Escherichia coli

Family Enterobacteriaceae

More than 25 genera and 110 species .Genera: Escherichia, Klebsiella, Proteus, Morganella, Providencia, Enterobacter, Serratia, Citrobacter, Shigella, Salmonella, Yersinia.Some of them are part of normal flora of GIT.The most frequently common bacterial isolates recovered from clinical specimens.All are gr-ve rods, catalase +ve, oxidase –ve, nitrate reducers, glucose fermenters.Some motile, others not .Grow well on MacConkey agar.Two major groups : Lactose fermenters or non.Virulence factors :Fimbria, capsule, exotoxin, endotoxin, antigenic phase variation, intracellular survival.Major antigens are O, K, H .

Virulence Factors

Fimbria , allow attachment of organism & persistence of infection. Capsule, to prevent phagocytosis. Exotoxin , liberated protein toxin. Endotoxin , associated with cell wall such as LPS. Antigenic variation, to evade antibody response. Intracellular survival, organism persist despite the host immune response

Cultural Characteristics

Grow on a variety of non- selective media such as nutrient, blood, brain heart infusion agar, as large gray , dry or mucoid colonies. Some produce B- hemolysis on blood agar. Differential media: MacConkey agar, either lactose fermenter (pink) or non fermenters ( transparent or colorless)

Cultural characteristics

On EMB : Eosin & methylene blue dyes inhibit gr+ , contain lactose. LF (E. coli) produce green black colonies with metallic sheen due to precipitation of the dyes in the colonies at acid pH. NLF, transparent , non- pigmented colonies.
On EMB : eosin & methylene blue dyes inhibit gr+ , contain lactose , LF (E. coli) produce green black colonies with metallic sheen due to precipitation of the dyes in the colonies at acid pH, NLF, transparent , non- pigmented colonies. Selective media, DCA, excellent selective media for isolation of Salmonella & Shigella.SS agar, high bile salt & Na citrate inhibit gr+ve & many gr-ve bacteria , it contain lactose, sodium thiosulfate to detect production of H2S. Salmonella : colorless with black centers, Shigella colorless with no black center.
On EMB : eosin & methylene blue dyes inhibit gr+ , contain lactose , LF (E. coli) produce green black colonies with metallic sheen due to precipitation of the dyes in the colonies at acid pH, NLF, transparent , non- pigmented colonies. Selective media, DCA, excellentnella & Shigella.SS agar, high bile salt & Na citrate inhibit gr+ve & many gr-ve bacteria , it contain lactose, sodium thiosulfate to detect production of H2S. Salmonella : colorless with black centers, Shigella colorless with no black center.

Cultural characteristics

Selective media, DCA, excellent selective media for isolation of Salmonella & Shigella. SS agar, high bile salt & Na citrate inhibit gr+ve & many gr-ve bacteria , it contain lactose & sodium thiosulfate to detect production of H2S. Salmonella : colorless with black centers. Shigella colorless with no black center.


Cultural Characteristics
XLD : contain xylose, lysin , lactose , sucrose ,Na thiosulfate, Na deoxycholate & phenol red as indicater. E.coli may utilize more than one sugar & produce yellow colonies. Salmonella , red colonies with black center from H2S. Shigella & Providencia not utilize any of the sugars, translucent colonies with no black center. Proteus: translucent colonies with black center.

Cultural characteristics

Enrichment brothSelenite broth : ↑Salmonella & Shigella, ↓inhibit E.coli & other coliform.Tetrathionate broth: S. typhi, S. paratyphi and Shigella.GN broth: Salmonella and Shigella.

Antigenic structure: O, K, H

Antigenic Structure

Antigenic Structure

K Antigen: is capsular antigen, in the form of polysaccharide ( K- Ag of Klebsiella) . K- Ag may be associated with virulence of the organism , E.coli producing K1-Ag are prominent in neonatal meningitis. Klebsiella is the main organism that form large capsule, can be identified by capsular swelling test with specific antisera.

