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.