Psuedomonaceae
Gram Negative rods
Nonfermentative (Strict aerobic)
Oxidation of sugars
Cytochrome C oxidase
Motile
Pseudomonas aeroginosa (Piocianic bacillus)
Growth in soil and water containing only traces of
nutrients.
A remarkable ability to withstand disinfectants
(found in soap solutions, in antiseptics and in
detergents).
Persistent in the hospital environment
An important role in hospital-acquired infections
P.a. Producing 2 pigments:
Pyocyanin (colors the pus in a wound blue-green)
Pyoverdin /Fluorescein (a yellow-green pigment that
fluoresces under ultraviolet light
In the lab, these pigments diffuse into the agar,
imparting a blue-green color that is useful in
identification of the species.
In cystic fibrosis patients, P. aeroginosa has a slime
layer (glycocalyx):
very mucoidal colonies. The slime layer mediates
adherence of the organism to mucous membranes
of the respiratory tract and prevents antibody from
binding to the organism.
Pathogenesis
Virulance factors:
Endotoxin
Exotoxin A (inhibits eukaryotic protein synthesis
by the same mechanism as diphteria
exotoxin)
An opportunistic pathogen when
neutrophil counts is below 500/uL
In those with extensive burns (skin host defenses are
destroyed)
In those with chronic respiratory disease (such as
cystic fibrosis)
10-20% of hospital-acquired infections.
In immunosuppressed
In those with catheters
Clinical finding
Can cause infections virtually anywhere in the
body, but more frequent in:
Urinary tract infections (UTIs)
Pneumonia
External otitis
Wound infections (especially burns).
Sepsis with mortality rate of over 50%.
Epidemiology
10% of people carry it in the normal flora of the
colon and on the skin in moist areas.
It can colonize the upper respiratory tract of
hospitalized patients.
Its ability to grow in simple aqueous solutions has
resulted in contamination of respiratory therapy
and anesthesia equipments, and even distilled
water.
Lab diagnosis
Non-lactose-fermenting (colorless) colonies on
MacConkey or EMB agar.
Blue-green pigment on nutrient agar
Catalaze and gelatinase positive
In TSI: Alkalin/Alkalin
Gram negative rods
Oxidase-positive
Fruity aroma
Oxidase Test
Detecting cytochrome C oxidase enzyme
Indicator: 1% tetra methyl-para-phenylene diamine
dihydrochloride
Treatment
Resistant to many antibiotics
Antibiogram test is essential
Usually is chosen from penicillins or cephalosporins
along with an aminoglycoside.
Prevention
Keeping neutrophil counts above 500/uL
Removing indwelling catheters promptly
Taking special care of burned skin
Brucella
Microbiology characteristics
Small bacilli
Gram negative
Aerobic
Capsule
Nonmotile
Co2 needed
Fastidious
Virulence factors
Endotoxin
No exotoxin
The organism is an obligative intracellular parasite.
Transmission
A zoonotic organism
From domestic animals:
B. melitensis from goat
B. abortus from cow
B. suis from pig
B. canis from dog
Entering portals: Mouth, conjunctive, respiratory
tract, abraded skin.
Pathogenesis
Entering the body through ingestion / skin / mucosa
Localization in mononuclear phagocytes to the
reticuloendothelial system: lymph nodes, liver,
spleen, and bone marrow
Small granulomas reveal a mononuclear response
Effective host defense depends primarily on cellmediated immunity.
Some organisms survive within macrophages.
The host responses by granulomatous along with
lymphocytes and epithelioid giant cells, which can
progress to form focal abscesses and caseation.
Clinical findings
Enlarged lymph nodes, liver and spleen
The onset may be insidious or abrupt.
Undulant (rising and falling )fever
Subclinical infection is common
Sweating, weakness and fatigue
Incubation period: 2-4 weeks
Severe limb and back pains
Influenza like onset
B. melitensis infections tend to be more severe and
prolonged, whereas those caused by B. abortus are
more self-limited.
Osteomyelitis is the most frequent complication.
In untreated cases, symptoms may continue for 2-4
weeks.
Most patients recover entirely within 3-12 months but
some develop complications marked by involvement
of various organs.
Laboratory diagnosis
Diagnosis can be made clinically if there is a history
of exposure.
Recovery of the organism requires the use of enriched
culture media and incubation in 10% co2.
Blood cultures are positive in early disease, but
serology is the mainstay of diagnosis.
Interpretation is complicated by subclinical infections
and persistent antibodies.
Treatment
Doxycycline
Streptomycin
Rifampin
Control
Pasteurizing milk
Eradicating infection from herds by immunization of
animals and slaughtering of infected animals.
Using safety precautions (protective clothing and
laboratory safety).
Campylobacter
Microbiology properties
Curved (comma- or S-shaped)
Gram-negative rods
Microaerophilic (growing in 5% oxygen)
Nonfermenting
Motile(darting motility) with single flagellum
Oxidase positive
Important species
Campylobacter jejunui :
Gastroenteritis
Campylobacter fetus:
An opportunistic organism
Bacteremia in compromised hosts and self-limited
diarrhea in previously healthy individuals.