Antigenic Structure

H- Ag : located on flagella, the antigen variation is due to difference in the amino acid sequence in the flageller protein ( flagellin). Klebsiella has no H-Ag. Within single serotype, the H- Ag may be present in either one or both of 2 forms. Phase 1: specific phase not shared by many m.o. Phase 2 : non specific phase & is present in many organism. Used for classification of the m.o. and serological typing. Antigenic formula of E. coli is O55:K5:H:21

Toxins

1. Endotoxins complex LPS in their cell wall, liberated after bacterial cell lysis causing septic shock. LPS , heat-stable, high mol. wt. When released in blood , stimulate macrophages and other immune cells to produce IL-1 and TNF, activate complement and coagulation factors. Fever, leukocytosis, hyopglycemia, hypotention and shock leading to decrease perfusion of essential organs (brain, kidney, heart). DIV and death from massive organ failure. Exotoxin Proteins released from intact cells. Cause transduction of fluid into ileum.



Genus EscherichiaOne of the most important members of Enterobacteriaceae.It is part of the normal flora of intestine .There are 5 species in Genus Escherichia, of these E.coli is the species most commonly isolated from clinical specimensCultural and biochemical characteristics :1.E. coli is motile, lactose fermenter.2.IMVC test is : ++--3.Urease test : -ve4.Do not produce: H2S

Antigenic structure :E.coli comprises many serotypes which are: for O - Ag : 173 for H- Ag : 56 for K- Ag : 100Serological test have enabled association to be made between O or O:H groups of E. coli and specific human disease.e.g.: strains of O1,O2,O4,O6,O9,O75 associated with U.T.I.

Pathogenesis and clinical features:Diarrhea

1.E.coli as primary intestinal pathogen , are classified into 5 groups: Enterotoxigenic E.coli , ETEC : two plasmid encoded toxins: 1.Heat labile : adenyl cyclase is activated with the production of cAMP , increases secretion of water and ions. 2.Heat stable : gunylate cyclase is activated which inhibits ionic uptake from the gut lumen. Strains with both toxins produce severe diarrhea. Toxins are produced in the small intestine. The bacteria remain on the surface. Increase secretion of water & chloride and inhibition of Na re-absorption Gut will be filled with water, hypermotility & diarrhea The mucosa becomes hyperemic but is not injured. There is no invasion or inflammation.

Cont,

Transmission is by consumption of food & water contaminated by infected human or convalescent carrier.Is the most important cause of traveler҆s diarrhea in visitors to developing countries.Causative agent of diarrhea in infants less than 2yrs.Treatment : co-trimoxazole, doxycycline & ciprofloxacin.

Enteropathogenic E.coli ,EPEC:

Firm adherence to the mucosal cells of the S. intestine by the pili. Destruction of microvilli without invasion of m.o. , watery, non bloody diarrhea. Causes diarrhea in infants & young toddlers. Usually self-limiting but could be chronic. Treatment with co-trimoxazole.

Enteroinvasive E.coli, EIEC

Penetrates the epith. cells of the Large intestine multiply intracellulary producing inflammatory diarrhea (blood, mucus, segmented neutrophils). The disease is a mild version of shigellosis. Treatment with ciprofloxacin.

It causes acute and chronic diarrhea. It is seen in infants & children in developing countries. Characterized by tight adherence to enteric cells. Attacks the colon rather than the s. intestine. production of Stx and hemolysin. Watery diarrhea, sometimes with blood & mucus.
Enteroaggregative E.coli: EAEC

Enterohemorrhagic E.coli, EHEC:

An outbreak of bloody diarrhea in 1982. Consumption of animal products colonized with EHEC. More in developed countries. Low infecting dose ( 100). verotoxin , biochemically similar to Stx , encoded by lysogenic phage. Causes inflammation of colonic mucosa Circulating verotoxin binds renal tissue causing glomerular swelling & deposition of fibrin & platelets in the microvasculature. Hemolysin (plasmid encoded)

Cont,

Hemorrhagic colitis. It causes profuse bloody diarrhea, intense abdominal pain, mild fever. Hemolytic uremic syndrome can develop as a complication in 10% of cases with a fatality rate of 5 %. Transmitted by contaminated meat , apple juice and raw milk, fresh vegetables Person to person transmission can occur.

