micro oppurtunistic enterobacteriae

RaRoRoMiKi RaRoRoMiKi

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Oppurtunistic Enterobacteria

Commensals of large intestine

Infections found outside intestine

Can infect any tissue of the body

Usual type of infection – Urinary tract infection o UTI, wound infection, pneumonia,

meningitis, septicaemia, GI disorders

KLEBSIELLA – ENTERO – SERRATIA GROUP

Lactose fermenters except Serratia pink colonies

Give (+) Vogus Proskauer reaction (+)acetylmethylcarbinol

Have similar biochemical characteristics

Resistant to ampicillin Klebsiella

Gram (-), Non-motile

Encapsulated – large polysaccharide capsule mucoid colonies

Weak urease producer

IMViC: - - + +

TSI: A/A + gas

(+) test for lysine decarboxylase and citrate

I – Indole test M – methlene red Vi – Vogus Proskauer reaction (presence of acetylmethyl carbinol) C – Citrate TSI – Triple Sugar Iron

- Test for fermentation of sugars - Red = no fermentation - Yellow = with fermentation - Break in agar = gas = gas

producer

Klebsiella pneumoniae

Also known as Friedlander’s bacillus

Most commonly isolated member

Present in the respiratory tract and feces of about 5% of normal individuals

(+) necrosis and hemorrhage producing currant jelly sputum

Causes nosocomial and community-acquired infections

TSI: A/A + gas

IMVic: ( - - + +) Infections: Primary Lobar Pneumonia

Individuals with underlying medical problems

At risk: alcoholics and people with compromised pulmonary function

Extensive hemorrhagic necrotizing consolidationof the lung thick nonputrid, bloody sputum

UTI Endopthalmitis Wound Infection Bacteremia Meningitis Klebsiella oxytoca

Biochemically similar to Klebsiella pneumoniae but indole (+)

Similar infection to Klebsiella pneumoniae

IMViC: + - + + Klebsiella ozoenae

Fetid, progressive atrophy of mucus membrane of nose chronic atrophic rhinitis

Klebsiella rhinoscleromatis

Rhinoscleroma

Chronic granulomatous destruction of nose and pharynx

Enterobacter

Also known as aerobacter

Causes nosocomial infection UTI

Characteristics:


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o Motile o Non-encapsulated o (-) urease o (+) citrate and ornithine

decarboxylase o IMViC: - - + + o TSI: A/A + gas

E. cloacae

Causes majority of infection

Most frequently associated with urinary tract infection

E. aerogenes

With small capsule

Maybe found free-living as well as in intestinal tract

Causes urinary tract infection and sepsis

Serratia

Able to produce DNase, lipase, and gelatinase

Resistant to colistin and cephalotin

Usually non-pigmented except for S.marcescens red pigment prodigiosin

Serratia marcescens

Most frequently isolated species in hospitalized patient

Associated with UTI, pneumonia, wound infections, and septicaemia

Resistant to penicillin and aminoglycosides

Infection associated with o Invasive procedures o Respiratory therapy procedures o Narcotic addicts

Diseases o Pneumonia o Bacteremia o Endocarditis o Wound infection o Septicaemia o Outbreaks of UTI

Serratia liquifasciens

Less common than S. Marcescens but have almost the same disease spectrum

PROTEUS – MORGANELLA – PROVIDENCIA GROUP

Mostly isolated from UTI

Also isolated from infections of the other body sites

Has the ability to produce phenylalanine deaminase

Motile

Grow on potassium cyanide (KCN) medium

Ferments xylose, non-lactose fermenter

Urease (+) Proteus

Highly motile via peritrichous flagella (+) swarming on solid media (expanding ring or waves or organisms over the surface of the agar)

Cell wall antigen (OX2, OX19, OXK) of certain strains (P.vulgaris) cross react with several species of Rickettsiae (+) Weil felix test

Present in human colon, soil and water

Virulence factor: o Rapid motility at 37°C o Urease production alkalinize

urine higher risk for the development of urinary stones

(+)H2S production blacken butt of TSI agar

Diseases associated other than UTI: o Pneumonia o Wound infection o Septicaemia


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Proteus mirabilis

Causes most community acquired and nosocomial infections

2nd leading cause of community acquired UTI

Inhibited by penicilllins

Indole (-) Proteus vulgaris

Mainly nosocomial

Indole (+)

Cross react with Rickettsiae (+)Weil Felix test

Morganella morganii

Formerly Proteur morganii

Urease (+)

