhea
• severe colitis
• wound infection - direct inoculation

A primary bacteremic syndrome, sometimes complicated by meningitis, has a 40% case-fatality rate.

• Visceral (primarily hepatic) and intraperitoneal abscesses also occur.

Diagnosis: isolation and identification is possible but not routinely done

Treatment:

• Gastroenteritis - self-limited
• severe sepsis - fluoroquinolones, cephalosporins III and IV, carbapenems, and amikacin

Diagnosis - isolation and identification in the laboratory.

Treatment:

• Ampicillin and cephalosporins - no activity
• Carbapenems, amikacin, and fluoroquinolones - excellent activity (90–99% of isolates susceptible).

it is critical to use the most appropriate narrower-spectrum agent whenever possible.

fluoroquinolones. Imipenem, cephalosporins IV, amikacin, TMP-SMX