EHEC

Transmission electron micrograph of Escherichia coli O157:H7

Cont,

Extra-intestinal infections
Urinary tract infection : causes up to 80 % of U.T.I. in young women , the virulence factor is the unique adherence factor (fimbria) , that allow them to adhere to the urethral epithelia . Vast majority of UTI are ascending from normal flora. It can cause septicemia , endotoxic shock, cholecystitis, septic wound ,meningitis ( neonatal with E. coli producing K 1Ag), pneumonia in immunocompromised and hospitalized patients .

Treatment

Ampicillin, cephalosporins ,aminoglycosides ,fluoroquinolones. Multiple drug resistance is common

Genus Klebsiella

General characteristics:Widely distributed in nature , on the skin, nasopharynx and in the intestinal tract of humans and animals.Lactose fermenters , with pinkish mucoid colonies.IMVC test : --++Urease test :-ve, except K. pneumoniae (+) in 48 hrs.Non motile , has no H- Ag.It has only O and K –Ag .K- Ag in the form of compact polysaccharides, there are 77 K-Ag.Human infection of R.T.I. caused by capsular serotype 1 and 2 U.T.I. caused by capsular serotypes 8,9,10,24 .

Klebsiella on MacConkey agar

Important species of genus Klebsiella
1. Klebsiella pneumoniae (Fridlander҆s bacillus).It cause primary pneumonia in debilitating patients (COAD), lead to destructive necrosis and hemorrhage resulting in the production of thick mucous red sputum.It cause extra-pulmonary infection such as surgical wound infections , septicemia , U.T.I. , meningitis .It accounts for a significant cases of hospital acquired UTI, pneumonia, septicemia and soft tissue infections.

Genus Klebsiella

2. Klebsiella ozaenae : causes a condition called ozena , purulent infection of the nasal mucosa with atrophic rhinitis and fetid odor. 3. Klebsiella rhinoscleromatis : causes granulomatous disease called scleroma, an infection of the upper respiratory tract .

Cont,

Treatment : are usually resistant to ampicillin and carbencillin ( susceptible to B-lactamase), lab . test for antibiotic sensitivity should be done. In general aminoglycosides and cefotaxime are used empirically until the result of sensitivity Nosocomial outbreaks of multiple drug resistant Klebsiella spp. (serotype K-55), especially in neonatal wards are often caused by the so called ESBL producers Imipenem and meropenem are the drugs of choice for ESBL producers

Genus Enterobacter

It has the general characteristics of Klebsiella but is motile Part of the normal flora of the intestine. E. aerogenes and E. cloacae are the two pathogens that do not cause diarrhea but are associated with opportunistic infections such as U.T.I. and R.T.I., wound infections and septicemia.

Genus Serratia

S. marcescence is the most important member of this genus. Well known as harmless organisms that produce a red pigment Is found as saprophytic in soil. Differ from other members of Enterobacteriacea in possessing DNase, lipase and gelatinase. Can cause a variety of human infections such as U.T.I. ,wound infections , septicemia and pneumonia It has many antibiotic resistance , to colistin , aminoglycosids, cephalothin but infections can be treated with third generation cephalosporins

Genus Proteus

Four important species: P.mirabilis P.vulgaris P.penneri P.myxofaciens General characteristics NLF Proteus is unique , it is highly motile, forms what is known as swarming over the surface of most plating media with fishy smell

Biochemical tests

Guthrie test is (+) in all members of Proteus, Morganella and Providencia All species of Proteus produce H2S Indole test is (-) in P.mirabilis and is (+) in P. vulgaris. Proteus is rapid urease test (+) It hydrolyse urea with the production of ammonia and CO2 result in increase pH of the media. Alkalinization of urine will lead to decrease solubility of Ca and Mg phosphate lead to stone formation . Ammonia produced by urease may damage the epithelia of the urinary system .

