بسم الله الرحمن الرحيم

1. بسم الله الرحمن الرحيم

2. Brucella Species (B. abortus, B. suis, B. melitensis) Dr. Manal El Said Head of Medical Microbiology Department

3. Brucella Species (B. abortus, B. suis, B. melitensis) Diseases Brucellosis (undulant fever). • Incubation period of 1 to 3 weeks & onset acute or gradual • Nonspecific symptoms: fever, chills, fatigue, malaise, anorexia, & weight loss occur. • Undulating (rising-and-falling) fever pattern. • Enlarged lymph nodes, liver & spleen are frequently found. • Pancytopenia occurs. • B. melitensisinfections more severe & prolonged whereas B. abortusare more self-limited. • Osteomyelitis is the most frequent complication. • Secondary spread from person to person is rare.

4. Brucella Species (B. abortus, B. suis, B. melitensis)

5. Brucella Species (B. abortus, B. suis, B. melitensis) Characteristics Small gram-negative rods. Habitat and Transmission • Reservoir is domestic livestock. • Transmission is via: • - Unpasteurized milk & cheese • - Direct contact with infected animal.

6. Brucella Species (B. abortus, B. suis, B. melitensis)

7. Brucella Species (B. abortus, B. suis, B. melitensis)

8. Brucella Species (B. abortus, B. suis, B. melitensis) Pathogenesis • Organisms localize in reticuloendothelial cells, especially liver & spleen. • Able to survive and replicate intracellularly. • Predisposing factors include consuming unpasteurized dairy products & working in abattoir.

9. Brucella Species (B. abortus, B. suis, B. melitensis)

10. Brucella Species (B. abortus, B. suis, B. melitensis)

11. Brucella Species (B. abortus, B. suis, B. melitensis) Laboratory Diagnosis • Gram-stained smear plus culture on blood agar plate. • Identified by biochemical reactions & by agglutination with known antiserum. • Serologically by detecting antibodies in patient's serum.

12. Brucella Species (B. abortus, B. suis, B. melitensis) Treatment Tetracycline plus rifampin. Prevention • Pasteurize milk; vaccinate cattle. • No human vaccine is available

13. Francisella tularensis Dr. Manal El Said Head of Medical Microbiology Department

14. Francisella tularensis Diseases Tularemia. • Presentation can vary from sudden onset of influenzalike syndrome to prolonged onset of low-grade fever & adenopathy. • Approximately 75% of cases are "ulceroglandular" type, in which site of entry ulcerates & regional lymph nodes are swollen & painful. • Less frequent forms of tularemia include glandular, oculoglandular, typhoidal, gastrointestinal, & pulmonary. • Disease usually confers lifelong immunity.

15. Francisella tularensis Characteristics Small gram-negative rods. Habitat and Transmission • Reservoir is many species of wild animals, especially rabbits, deer & rodents. • Transmission is by ticks , aerosols, contact & ingestion.

16. Francisella tularensis Pathogenesis • Organisms localize in reticuloendothelial cells. Francisella tularensis enters respiratory tract & (2) lamina propria of respiratory bronchioles via M cells; (3) Digested antigen is taken up by dendritic cells; dendritic cells travel to regional lymph nodes &present F. tularensis antigens to T-helper 1 cells; (4) T-helper 1 cells proliferate; they may return to site of initial infection; (5) restimulation by local antigen presenting cells results in interferon-γ production & macrophage activation; (6) Failure to clear F. tularensis results in granuloma formation.

17. Francisella tularensis Laboratory Diagnosis • Culture is rarely done because special media are required & there is high risk of infection of laboratory personnel. • Serologic tests detect antibodies in patient's serum. Francisella tularensis in a liver cell.

18. Francisella tularensis

19. Francisella tularensis Colonization of Francisella tularensis on various media, namely: (A) buffered charcoal yeast extract; (B) chocolate agar medium; (C) sheep’s blood agar; (D) cysteine heart agar.

20. Francisella tularensis Treatment Streptomycin. Prevention • Live, attenuated vaccine for persons in high-risk occupations. • Protect against tick bites.

21. Pasteurella multocida Dr. Manal El Said Head of Microbiology Department

22. Pasteurella multocida Diseases Wound infection, e.g., cellulitis • Rapidly spreading cellulitis at site of animal bite is indicative of P. multocida infection. • Incubation period is brief, less than 24 hours. • Osteomyelitis can complicate cat bites, because cats' sharp, pointed teeth can implant organism under periosteum.

23. Pasteurella multocida Characteristics Small gram-negative rods. Habitat and Transmission • Reservoir is mouth of many animals, especially cats & dogs. • Transmission is by animal bites.

24. Pasteurella multocida Pathogenesis • Spreads rapidly in skin & subcutaneous tissue.

25. Pasteurella multocida Laboratory Diagnosis Gram-stained smear and culture.

26. Pasteurella multocida Treatment Penicillin G.. Prevention • Ampicillin should be given to individuals with cat bites. • There is no vaccine.

27. Capnocytophaga • Capnocytophagagingivalis • It is gram-negative fusiformrod that is associated with periodontal disease • It can be opportunistic pathogen, causing sepsis in immunocompromised patients.

28. Capnocytophaga • Capnocytophagacanimorsus • It is a member of the oral flora of dogs and causes infections following dog bites. • It cause sepsis in immunocompromised patients, especially those without spleen.