Causes nosocomial UTI

Morganella morganii panopthalmitis o Conjunctiva is hemorrhagic and

necrotic with mucopurulent greenish pus discharge

o Cornea is edematous Providencia rettgeri

Formerly Proteus rettgeri

Member of normal intestinal flora

Causes UTI

Often resistant to antimicrobial therapy

Citrobacter (Bethesda-ballerup Group)

Citrate (+)

Do not carboxylate lysine

Slowly ferments lactose

Occurs in the environment and human colonbut majority of the isolates are from the urinary tract

Causes UTI and sepsis in immunocompromised patients

Citrobacter diversus o Associated with neonatal brain

abscess and meningitis

Citrobacter freundii

Citrobacter amalonaticus

E. coli Greenish metallic

E. cloaca Usually nosocomial infection and often drug resistant

K. pneumonia

Large mucoid capsule and viscous colonies

S. marcescens

Red pigment produced, nosocomial infection, drug resistant

P. mirabilis Swarming phenomenon, produces urease

Pseudomonas aerogenes

Drug resistant; blue green pigment, fruity odor, nosocomial

TSI Gas H2S

Acid Acid + - Escherichia, Klebsiella, Enterobacter

Alkaline Acid - - Shigella, Serratia

Alkaline Acid + + Salmonella, Proteus

Alkaline Alka-line

- - Pseudo-monas

Diseases Caused by Members of Enterobacteria

Major Pathogen

Represen-tative Disease

Minor related Genera

Escherichia UTI, diarrhea, neonatal meningitis

Shigella Dysentery

Salmonella Typhoid fever, enterocolitis

Arizona, Citrobacter, Edwardsiella

Klebsiella Pneumonia, UTI

Enterobacter Pneumonia, UTI

Serratia Pneumonia, UTI

Proteus UTI Providencia, Morganella

Yersinia Plague, enterocolitis, mesenteric adenitis


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CORYNEBACTERIUM MORPHOLOGY:

Aerobic (+) bacilli, irregular shape, non-sporeforming

Reveals short chains (V or Y) resembling CHINESE LETTERS.

Metachromatic granules (Babes – Ernst bodies) –it is used as storage depot for high energy phosphate compounds

Pathogenesis:

Toxicity is directly attributed to an exotoxin production (virulence factor)

Do not need to enter the blood stream to produce systemic signs of the disease

Tox gene is introduced into the strain by a lysogenic bacteriophage

3 Functional regions exist on the toxin molecule:

a. Receptor binding protein- receptor of the toxin is in the heparin epidermal growth factor

b. Translocation region on B subunit- inserted into the endosomal membrane facilitating the movement of the catalytic region into the cytosol.

c. Catalytic region on the A subunit- terminates host cell CHON synthesis by inact. Elongation factor 2 (EF-2), factor required for the movement of the peptide chains on the ribosomes

**toxin synthesis is regulated by a chromosomally encoded element, diphtheria toxin repressor (DTxR). -Can bind to the toxin gene operator and prevent toxin production. EPIDEMIOLOGY:

MOT: person to person by respiratory droplets or skin contact maintained in the population by asymptomatic carriage

Humans are the known reservoir.

Diseases Associated with Corynebacterium Species

Organism Human Disease

C. diphtheria Diphtheria (respiratory, cutaneous), pharyngitis, endocarditis

C. ulcerans Respiratory diphtheria

C. glucoronylyticum GUT infections (males)

C. rieglii GUT infections (females)

C. pseudotuberculosis

Lymphadenitis, ulcerative lymphangitis, abscess formation

C. jeikenium (group JK)

Septicaemia, endocarditis, wound infections, FB infections (shunts, catheter, prosthesis), 40% can affect the skin, resistant to antibiotics

C. urealyticum (group D2)

UTI, septicaemia, wound infections, resistant to antibiotics, , can form struvite, calculi, or stones

C. amycolatum Wound infections, septicaemia, UTI, FB infections, RT infections, resistant to antibiotics, resides on the skin surface but not in the oropharynx

C. macginleyi Eye infections

C. pseudodipthericum

RT infections, endocarditis

C. minutissimum Wound infections, RT infections, colonizes the skin


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of healthy people, associated with erythrasma

CLINICAL DISEASES

CLINICAL PRESENTATION IS DETERMINED BY:

Site of infection Immune status of the px Virulence of the organism

A. Respiratory Diptheria

IP: 2-6 days

Organism multiply locally on the epithelial cells in the pharynx

The exudates evolves into a thick pseudomembrane composed of bacteria, lymphocytes, plasma cells, fibrin, and dead cells that can cover the tonsils, uvula, palate and nasopharynx down to larynx

Firmly adheres to the respiratory tissues and is difficult to dislodge w/o making underlying tissue bleed.