Antigenic structure

Treatment : the most active antibiotic are aminoglycosides and cephalosporins , P. mirabilis is sensitive to ampicillin, other species are resistant

Genus Morganella

M. morganii is the most important species of this genus. It can cause U.T.I., wound infections as well as diarrhea Urease test + Indole test + Citrate + Does not produce H2S .

Genus Providencia

Although rare, Providencia has been associated with nosocomial infections and U.T.I. P. alcalifaciens has been associated with some cases of diarrhea among children Urease test -ve Does not produce H2S

Genus Shigella

General characteristics: Non lactose fermentors except S.sonnei which can slowly ferment lactose on prolonged incubation Non motile. Does not produce H2S Anaerogenic. There are four species : Serotype A- S. dysenteriae, cause epidemics. Serotype B- S.flexeneri , most endemic in developing countries . Serotype C- S. boydii , relatively uncommon except in Indian subcontinent. Serotype D- S. sonnei , most commonly isolated in U.S. and U.K. cause mild disease.


Antigenic structure
Shigella are differentiated by their somatic (O) Ag into serotypes :A : 12 serotypes B : 8 serotypesC : 18 serotypesD : 1 serotypeK –Ag : some strains possess K –Ag which may or may not be visible as a capsule and covers the O. Ag .

Resistance of Shigella

All types are killed by moist heat at 55 ᴼ C in 1 hr. & by strong disinfectantShigella are sensitive to acid , that’s why fecal samples should be transported to the lab. immediately .

Cultural characteristics

It can grow on nutrient , blood agar .On MacConkey҆s agar : transparent, (non L.F.)On DCA : excellent selective media for Shigella , it appear pale , small , translucent , with no black center On S.S. agar : transparent with no black center.On XLD agar : best selective media for Shigella , transparent , no black center.

Shigella on MacConkey agar

Pathogenesis
Shigella infection are almost always limited to the intestinal tract. Shigella initially invades the epithelial cells , M cells overlying the lymphoid follicle in the distal colon and rectum. The bacteria then engulfed by the macrophages in the subepithelial space. Inside the macrophages, the organism escape from the phagosome into the cytoplasm & induce apoptosis of macrophage cell. Then invade the adjacent epithelial cells, where they can proliferate and migrate from cell to cell. This results in release of cytokines, interleukin - 1 and interleukin - 8 which direct massive influx of neutrophils into the colonic mucosa. This inflammatory response will prevent the systemic spread of Shigella but at the same time it causes ulceration and destruction of colonic mucosa , tissue necrosis and bleeding . Then granulation tissue fills the ulcer and scar tissue forms.


Toxins1. Endotoxin : all shigella release their toxic LPS after lysis , this is probably contributes to the irritation of the bowel wall.2. Shigella dysenteriae produce a heat labile exotoxin (shiga toxin ) that affect both the gut and CNS , acting as enterotoxin ,it produces diarrhea as does the E.coli verotoxin ( causes cell death and necrosis of colonic epith.As a neurotoxin , it causes CNS reactions such as meningism and coma.The toxin produces an early non bloody voluminous diarrhea and the invasion of large intestine results in later dysentery with blood and pus in the stool.

Clinical picture

After I.P. of 1-2 days, there is sudden attack of abdominal pain ,fever, watery diarrhea. After 2-3 days , bowel movement become less frequent but the presence of blood and mucus in the stool , and the onset of tenesmus . Symptoms subside in 2-5 days. In children and elderly there may be dehydration , acidosis and rarely death from complications such as intestinal perforation, HUS ( in infection with S. dysenteriae ).

