2. Psuedomonaceae Gram Negative rods Nonfermentative (Strict aerobic)
Oxidation of sugars
Cytochrome C oxidase
Motile

3. 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

6. 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.

7. In cystic fibrosis patients, P
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.

8. Pathogenesis
Virulance factors:
Endotoxin
Exotoxin A (inhibits eukaryotic protein synthesis by the same mechanism as diphteria exotoxin)

9. 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

10. 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%.

11. 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.

15. 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

17. Detecting cytochrome C oxidase enzyme
Oxidase Test
Detecting cytochrome C oxidase enzyme
Indicator: 1% tetra methyl-para-phenylene diamine dihydrochloride

18. OF (Oxidation Fermentation) Test Indicator: Bromothymol blue PH: 7.1

19. Treatment Resistant to many antibiotics Antibiogram test is essential
Usually is chosen from penicillins or cephalosporins along with an aminoglycoside.

20. Prevention
Keeping neutrophil counts above 500/uL
Removing indwelling catheters promptly
Taking special care of burned skin

21. Brucella Microbiology characteristics Small bacilli Gram negative
Aerobic
Capsule
Nonmotile
Co2 needed
Fastidious

22. Virulence factors Endotoxin No exotoxin
The organism is an obligative intracellular parasite.

23. 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.

24. 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 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.

25. 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

26. 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.

27. 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.

28. Treatment
Doxycycline
Streptomycin
Rifampin

29. Control Pasteurizing milk
Eradicating infection from herds by immunization of animals and slaughtering of infected animals.
Using safety precautions (protective clothing and laboratory safety).

30. 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

31. Important species Campylobacter jejunui : Gastroenteritis
Campylobacter fetus:
An opportunistic organism
Bacteremia in compromised hosts and self-limited diarrhea in previously healthy individuals.
Campylobacter coli:

32. Enterotoxin that acts in the same manner as cholera toxin
Campylobacter jejuni
Virulence factors
Endotoxin
Enterotoxin that acts in the same manner as cholera toxin

34. 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)

35. Campylobacter jejuni and C
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.

36. 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.

37. 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.

38. Detection of C jejuni and related enteric bacteria.

39. 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.)

40. 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

41. Treatment Erythromycin in C. jejuni enterocolitis
An aminoglycoside in C. fetus bacteremia

42. Prevention No vaccine Proper sewage disposal
Personal hygiene (hand washing)

43. Helicobacter pylori
Multiple flagella
Urease

44. 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

46. Seventy-two hour culture of H pylori showing typical thin, comma- or S-shaped forms

47. Virulence factors
Urease
Cytotoxin
Protease
Flagella

48. 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.

56. 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.

57. Detection methods for H pylori

58. 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

59. Skirrow’s medium (containing vancomycin, trimethoprim, polymyxin, and amphotericin B.)

60. Laboratory diagnosis
Serological tests for antibodies on blood or saliva
13C or 14C urea breath tests
Faecal antigen testing

61. 13C or 14C urea breath tests (CUBT) for Helicobacter pylori detection

63. 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.

65. 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.

66. Serological tests for H. pylori
Elisa
Complement fixation
Latex agglutination

67. 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.

68. 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

71. Brucella
Portals of entry for Brucella species

73. Spread of Brucella in the body

77. 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.