If patient recovers after the approx. 1 week course of the dse., the membrane dislodge (by itself) and is expectorated.

B. Cutaneous Diptheria

MOT: Skin contact

Papule -> chronic nonhealing ulcer -> covered with a grayish membrane

LABORATORY DIAGNOSIS:

I. CULTURE

Medium: Loeffler’s Medium; Serum Tellurite agar; Cysteine Tellurite agar

3 types of colonial morphologies on cysteine tellurite agar

Gravis colonies- small, gray

Intermedius colonies- small, flat, gray

Mitis colonies- small, round, convex, and black

The precise identification is determined by the results of the specific biochem. test.

Sugar fermentation

C. diptheria- glu, mal,+/- suc

C. xerosis- glu, suc

C. pseudodiptheriticum- none

II. TOXIGENICITY TESTING

Done by:

In vitro immunodiffusion assay (ELEK TEST) - (+) test result –formation of

precipitin lines - Uses specific antitoxin using

guinea pigs injected subq with the isolate from the px

PCR - An amplification test w/c directly

detects the tox gene in the clinical specimen

- The diagnostic test of choice **nontoxic strains have been assoc. with the significant dses. (septicemia, endocarditis, osteomyelitis, abscess formation)

Animal inoculation (Rabbit Pathogenecity test) – presence of necrosis

TREATMENT, PREVENTION AND CONTROL

Early admin. of the diphtheria antitoxin for neutralization

Penicillin or erythromycin – reduces toxin production, decreases chronic carriers

Diphtheria toxoid during childhood with booster doses given every 10 years throughout life

Immunity to diphtheria can be determined by measuring the neutralizing Abs in the person -> SCHICK TEST - Involves intradermal injection of

diphtheria toxin - (+)Neutralizing Abs -> no

reaction


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- (-) neutralizing Abs -> localized edema with necrosis (susceptible to diphtheria)

LEGIONELLA MORPHOLOGY:

gram (-) short coccobacilli

stain used- Dieterle’s silver stain

weakly staining pleomorphic, thin, gram (-) bacilli

PROPERTIES:

causes pneumonia in both the community and hospitalized immunocompromised px.

Its growth is enhanced with iron salts and depends on the supplementation of media with L-cysteine

Non-fermentative; motile; catalase (+)

SPECIES

L.pneumophilia- cause of multiple epidemic and sporadic infxns

PATHOGENESIS:

Are facultative intracellular parasite

Can multiply in the alveolar macrophages and monocytes

Prevents phagolysosome fusion

Are associated chiefly with environmental water sources such as Aircon and water cooling towers

Outbreaks of pneumonia in hospitals have been attributed to the presence of the organism in the water taps, sinks and showers.

MOT: inhalation of aerosol water sources

In severe cases, bacteremia occurs accompanied with damage to the vascular endothelium in multiple organs esp. the brain and kidneys

Person to person contact does not occur

CLINICAL DSES:

Pontiac fever - Fever, chills, myalgia, malaise

and headache but no evidence of pneumonia

- Self limiting - IP: 1-2 days

Legionnaire’s dse - Legionellosis - One of the most common

causes of community acquired pneumonia

- Fever, chills, dry productive cough, headache (underlying pulmonary dse), severe can lead to death

- Primary manifestation is pneumonia with multilobar consolidation and abscess

- IP: 2-10 days LABORATORY DIAGNOSIS:

- Medium: BCYE agar - Can grow in air or 3% -5%

CO2 at 35°C after 3-5 days - Colonies- ground glass

appearance - Antigenic detection: ELISA,RIA,

NUCLEIC ACID ANALYSIS - Serology”: indirect fluorescent

antibody test

TREATMENT

Azithromycin or levofloxacin for immunocompromised px

Erythromycin or tetracycline for community acquired infxns

Organisms w/ beta-lactamase are resistant to PEN

LISTERIA MORPHOLOGY:

Aerobic, non-sporeforming, gram (+) bacilli


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Motile at RT

Exhibit a characteristic “tumbling motility” in liquid medium and “umbrella motility” in agar medium.

PATHOGENESIS:

Facultative intracellular pathogen that can grow in macrophages, epithelial cells and cultured fibroblasts

Virulent strains produce Internalisins – cell

attachment factors Hemolysins – listeriolysin O,

2 phospholipase Cs. ActA – a protein that

mediates actin-directed motility.