Lab diagnosis

Fresh stool or rectal swab should be cultured on proper media. Sero-diagnosis in not important in the diagnosis of Shigella Treatment : Ciprofloxacin, ampicillin , tetracycline and co-trimoxazole . Fluid and electrolytes replacement in cases of dehydration

Epidemiology

Shigella infection is confined to the humans , and is distributed all over the world. It is transmitted by feces , flies , food and fingers from person to person. Most cases occur in children under 10 yrs, it is highly prevalent in children institutions, camps and mental hospitals. S. sonnei cause a mild form of the disease. S. dysenteriae is the least commonly recovered but is the most virulent . The infective dose is very low , (10 -100 ) organism .

Genus Yersinia

Three important species:Y. pestisY.enterocoliticaY. pseudotuberculosis General characteristicsPrimary animal pathogens which can be transmitted to humansSmall gr –ve rods, bipolar staining , safety pin with central clear areaIMVC tests : -+--

Cont,

Yersinia enterocoliticaYersinia pseudotuberculosis
General characteristics: Cause enterocolitis similar to that of Salmonella and Shigella infections & are called enteropathogenic yersinia. Both cause mesenteric lymphadenitis resemble appendicitis. Y. pseudotuberculosis causes pseudotuberculosis, a disease characterized by local necrosis & granulomatous inflammation in the lymph nodes, liver & spleen. The portal of entry of both m.o. is the GIT.

Cont,

NLF, grow on MacConkey҆s agar as pin-point colorless colonies.Optimum temp. 25- 32ᴼ C Do not produce H2SThe organism is urease-positiveMotile at 25°C and nonmotile at 37°C. Ornithine decarboxylase test +ve


1.Bipolar staining.2. On MacConkey agar


Enteropathogenic yersinia enter the human in contaminated food & invade M cells of the Peyer҆s patchThe invasion is mediated by 3 virulence factors , invasin and 2 major effector proteins called Yops (yersinia outer membrane proteins).Invasion of human epithelial cells and penetration of the mucosa occurs in the ileum, followed by multiplication in Peyer҆s patch.The pathogenic strategy of this organism is to paralyze the phagocytic activity of the defending macrophages & neutrophils. The outcome is the entrance & replication within REC Pathogenesis

Cont,

A direct lymphatic link between the Peyer҆s patches and mesenteric lymph nodes may result in bacterial dissemination to these sites, resulting in mesenteric lymphadenitisInfection may result in mucosal ulceration (usually in terminal ileum, necrotic lesions in Peyer҆s patches, mesenteric lymph node enlargement & microabscessesThe systemic symptoms seen with dissemination is due to effect of endotoxin

Clinical picture

The usual presentation is characterized by diarrhea, low-grade fever, and abdominal pain which may mimic acute appendicitis. Diarrhea may be bloody in severe cases. It also cause enteric fever. Septicemia is reported most commonly in patients who have underlying immune defect. Reactive arthritis (associated with HLA-B27 antigen). Metastatic infections following Y enterocolitica & Y pseudotuberculosis septicemia include focal abscesses in the liver, kidneys, spleen, and lungs.

Epidemiology

Y enterocolitica is much more common in northern Europe, Scandinavia, and Japan. Isolation of Y enterocolitica in developing countries is uncommon. Y enterocolitica is potentially transmitted by contaminated unpasteurized milk and milk products, raw pork, meats, oysters, and fish. Y. pseudotuberculosis, in most cases animals including wild animals are the most likely source of infection.

Yersinia pestis

Not an enteric pathogen. Multiple pathogenicity factors: a. protein capsule has ability to adapt to IC survival. b. exotoxin , endotoxin , coagulase and fibrinolysins Y. pestis : non motile at room temp. Ornithine decarboxylase test : -ve Urease test : -ve Causes plaque, an infection of rodents transmitted to human by the bite of infected fleas.

