PsuedomonaceaePsuedomonaceae
Gram Negative rods
Nonfermentative (Strict aerobic)
Oxidation of sugars
Cytochrome C oxidase
Motile
Pseudomonas aeroginosa (Piocianic bacillus)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: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.
PathogenesisPathogenesis
Virulance factors:
Endotoxin
Exotoxin A (inhibits eukaryotic protein synthesis by the same mechanism as diphteria exotoxin)
An opportunistic pathogen when An opportunistic pathogen when neutrophil counts is below 500/uLneutrophil 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 findingClinical finding
Can cause infections virtually anywhere in the body, but more frequent in:
Urinary tract infections (UTIs)PneumoniaExternal otitisWound infections (especially burns).Sepsis with mortality rate of over 50%.
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.
EpidemiologyEpidemiology
Lab diagnosisLab 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 TestOxidase TestDetecting cytochrome C oxidase enzyme
Indicator: 1% tetra methyl-para-phenylene diamine dihydrochloride
TreatmentTreatment
Resistant to many antibiotics
Antibiogram test is essential
Usually is chosen from penicillins or cephalosporins along with an aminoglycoside.
PreventionPrevention
Keeping neutrophil counts above 500/uL
Removing indwelling catheters promptly
Taking special care of burned skin
BrucellaBrucella
Microbiology characteristicsSmall bacilliGram negativeAerobic CapsuleNonmotileCo2 neededFastidious
Virulence factorsVirulence factors
Endotoxin
No exotoxin
The organism is an obligative intracellular parasite.
TransmissionTransmissionA zoonotic organism
From domestic animals:B. melitensis from goatB. abortus from cowB. suis from pigB. canis from dogEntering portals: Mouth, conjunctive, respiratory
tract, abraded skin.
PathogenesisPathogenesis
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 cell-mediated 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 findingsClinical findingsEnlarged 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 diagnosisLaboratory 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.
TreatmentTreatment
Doxycycline
Streptomycin
Rifampin
ControlControlPasteurizing milk
Eradicating infection from herds by immunization of animals and slaughtering of infected animals.
Using safety precautions (protective clothing and laboratory safety).
CampylobacterCampylobacter
Microbiology propertiesCurved (comma- or S-shaped)Gram-negative rodsMicroaerophilic (growing in 5% oxygen)NonfermentingMotile(darting motility) with single flagellumOxidase positive
Important speciesImportant 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 jejuniCampylobacter jejuni•
Virulence factorsVirulence factors
EndotoxinEndotoxin
Enterotoxin Enterotoxin that acts in the same manner as cholera toxin
Transmission and EpidemiologyTransmission 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.
PathogenesisPathogenesis
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 findingsClinical findings
EnterocolitisEnterocolitis, 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 diagnosisLaboratory diagnosisfor C. jejunifor 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 diagnosisLaboratory diagnosisfor C. jejunifor 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
TreatmentTreatment
Erythromycin in C. jejuni enterocolitis
An aminoglycoside in C. fetus bacteremia
PreventionPrevention
No vaccine
Proper sewage disposal
Personal hygiene (hand washing)
Helicobacter pyloriHelicobacter pylori
Multiple flagella
Urease
Helicobacter pyloriHelicobacter pylori
Microbiology propertiesMotile(darting motility) with lophotrichous
flagellumMicroaerophilic (growing in 5% oxygen)Curved (comma- or S-shaped)Oxidase & Catalase positiveGram-negative rodsNonfermenting
Seventy-two hour culture of H pylori showing typical thin, comma- or S-shaped forms
Virulence factorsVirulence factors
Urease
Cytotoxin
Protease
Flagella
PathogenesisPathogenesis
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.
EpidemiologyEpidemiologyThe 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% 20% people under 30 years under 30 years but in 40 – 60 % 40 – 60 % of 60 years old60 years old.
Detection methods for H pylori
Laboratory diagnosisLaboratory diagnosis
Using endoscopic biopsy samples endoscopic biopsy samples where the organism can be detectedon histological examinationCulturePCR (polymerase chain reaction)A rapid urease test on the sample
Skirrow’s medium (containing vancomycin, trimethoprim, polymyxin, and amphotericin B.)
Laboratory diagnosisLaboratory diagnosis
Serological tests for antibodies on blood or saliva13C or 14C urea breath tests
Faecal antigen testing
1313C or C or 1414C C urea breath testsurea breath tests(CUBT) for (CUBT) for Helicobacter pylori Helicobacter pylori detectiondetection
The Carbon urea breath test (CUBT)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 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. pyloriSerological tests for H. pylori
Elisa
Complement fixation
Latex agglutination
SerologySerology
Testing IgGIgG is the most sensitive as seen in 95%95%..
Testing IgAIgA responses in 68-80%.
Testing IgMIgM responses in only 14% 14% of infected patients.
ControlControl
A three drug treatment for 2 weeks2 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
BrucellaBrucella
Portals of entry for Brucella species
Spread of Spread of BrucellaBrucella in the body 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.