Campylobacter coli:
Gastroenteritis
•
Campylobacter jejuni
Virulence factors
Endotoxin
Enterotoxin that acts in the same manner as
cholera toxin
Transmission and Epidemiology
Source of the organisms:
Domestic animals, such as cattle, chickens and dogs
Person-to-person transmission:
oral-fecal
The major cause of bacterial diarrhea in developed
countries (4.6% of patients with diarrhea, compared
with 2.3 and 1% for salmonella and Shigella)
Campylobacter jejuni and C. coli are endemic
worldwide and hyperendemic in developing
countries.
Infant and young adults are most often infected.
The incidence peak in the summer.
Sporadic outbreaks are associated with
contaminated animal products or water.
Pathogenesis
Invasion to the epithelial cells and colonization the
small and large intestines often occurs, accompanied
by blood in stool causing inflamatory diarrhea and
fever.
Systematic infections, eg, bacteremia, occur most
often in neonates or debilitated adults.
Clinical findings
Enterocolitis, begins as watery, fuel-smelling
diarrhea followed by bloody stools accompanied by
fever and severe abdominal pain.
Systemic infections, most commonly bactermia, are
caused by C. fetus showing symptoms of fever and
malaise.
Detection of C jejuni and related enteric bacteria.
Laboratory diagnosis
for C. jejuni
A stool specimen
Blood agar culture
Incubation at 42c in a microaerophilic atmosphere
(5% O2 and 10% CO2)
Skirrow’s medium (containing vancomycin,
trimethoprim, cephalothin, polymyxin, and
amphotericin B.)
Laboratory diagnosis
for C. jejuni
Failure to grow at 25 C
Oxidase positive
Sensitivity to nalidixic acid
The identification of C. fetus is confirmed by:
Failure to grow at 42 C
Ability to grow at 25 C
Resistance to nalidixic acid
Treatment
Erythromycin in C. jejuni enterocolitis
An aminoglycoside in C. fetus bacteremia
Prevention
No vaccine
Proper sewage disposal
Personal hygiene (hand washing)
Helicobacter pylori
Multiple flagella
Urease
Helicobacter pylori
Microbiology properties
Motile(darting motility) with lophotrichous
flagellum
Microaerophilic (growing in 5% oxygen)
Curved (comma- or S-shaped)
Oxidase & Catalase positive
Gram-negative rods
Nonfermenting
Seventy-two hour culture of H pylori showing typical thin, comma- or S-shaped forms
Virulence factors
Urease
Cytotoxin
Protease
Flagella
Pathogenesis
H. pylori is associated with type B gastritis (antral
stomach inflammation/ peptic ulcer).
It shelters from gastric acid in the gastric mucous
layer and probably is able to adhere to gastric
epithelial cells.
Production of urease and cytotoxin is associated with
injury to the gastric epithelium.
Epidemiology
The prevalence of infection increases with age.
The source and mode of transmission are not
known.
H. pylori is in the mucosa of the stomach of
20% people under 30 years but in 40 – 60 % of
60 years old.
Detection methods for H pylori
Laboratory diagnosis
Using endoscopic biopsy samples where the organism
can be detected
on histological examination
Culture
PCR (polymerase chain reaction)
A rapid urease test on the sample
Skirrow’s medium (containing vancomycin,
trimethoprim, polymyxin, and amphotericin B.)
Laboratory diagnosis
Serological tests for antibodies on blood or saliva
13C or 14C urea breath tests
Faecal antigen testing
13C
or 14C urea breath tests
(CUBT) for Helicobacter pylori detection
The Carbon urea breath test (CUBT)
The breath tests are performed by asking the
patient to swallow carbon-labeled urea
which is metabolised by H. pylori’s urease to
produce labeled carbon dioxide.
Two forms of urea breath tests by using 13C
urea or 14C urea is available.
This is absorbed into the blood stream and
then exhaled in the breath of infected
individuals.
The rapid urease test
Least expensive and can be performed on
endoscopic biopsy specimens.
The urease produced by the organism converts urea
to ammonia resulting in a PH change detected by
phenol red.
The tests usually give a rapid result but typical
sensitivity at 1 hour is 71% which increases to 96% at
6 hours.
Serological tests for H. pylori
Elisa
Complement fixation
Latex agglutination
Serology
Testing IgG is the most sensitive as seen in 95%.
Testing IgA responses in 68-80%.
Testing IgM responses in only 14% of infected
patients.
Control
A three drug treatment for 2 weeks:
1. A proton pump inhibitor (such as
lansoprazole and omeprazole decreasing stomach's
production of acid allowing the ulcer to heal)
2. Methronidasol
3. Tetracycline
Brucella
Portals of entry for Brucella species
Spread of Brucella in the body
Brucellosis is a disease of mainly cattle, swine, goats,
sheep and dogs. The infection is transmitted to humans
by animals through direct contact with infected
materials like afterbirth or indirectly by ingestion of
animal products and by inhalation of airborne agents.
Consumption of raw milk and cheese made from raw
milk (fresh cheese) is the major source of infection in
man. Most of the fresh cheeses are sheep and goat
cheese. Next to this it is considered to be an
occupational disease for people who work in the
livestock sector. Human-to-human transmission is very
rare.