Clinical picture

Two forms of infections: a. bubonic b. pneumonic The bubonic form occurs within a week of being bitten by an infected flea. Multiplication of the bacteria produces the characteristic "bubo" (swollen, painful lymph node). Characterized by high fever, painful inflammatory swelling of axillary & groin LN Bacteremia follows, causing death in about 75% of those affected.



Pneumonic plaque
Characterized by malaise, pulmonary signs in the form of hemorrahgic pneumonia. Respiratory infection can occur as a consequence of bacteremic spread associated with bubonic plaque. Can be acquired by inhalation of infected air-born droplets during close contact with infected person, this form of plaque is rapidly fatal.

Lab diagnosis

Clinical specimens, sputum, bubonic aspirate & blood.Direct smear stained with Giemsa or methylene blue stain reveals bipolar stainingDirect Immunofluorescent detection (commercially available kits) for immediate identification of smears & culture.Isolation of the organism, it can grow on blood & MacConkey҆s agar.

Treatment

Y. enterocolitica is frequently resistant to ampicillin and first generation cephalosporins versus Y.pseudotuberculosis which is susceptible them and to aminoglycosides and tetracycline. Y. pestis is still susceptible to streptomycin, gentamicin. Chloramphenicol, tetracycline & ciprofloxacin are alternatives.

Genus Salmonella

Gr –ve, NLF, non sporing bacilli , motile ,some of them are capsulated (S. typhi)Aerobic and facultatively anaerobic , can grow on simple media .Ferment glucose with the production of acid and gas IMVic : -+-+Produce H2S Urease (-ve )Found in sewage , water , and soil .

Antigenic structure

O- Ag : more than 60 different O-Ag have been recognized and they are named by arabic numericals ( 1, 2, 3 , 4 -----). H-Ag :this antigen represent determinant group on flagellar protein, the production of H-Ag is biphasic (Phase 1 and phase 2) Capsular A-g : may possess capsular Ag called (Vi), : S. typhi , this Ag associated with the virulence of the m.o.

Classification

There are 2 species : S. enterica , S. bongori . S. enterica is divided into 6 subspecies : 1. enterica 2. salamae 3. A. arizona 3. B. diarizona 4. houtena 5. bongori 6 . Indica . There are also many serotypes ( more than 2300 ) within both species , the vast majority of human isolates (99%) are subspecies of S. enterica . Another classification is according to serology ( kauffman-White) , the main division is first by the somatic O antigen , then by the H- Ag which is further divided into phase 1 and phase 2.

Determinant of pathogenicity

Endotoxin : cause diverse toxic manifestation. Vi Ag . : protect bacteria from phagocytosis and from the bactericidal effect of serum . Fimbria : play a major role in the virulence of the bacteria. Salmonella may produce a heat labile toxin similar to enterotoxin of E. coli , shiga like toxin or cytotoxin. (property of invasiveness).

Clinical Diseases

1. Enterocolitis :(gastroenteritis) , is caused mainly by S. typhimurium and S. enteritidis after I.P. of 12 – 48 hrs.Nausea, vomiting, abdominal cramps , watery diarrhea , low grade fever .Stool culture is (+), while blood culture is –Bacteremia is rare (2 – 4 % ).Follow consumption of food or drink contaminated with animal feces .It is self limiting disease, antibiotics are contraindicated except for those at risk of septicemia. Replacement of fluid and electrolytes .

2.Bacteremia

Bacteremia with localized pyaemic infections : Caused mainly by S. cholerasuis . An acute illness with abrupt onset and early invasion of blood stream with possible focal lesions in lung , bones ,joints, serous cavities and meninges . May occur in patients with chronic diseases such as sickle cell anemia or malignancy. Blood culture is (+) while stool culture is (-)

3. Enteric fever

Is usually caused by S. typhi and S. paratyphi A ,S. paratyphi B and . S paratyphi C.I.P. is 10 – 14 days Human is the only reservoir of the infection Follows consumption of food or drink contaminated with human feces .

