Gram Negative Bacilli Dr. Nahed Gomaa. True Bacteria Gm +ve Cocci Bacilli Gm -ve Cocci Neisseria...
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Transcript of Gram Negative Bacilli Dr. Nahed Gomaa. True Bacteria Gm +ve Cocci Bacilli Gm -ve Cocci Neisseria...
Gram Negative Bacilli
Dr. Nahed Gomaa
True Bacteria
Gm +ve Gm -ve
Cocci BacilliCocci
•Neisseria gonorrhea•Neisseria meningitidis
Bacilli
Pleomorphic (cocco-bacilli)•Haemophilus
•Brucella•Bordetella
Vibrios and spirilla•Vibrio cholera•Campylobacter
•Helicobacter
Gm –ve bacilli
Oxidase +vePseudomonas
Vibrio
Oxidase –veEnterobacteriaceae
Oxidase testSome bacteria like pseudomonas and vibrio produce the Oxidase enzyme which oxidize the reagent phenylenediamine producing a blue color.
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
Pseudomonas green pigment
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
Vibrio choleraeIt causes rice watery diarrhea →dehydration
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
V. Cholera on TCBS
• 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 -therapyCholera -therapy
EnterobacteriaceaeEnterobacteriaceae
• 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.
According to lactose fermentation they are classified According to lactose fermentation they are classified intointo
Lactose fermenters• Citrobacter, Enterobacter• Escherichia coli• Klebsiella
Non-lactose fermenters• Salmonella• Shigella• Proteus• Yersinia
Escherichia coli
• Gram –ve, motile, FA, lactose fermenting• Biochemically indole positive• Antigens Antigens
O (lipopolysaccharide) O (lipopolysaccharide) H (flagellar) H (flagellar) K (capsular) K (capsular)
Escherichia coliEscherichia coli
Pathogenesis and Clinical Findings1- Diarrheal diseases 2- Urinary tract infection nearly 90% of UTI in young women is
caused by E. coli3- 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.
Shigella
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).
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.
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 CO2e) They produce H2S
ProteusSwarming due to motility
Pathogenesis and Clinical Findings
• Urinary tract infection • Pneumonia• Wound infections• Septicemia • Most strains are sensitive to
aminoglycosides and trimethoprim sulfamethoxazole
Salmonella
Salmonella• 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
Salmonella2- 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.
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.
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)
Typhoid -Therapy• Antibiotics
– essential Chloramphenicol is the drug of choice. Certain resistant cases respond to ampicillin
Helicobacter pylori Gram-negative organisms are
curved or spiral shaped
Pathogenesis1- 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).
Laboratory Diagnosis1- 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-
TreatmentCombined therapy with
metronidazole, amoxacillin or tetracycline and bismuth salt
eliminates the organism, peptic ulcers heal and relapses are
generally avoided.