29. HACEK Group • This is group of small gram-negative rods that have in common the following: • Slow growth in culture, • Requirement for high CO2 levels to grow in culture • Ability to cause endocarditis. • -They are members of the human oropharyngealflora and can enter the bloodstream from that site. • -The name "HACEK" is an acronym of the first letters of the genera of the following bacteria: Haemophilusaphrophilus and Haemophilusparaphrophilus, Actinobacillusactinomycetemcomitans, Cardiobacteriumhominis, Eikenellacorrodens, and Kingellakingae.

30. Vibrio cholerae Diseases Cholera. • Watery diarrhea (Rice-water stool) in large volumes. • There are no red blood cells or white blood cells in stool. • There is no abdominal pain & subsequent symptoms are referable to marked dehydration. • Loss of fluid & electrolytes leads to cardiac & renal failure. • Acidosis & hypokalemia occur as result of loss of bicarbonate & potassium in stool.

31. Vibrio cholerae Diseases

32. Vibrio cholerae Characteristics • Comma-shaped gram-negative rods. • Oxidase-positive Habitat and Transmission • Habitat is human colon. • Transmission is by fecal–oral route.

33. Vibriocholerae Pathogenesis • Massive, watery diarrhea caused by enterotoxin that activates adenylate cyclase by adding ADP-ribose to stimulatory G protein. • Increase in cyclic AMP causes outflow of chloride ions & water. • Toxin has two components: • - Subunit A: ADP-ribosylating activity • - Subunit B: binds toxin to cell surface receptors.

34. Vibriocholerae Pathogenesis • Organism produces mucinase, which enhances attachment to intestinal mucosa. • Infectious dose is high (>107 organisms). • Carrier state rare string test

35. Vibrio cholerae Laboratory Diagnosis • Gram-stained smear and culture. (During epidemics, cultures not necessary.) • Agglutination of the isolate with known antisera confirms the identification. string test Vibrio cholerae on TCBS agar

36. Vibrio cholerae Treatment • Treatment of choice is fluid and electrolyte replacement. • Tetracycline is not necessary but shortens duration and reduces carriage. Prevention • Public health measures, e.g., sewage disposal, chlorination of the water supply, stool cultures for food handlers, and handwashing prior to food handling. • Vaccine containing killed cells has limited effectiveness. • Tetracycline used for close contacts.

37. Vibrio parahaemolyticus • Comma-shaped gram-negative rod found in warm sea water. • Causes watery diarrhea • Acquired by eating contaminated raw seafood. • Outbreaks have occurred on cruise ships in Caribbean. • Diarrhea is mediated by enterotoxin similar to cholera toxin. • . Forms GREEN non-sucrose fermenting agars

38. Vibrio vulnificus • Comma-shaped gram-negative rod found in warm sea water. • Causes cellulitis & life-threatening sepsis with hemorrhagic bullae. • Acquired either by trauma to skin, especially in shellfish handlers, or by ingestion of raw shellfish, especially in patients who are immunocompromised or have liver damage.

39. Campylobacter jejuni Dr. Manal El Said Head of Medical Microbiology Department

40. Campylobacter jejuni Diseases Enterocolitis. Characteristics • Comma-shaped gram-negative rods. • Microaerophilic. • Grows well at 42°C Habitat and Transmission • Habitat is human & animal feces. • Transmission is by fecal–oral route.

41. Campylobacter jejuni Pathogenesis • Invades mucosa of colon but does not penetrate • Sepsis rarely occurs. Laboratory Diagnosis • Gram-stained smear plus culture on special agar, e.g., Skirrow's agar, at 42°C in high-CO2, low-O2 atmosphere.

42. Campylobacter jejuni Treatment Usually symptomatic treatment only; erythromycin for severe disease. Prevention • Public health measures, e.g., sewage disposal, chlorination of the water supply, stool cultures for food handlers, and handwashing prior to food handling. • No preventive vaccine or drug is available.

43. Helicobacter pylori Dr. Manal El Said Head of Medical Microbiology Department

44. Helicobacter pylori Diseases • Gastritis & peptic ulcer. • Risk factor for gastric carcinoma. Characteristics Curved gram-negative rod. Habitat and Transmission • Habitat is the human stomach. • Transmission is by ingestion.

45. Helicobacter pylori Pathogenesis • Organisms synthesize urease, which produces ammonia damages gastric mucosa. • Ammonia neutralizes acid pH in stomach, which allows the organism to live in gastric mucosa.

46. Helicobacter pylori Laboratory Diagnosis • Gram stain and culture. • Urease-positive. • Serologic tests for antibody • "urea breath" test are useful.

47. Helicobacter pylori Treatment Amoxicillin, metronidazole & bismuth (Pepto-Bismol). Prevention No vaccine or drug is available.

48. Bacteroides fragilis Dr. Manal El Said Head of Medical Microbiology Department

49. Bacteroidesfragilis Diseases Sepsis, peritonitis, and abdominal abscess. Characteristics Anaerobic, gram-negative rods Habitat and Transmission • Habitat is the human colon, where it is the predominant anaerobe. • Transmission occurs by spread from the colon to the blood or peritoneum.

50. Bacteroidesfragilis Pathogenesis • Lipopolysaccharide in cell wall is chemically different from & less potent than typical endotoxin. • No exotoxins known. • Capsule is antiphagocytic. • Predisposing factors to infection include bowel surgery and penetrating abdominal wounds.