Pathogenesis of enteric fever

S.typhi invades mucosa via particularly M- cells overlying peyer҆s patch, they are then phagocytosed by resident macrophages, but instead of being killed they survive and replicate. Then the m.o. migrate with infected macrophages to the mesenteric L.N. then to the blood stream through the thoracic duct and give rise to a primary bacteremia .

Pathogenesis

During primary bacteremia , m.o. are shed in the liver , gall bladder ,spleen , bone marrow , L.N. , kidneys , where they further multiply.Transitory bacteremia which occurs 24 – 72 hr. after ingestion of m.o. is rapidly brought to an end by the removal of the bacilli by REC .Salmonella has the ability to reside within the cells of RES , there will be active proliferation of m.o. in liver and spleen .After IC multiplication, the m.o. enter the blood stream again with large numbers, continuous 2ndry bacteremia associated with a generalization of infection throughout the tissues.

Pathogenesis

As bile is a good culture medium , the m.o. multiply in the gall bladder and are continuously discharged into intestineHere it involves the peyer҆s patch and the lymphoid follicle of the ileum producing characteristic lesions .

Clinical picture:

Appears after I.P. of 2 wks and include 3 stages: In the 1st wk, the classical sign is fever, that starts low and increases as the disease progress ( step-ladder fever), there is abdominal pain, constipation, malaise, headache. 2nd wk, splenomegaly, relative bradycardia, rose spot rash.


Cont,
3rd wk, more toxic and anorexic , diarrhea, the disease may be complicated by intestinal ulceration or even perforation, meningitis, pneumonia. By the end of the 3rd wk there will be improvement and fever subsides

Diagnosis

Culture of clinical specimens : Blood culture is (+) in the 1st week of disease. Urine culture may be +ve after the 2nd week . Stool culture is +ve in 2nd and 3rd week . Culture media: Salmonella can grow on simple media , MacConkey , DCA, S.S. EMB . On selective media such as BBSA : Salmonella appear as large colonies with black centers , metallic sheen due to H2S production . Enriched media such as tetrathionate , GN, selenite broth . Suspected colonies are identified by slide agglutination test with specific O and H antisera

1.Brilliant bismuth sulphate agar2. Salmonella Shigella agar

Serological diagnosis :
Widal test : Serum antibodies rise sharply during the 2nd and 3rd week of salmonella infection . A titer of O equal or more than 1/160 suggest an active infection . A titer of H equal or more than 1/160 indicate acute or past infection or past immunization. It is unreliable test : main problems are A.Due to cross reaction with other m.o. that cause U.T.I. B. also in case of prior vaccination give false +ve reaction C. Difficulty in interpreting the test results increases in areas where S. typhi is endemic and where the antibody titers of the normal population are often not known. New tests are ELISA and PCR

Treatment

Ampicillin , amoxicillin , co- trimoxazole , chloramphenicol . Multiple drug resistance transmitted genetically by plasmid among Enterobacteriacea. Ciprofloxacin is the drug of choice for many years , but resistance is increasing . Ceftriaxone , cefotaxime are currently reliable alternative in resistant cases Cholecystectomy for carrier cases, or by using ampicillin or ciprofloxacin .

Epidemiology

Gastroenteritis is common worldwide. Follows consumption of food , water or milk contaminated with animal feces. In developed countries , most human infections is related to ingestion of infected meat (poultry) , eggs or diary products . Enteric fever is a disease of developing countries affecting children over 5 yrs and young adults . The inoculum dose is 1000 m.o.

Prevention

Sanitary measures should be taken to prevent contamination of food and water from animal excretionsTyphoid carrier must not work as food handler.2 types of vaccine :1. acetone – killed bacterial suspension of S. typhi , it give partial protection , given by I.M. injection .A live avirulent mutant strain of S. typhi given orally.