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Gram Negative Bacilli Dr. Nahed Gomaa. True Bacteria Gm +ve Cocci Bacilli Gm -ve Cocci Neisseria gonorrhea Neisseria meningitidis Bacilli Pleomorphic.

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Presentation on theme: "Gram Negative Bacilli Dr. Nahed Gomaa. True Bacteria Gm +ve Cocci Bacilli Gm -ve Cocci Neisseria gonorrhea Neisseria meningitidis Bacilli Pleomorphic."— Presentation transcript:

1 Gram Negative Bacilli Dr. Nahed Gomaa

2 True Bacteria Gm +ve Cocci Bacilli Gm -ve Cocci Neisseria gonorrhea Neisseria meningitidis Bacilli Pleomorphic (cocco- bacilli) Haemophilus Brucella Bordetella Vibrios and spirilla Vibrio cholera Campylobacter Helicobacter

3 Gm –ve bacilli Oxidase +ve Pseudomonas Vibrio Oxidase –ve Enterobacteriaceae

4 Oxidase test Some bacteria like pseudomonas and vibrio produce the Oxidase enzyme which oxidize the reagent phenylenediamine producing a blue color.

5 PSEUDOMONAS Gram-negative, motile, aerobic rods Some of which produce water-soluble pigments. On agar medium it produces colonies with fluorescent greenish colour Common saprophytes in soil, water, plants and animals. It does not ferment carbohydrates, and is oxidase positive

6 Pseudomonas green pigment

7 Pseudomonas P. aeruginosa is primarily a nosocomial pathogen, It causes: Infection of wounds and burns, giving rise to blue-green pus. Urinary tract infection when introduced by catheters and instruments. Pneumonia, severe otitis media and corneal infections in contact lens users It is multi-drug resistant

8 Vibrio cholerae It causes rice watery diarrhea →dehydration

9 Vibrios Gram negative rods Motile with comma shaped flagellum Aerobes Oxidase positive Cultivated on alkaline pH and Subculture into thiosulphate citrate bile sucrose agar (TCBS) medium. V. cholera produce yellow colonies Produces a heat-labile enterotoxin Transmitted by feco-oral route, no blood invasion, causes a watery diarrhea

10 V. Cholera on TCBS

11 massive secretion of ions/water into gut lumen dehydration and death therapy – fluid replacement – antibiotic therapy (tetracycline) vaccination – partially effective ( heat killed vaccine) – not generally used – international travelers Cholera -therapy

12 Enterobacteriaceae These are Gram negative facultative anerobic rods. They are oxidase negative. All members ferment glucose Often isolated from fecal matter Important serotypes can be differentiated by their O (lipopolysaccharide), H (flagellar) and K (capsular) antigens.

13 According to lactose fermentation they are classified into Lactose fermenters Citrobacter, Enterobacter Escherichia coli Klebsiella Non-lactose fermenters Salmonella Shigella Proteus Yersinia

14 Escherichia coli

15 Gram –ve, motile, FA, lactose fermenting Biochemically indole positive AntigensAntigens O (lipopolysaccharide) O (lipopolysaccharide) H (flagellar) H (flagellar) K (capsular) K (capsular) Escherichia coli

16 Pathogenesis and Clinical Findings 1- Diarrheal diseases 2- Urinary tract infection nearly 90% of UTI in young women is caused by E. coli 3- Sepsis: Newborns are highty susceptible to E. coli sepsis. It may occur secondary to urinary tract infection. 4- Meningitis : E. coli and group B streptococci are the leading causes of meningitis in infants. 5- Fecal pollution of water: Some intestinal flora if excreted in stools and contaminated water, will indicate fecal pollution, these organisms are; E.coli, enterococci, Closiridium perfringens.

17 Shigella

18 Structure, Classification, and Antigenic Types Shigellae are Gram-negative, nonmotile, facultatively anaerobic, do not produce gas non-spore-forming rods. Do not ferment lactose The genus is divided into four serogroups with multiple serotypes: A (S dysenteriae, 12 serotypes); B (S flexneri, 6 serotypes); C (S boydii, 18 serotypes); and D (S sonnei, 1 serotype).