EPIDEMIOLOGY:

L.monocytogenes is isolated from water, vegetations, and the intestinal contents of a variety of animals.

Human fecal carriage is estimated to occur in 1%-5% of healthy normal people.

Focal epidemics and sporadic causes have been associated with the consumption of contaminated cheese, undercooked meat, unwashed raw vegetables and cabbage.

Can grow on cold temperature, esp., those in prolonged refrigeration.

If the food is uncooked or inadequately cooked (microwave meals) before consumption, disease can occur.

CLINICAL DISEASE

NEONATAL DISEASE EARLY ONSET

Acquired transplacentally in utero

Also called “granulomatosis infantisepticca”

Characterized by the formation of disseminated abscesses and granulomas in multiple organs

LATE ONSET Acquired at or soon after

birth Occurs 2-3 weeks after birth

in the form of meningitis or meningoencephalitis with septicaemia.

HEALTHY ADULTS Influenza like illness

MENINGITIS IN ADULTS Most common form of listeria in

adults Suspected in cases of organ

transplants or cancer Unremarkable history of chills, fever

and hypotension


Gram stain in preparations of CSF are generally present in concentrations below the limit of detection (10 bacteria per mL CSF or less)

Culture: selective media and cold enrichment

Characteristic “tumbling motility” in liquid medium

Test for pathogenecity: Ocular test Tryptose agar slant culture

introduced into conjunctival sac of rabbit – (+) purulent conjunctivitis will develop.

TREATMENT:

Penicillin or Ampicillin either alone or with gentamycin

ACTINOMYCETES:

Aerobic, gram (+), catalase (+) bacilli

Are found on soil and decaying vegetations


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Some have delicate filamentous form (hyphae)

Nocardiaceae is one of the mycolic acid containing members.

Stain irregularly with gram stain and are partially acid fast

Genus: 1. Nocardia – pulmonary disease 2. Rhodococcus – pulmonary

disease 3. Tsukamurelle – opportunistic

infxns 4. Gordona – opportunistic infxns

Actinomycetes with no mycolic acid:

1. Actinomadura – mycetoma 2. Nocardiosis – mycetoma 3. Streptomyces – mycetoma 4. Dermatophilus – exudative

dermatitis 5. Oerskovia – opportunistic infxns;

peritonitis 6. Rothia – dental plaque 7. Tropheryma – whipple’s disease

Disorder characterized by arthralgia, diarrhea, abdominal pain, weight loss, lymphadenopathy, fever, increase skin pigmentation

8. Thermophilic actinomycetes (farmer’s Lung)

Thermoactinomyces – allergic pneumonitis

Saccharopolyspora – allergic pneumonitis

Saccharomonospora – allergic pneumonitis

**Granulomatous changes in the lung with pulmonary edema, eosinophilia, and increase IgE. ACTINOMYCES MORPHOLOGY:

Gram (+) microaerophilic bacilli; obligate anaerobes that grow in mass of filaments; (-) for spores.

Species: A.bovis – causes lumpy jaw

in cattle A.israelii – causative agent of

Actinomycosis in humans

A.israelii Occurs as a part of the

normal flora in the crypts of the tonsils, dental carries, and occasionally in the intestinal tract or the lungs.

Clinical syndrome” Cervicofacial – most

common; infxns seen in the px with poor dental hygiene following a dental procedure.

Thoracic – have an history of aspiration

Abdominal – precede by trauma or surgery to the bowel

Pelvic- maybe a primary infxns iin women with IUD.


Grow best in anaerobic condition with 10% CO2

Colonies appear white and resemble a “molar tooth”

NOCARDIA MORPHOLOGY:

N.brasiliensis and N,otitidiscaviarum causes primary cutaneous infxns (mycetoma, lymphocutaneous infxns, cellulitis, superficial abscesses) in immunocompromised px.


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Bronchopulmunary infxns develop after the colonization of the oropharynx.

Primary cutaneous nocardiosis develops after traumatic inoculation.

CLINICAL DISEASE

Bronchopulmonary infxns

Cutaneous infxns Actinomycotic mycetoma Lymphocutaneous infxns

- Cutaneous nodules and ulcerations along the lymphatics and regional lymph nodes involvement


organism grow on most lab media inoculated in an atmosphere of 5% - 10% CO2.

BCYE agar is used for specimen contaminated with other bacteria

TREATMENT:

Combination of antibiotics and appropriate surgical intervention

DOC; SULFONAMIDES

micro oppurtunistic enterobacteriae

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