enteric fever(dr. b. erghan)-r.ppt

7/27/2019 Enteric fever(Dr. B. Erghan)-R.ppt

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Enteric fever

Eghan BA

24/2/2005


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Salmonella infections

Genus: Salmonella

Named after : Pathologist, Salmon

Family: enterobacteriacae

2300 serotypes

Grouped: O antigen (somatic)

Further serotyed:Flagella (H) and surface virulence(Vi) antigen

Most of which originating in animals eg poultry andtransmitted to man either directly or in food


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Based on DNA studies, all salmonellae are

now considered a single species (Scholeraesuis),

separated into 7 distinct subgroups.

By convention, these subgroups are often

referred to as separate species (eg, S typhiinstead ofS choleraesuis subgroup typhi)


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Mode of transmission

Ingestion of food derived from infected

animals contaminated with faeces of infectedindividual

Raw milk and raw milk products

Undercooked or raw eggs and egg products

Meat and meat products Contaminated water

Shellfish from water polluted by raw sewage.


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The bacteria must survive the pH in stomach

and colonize the small intestines. Attach and penetrate the intestinal mucosa

resulting in diarrhoea from direct mucosal

damage or by action of bacterial toxins.

Also invasion of the lymphoid tissue withinthe GI tract and multiplication within

macrophages leading to bacteraemia


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Factors predisposing an individual to

infection include

Studies suggest that infection may be inoculum-dependent. In healthyindividuals previously,ingestion of

105 organisms: clinical disease in 25% of volunteers

10

7

organisms: caused disease in 50% of volunteers 109 organisms caused disease in 95% of volunteers.

As the number of organisms increased, the incubation period decreased.

A gastric pH of less than 1.5 kills most salmonellae. Patients who continually ingest antacids

have had a gastrectomy

have achlorhydria due to aging

or other factors eg. Inflammatory bowel disease, malignancy

require lower numbers of organisms to produce clinical disease.

Possession of Vi antigen by S typhiis linked with increased pathogenicity.


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Syndromes of Salmonella infections

Gastroenteritis ( the most frequent manifestation)

Typhoid and paratyphoid fever (enteric fever)

Enterocolitis

Septicaemia

Metastastic lesions (complicating septicaemia) Osteomyelitis, septic arthritis, liver abscess, brain abscess

meningitis, pneumonia, endocarditis, arteritis, septicarthritis, splenic and hepatic abscesses, and soft tissueabscesses.


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Gastroenteritis

Incubation period; 8-48 hours

Presentation:

Nausea, vomiting progressing to abdominal cramping and

diarrhoea which may be bloody

Physical findings:

Fever > 38C

Abdominal tenderness or signs consistent to peritonitis

Gross or occult blood may be found on rectal examination.


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Typhoid fever or enteric fever

History

Incubation period: varies with the size of the infecting dose.

a median dose of one million to one billion organismsnecessary to produce symptoms

Typhoid fever: averages 10-20 (range 3-56) days.

In paratyphoid fever: 1-10 days.

The duration of illness in an untreated individual is usually four

weeks. In the incubation period, 10-20% of patients have transient

diarrhea.


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As bacteremia develops, Fever; 39-40C (Rising remittent fever as high as (39-40C.

Step-wise fashion over 2-3 days.) headaches.

malaise,.

Constipation

anorexia

myalgia,

cough,

sore throat

After 1 week if untreated patients condition worsen leadingmental confusion


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Physical findings


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First week

Rose spots: Crops of 2-4 mm diameter pink

papules which fades with pressure developon the upper abdomen and lower chest

between the 7th and 12th days. Caused by

bacterial embolization, and culture results of

skin snips of the spots may be positive. Relative bradycardia

Dicrotic pulse are also common at this time.


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Second week

Toxic appearance

Apathetic Fever sustained.

Abdomen distention

Splenomegaly


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Third week

Toxicity increases

Weight loss Fever persists

Delirious state (typhoid state or typhoidpsychosis ) emerges.

Pronounced abdominal distension liquid, foul, green-yellow diarrhea (pea soup

diarrhea).


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Third week (contd)

Patient is weak

thready pulse

Tachypnoic

Crackles may develop over the lung bases.

Death may occur at this stage from overwhelming

Toxemia. Myocarditis.

Intestinal hemorrhage.

Perforation.


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Fourth week

In patients surviving into the fourth week, the

fever, mental state, and abdominaldistension slowly improve over a few days,

but intestinal complications may still occur.


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Differentials

Abdominal abscess

Amoebic hepatic abscess


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Investigation

Complete blood count moderate anemia

Raised ESR

Thrombocytopenia relative lymphopenia

WBC increases with perforation

Sometimes a slightly raised prothrombin time (PT) and activated partialthromboplastin time, decreased fibrinogen levels, and circulating fibrindegradation products.

Liver Transaminases: Raised (2X or more) Raised serum bilirubin.

Electrolytes hyponatraemia

hypokalaemia.


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Clinical diagnosis is suggested by:

assays that identify Salmonella antibodies, antigens, or DNA

But definitive diagnosis of typhoid fever requires isolation of theorganism from blood or bone marrow

the most sensitive method of isolating S typhi and paratyphiisobtaining a bone marrow aspirate (BMA) culture.

S typhican be isolated from BMA even if patients have been takingantibiotics for several days

regardless of how long they have been ill. This test may be indicated in patients whose initial blood

culture results are negative, presumably because of priorantibiotic therapy.