19 Shigellosis = bacillary dysentry Habitat :the intestinal tracts of man and animals, where they produce bacillary dysentery. This is primarily a disease of young children occurring by fecal-oral contact. Adults can catch this disease from children. Although it can be transmitted by infected adult food handlers, contaminating food. The source in each case is unwashed hands. Symptoms of shigellosis include abdominal pain, tenesmus, watery diarrhea, and/or dysentery (multiple scanty, bloody, mucoid stools). Other signs may include fever, vomiting, dehydration, and convulsions.

20 PROTEUS The organisms are present in the human colon as well as in soil and water  Morphology: gram negative bacilli highly motile  Cultural Characters: a) Facultative anaerobes b) Due to their high motility, they produce a striking swarming growth c) On Mac Conkey’s medium, they produce pale non lactose fermenting colonies. d) produce the enzyme urease, which cleaves urea to form ammonia and CO 2 e) They produce H2S

21 Proteus Swarming due to motility

22 Pathogenesis and Clinical Findings Urinary tract infection Pneumonia Wound infections Septicemia Most strains are sensitive to aminoglycosides and trimethoprim sulfamethoxazole

23 Salmonella

24 Salmonellae are Gram-negative, flagellated, facultatively anaerobic bacilli possess three major antigens: H or flagellar antigen; O or somatic antigen; and Vi antigen (possessed by only a few serovars). 2000 antigenic "types” Serotypes of medical importance 1- Four serotypes of salmonellae cause enteric fever, these are; Salmonella Typhi, Salmonella Paratyphi A, Salmonella Paratyphi B, and Salmonella Paratyphi C

25 Salmonella 2- S. enteritidis and S. typhimurium  Cause food poisoning  is transmitted from contaminated food (such as poultry and eggs). 3- S. cholerae-suis (seen much less commonly) causes septicemia after invasion with focal lesion.

26 Enteric Fever (Typhoid and Paratyphoid) Enteric fever is a world wide disease caused by Salmonella Typhi, Salmonella Paratyphi A, Salmonella Paratyphi B and Salmonella Paratyphi C. The source of infection is the stools or urine of cases or carriers. The organisms almost always enter via the oral route, usually with contaminated food or drink. After ingestion the organisms multiply in Peyer’s patches, then carried via lymphatics to mesenteric lymph nodes, liver and spleen. Further multiplication of the organism leads to blood invasion (bacteremia) which persists for one week. From the blood, the organisms are carried to many organs including the liver then excreted with bile and appear in stools. The organism may reach the kidney, then excreted in urine. Antibodies appear during the second week of illness. After an incubation period of 10-14 days, fever, malaise, headache, constipation, bradycardia and myalgia may occur.

27 Laboratory Diagnosis of Enteric Fever 1- Isolation of the organism from a) blood during the first week of fever b) stool or c) urine usually positive during the second and subsequent weeks of fever.  2- - Serological diagnosis for detection of agglutinins (Widal test)

28 Typhoid -Therapy Antibiotics – essential Chloramphenicol is the drug of choice. Certain resistant cases respond to ampicillin

29 Helicobacter pylori Gram-negative organisms are curved or spiral shaped

30 Pathogenesis 1- H. Pylori has been accepted in the last few years as the major cause of stomach ulcers. 2- The organism chronically lives in and on the stomach mucosa of man. 3- The production of large amount of ammonia from urea by the organism”s urease leads to damage of mucosa predisposing to gastritis and peptic ulcer.. 4- Production of ammonia is a factor in pathogenesis (in locally neutralizing stomach acid).

31 Laboratory Diagnosis 1- Gram stained smear, of biopsy of the gastric mucosa. 2- Culture: The organism is microaerophilic. Culture Is done on Skirrow”s medium and growth identified by urease test. 3- Urea breath test: 13C or 14C labeled CO2 is detected in the breath after feeding labeled urea-microaerophiliclabel

32 Treatment Combined therapy with metronidazole, amoxacillin or tetracycline and bismuth salt eliminates the organism, peptic ulcers heal and relapses are generally avoided.


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