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If BMA cannot be performed,

blood, intestinal secretions, and stool culture findings are usually positive in approximately 85-90% of patients

with typhoid fever during the first week, declining to 20-30%later in the course of the disease.

A sensitivity of 63% has also been reported from culturingskin snips of rose spots.

A single rectal swab: sensitivity 30-40%.

S typhihas been isolated from the cerebrospinalfluid, peritoneal fluid, mesenteric lymph nodes,resected intestine, pharynx, tonsils, abscess, bone,and urine.


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Serology

Widal test ( traditional serologic test)

It measures agglutinating antibodies against flagellar

(H) and somatic (O) antigens ofS typhi.

In acute infection, O antibody appears first, rising

progressively, later falling, and often disappearing within a

few months.

H antibody appears slightly later but persists longer. Rising or high O antibody titers generally indicate acute

infection, whereas elevations of H antibody help to identify

the type of enteric fever.


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Numerous studies have shown that the sensitivity,

specificity, and predictive values of this test vary

dramatically among laboratories, rendering the test'svalue to the clinician questionable.

Wide variation is caused by differences in patient

population, antigens, and techniques.

The Widal reaction is indicative of typhoid fever inonly 40-60% of patients at the time of admission.


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New innovations

Indirect hemagglutination, indirect fluorescent Vi

antibody, and indirect enzyme-linked immunosorbent

assay for immunoglobulin M (IgM) andimmunoglobulin G antibodies to S typhi

polysaccharide are available.

Monoclonal antibodies against S typhiflagellin

DNA probes are also available.

Polymerase chain reaction


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Treatment

Medical Care

Nurses and doctors:

adequate hand washing and safe disposal of feces andurine.

Antibiotic therapy is essential and should beginempirically if the clinical evidence is strong.

Antimicrobials:

shorten the course, reduce the rate of complications if begun early

reduce the case-fatality rate.


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Surgical Care

Consultation with a surgeon is advised when typhoid fever is

complicated by gastrointestinal perforation.Surgical intervention for intestinal perforation

simple closure of a perforation

small bowel resection for patients with multiple perforations.

Early diagnosis is key to lower mortality.

Cholecystectomy not always successful because of persisting hepatic infection.

indicated for gallbladder disease but not for the purpose oferadicating the carrier state.


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Medication

Goal is to:

1. eradicate the infection2. reduce morbidity

3. prevent complications.


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antibiotics

Ciprofloxacin (250-500 mg bid for 7-14 d)

Levofloxacin (Levaquin) (250-500mg bid for7days)

Cefotaxime (2 g IV q6h )

Ceftriaxone (Rocephin) 1-2 g IV dly or bid

Chloramphenicol

Amoxicillin Trimethoprim and sulfamethoxazole

Azithromycin (Zithromax)


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Corticosteroids

Reduce mortality in severely ill patients with

depressed levels of consciousness or shock.

Dexamethasone


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Further management

Management of long-term carriers is as follows:

Prolonged courses of amoxicillin or co-trimoxazole. Failure

rate is high if the patient has chronic gallbladder disease.

Ciprofloxacin (750 mg bid) and norfloxacin (400 mg bid)

have been much more effective, with cure rates of 78% and

83%, respectively.

Long-term urinary carriers should be assessed for urinary

tract abnormalities, including schistosomiasis.


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Complications

Intestinal manifestations

intestinal hemorrhage perforation (3-4.6% of hospitalized patients).

Hepatobiliary manifestations

cholangitis, cholecystitis, or hemolysis.

Pancreatitis

Acute renal failure and hepatitis with

hepatomegaly


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Toxic myocarditis:

tachycardia, weak pulse and heart sounds,hypotension, and electrocardiographic

abnormalities.

Pericarditis


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Neuropsychiatric manifestations A toxic confusional state, characterized by disorientation, delirium,

and restlessness, is characteristic of late-stage typhoid.

Facial twitching or convulsions. paranoid psychosis or catatonia may develop during

convalescence.

Meningismus

Encephalomyelitis may develop, and the underlying pathology maybe that of demyelinating leukoencephalopathy.

Rarely transverse myelitis, polyneuropathy, or cranialmononeuropathy may develop.

spastic paraplegia, peripheral or cranial neuritis, Guillain-Barrsyndrome, schizophrenialike illness, mania, and depression.


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Hematologic manifestations

Subclinical disseminated intravascular

coagulation occurs commonly in persons

with typhoid fever.

Hemolytic-uremic syndrome is rare.

Haemolysis may also be associated with

glucose-6-phosphate dehydrogenasedeficiency.


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Genitourinary manifestations

Approximately 25% of patients excrete S typhiin

their urine at some point during their illness.

Immune complex glomerulonephritis and proteinuria

have been reported, and IgM, C3 antigen, and S

typhiantigen can be demonstrated in the glomerular

capillary wall.

Nephritic syndrome may complicate chronic S typhibacteremia associated with urinary schistosomiasis.


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Musculoskeletal manifestations

Skeletal muscle - shows Zenker

degeneration, particularly affecting the

abdominal wall and thigh muscles.

Polymyositis .


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CNS manifestations

Focal intracranial infections are uncommon.

Recently, multiple brain abscesses have been

reported.

enteric fever(dr. b. erghan)-r.ppt

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