Enteric Fever: Dr. Catherine Chunda-Liyoka 25.07.2018 5 Year Medical Students

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Dr.

Catherine Chunda-Liyoka
ENTERIC FEVER 25.07.2018
5th year Medical Students
HISTORY

Antonius Musa, a Roman physician who


achieved fame by treating the Emperor
Augustus 2,000 year ago, with cold baths
when he fell ill with typhoid.

Thomas Willis who is credited with the first


description of typhoid fever in 1659.
 
 
French physician Pierre Charles
Alexandre Louis first proposed
the name “typhoid fever”

William Wood Gerhard who was the first


to differentiate clearly between typhus
fever and typhoid in 1837.

 
Carl Joseph Eberth who discovered the
typhoid bacillus in 1880.

Georges Widal who described the  


‘Widal agglutination reaction’ of the blood in 1896.
1. The best known carrier was "Typhoid
Mary“; Mary Mallon was a cook in Oyster
Bay, New York in 1906 who is known to
have infected 53 people, 5 of whom died.

2. Later returned with false name but


detained and quarantined after another
typhoid outbreak.

3. She died of pneumonia after 26 years in


quarantine.
EPIDEMIOLOGY

♦  strongly endemic
♦  endemic
♦  sporadic cases
ETIOLOGY
S. typhi
S. paratyphi A,B and C
Gram negative rod
Motile
Non-sporing
Non-capsulated except S.typhi
Capable of aerobic and anaerobic respiration
Resistant to many physical agents
Can be killed by heat 54.4 deg for I hour or 60deg for 15min
Remain viable for ambient or reduced temp for days
May survive for weeks in sewerage, dried foodstuff, pharmaceutical agents, and
fecal matter
Has O (heat stable lipopolysaccharide) and H (heat labile protein)antigens
MODE OF TRANSMISSION
Humans are only reservoir of S.Typhi thus direct or indiredct contact with an infected
person is necessary for infection
Ingestion of food or water contaminated with human faeces is the commonest mode of
transmission
Oysters and shellfish cultivated in water contaminated by sewerage is source of spread
In USA due to international travel-travel to Asia, South and Central America usually
implicated.
Congenital and Intrapartum transmission can also occur from a bacteremic and chronic
carrier mother.
Sexual transmission from an asymptotic carrier
Incubation period: 7-14 days but can be as long as 3-30-60days
Period of communicability is from the first week to convalescence which can last
upto 3 months or even 1 year.
Susceptability: reported in preschool children and 5-19 years old in endemic areas;
those with impaired cellular immunity, SCD patients. Elderly, debilitated, poor
sanitary conditions, poor water sanitation, gastric achlorrhydria, HIV positive
PATHOGENESIS
Ingestion of contaminated food or water

Salmonella bacteria

Invade small intestine and enter the bloodstream

Carried by white blood cells in the liver, spleen, and bone marrow

Multiply and re-enter the bloodstream


Bacteria invade the gallbladder, biliary system, and the lymphatic tissue of the
bowel and multiply in high numbers

Then pass into the intestinal tract and can be identified for diagnosis in
cultures from the stool tested in the laboratory
HOW DOES THE BACTERIA CAUSE
DISEASE ?
Characterized by hyperplasia of the reticulo-endothelial system with proliferation of the
mononuclear cells.
Occurs in the Peyers patches where infection enters the GIT from.
Involves the mucosa and lymphatic tissue of the intestinal tract causing severe
imflammation and necrosis inflammation of the intestines can penetrate the deeper tissues
to cause perforation.
Liver, spleen, mesenteric nodes are hyperplastic with focal areas of necrosis
Inflammation can also occur in the bone marrow, gall bladder, meninges, lungs, kidneys
,eyes, joints, bones
Can cause meningitis, pneumonia, bronchitis, pyelonephritis, nephrotic syndrome,
endophthalmitis, optic neuritis, arthritis, osteomyelitis as complications
Bacteria invades peyers patches.
Transported to the intestinal lymph nodes
Mononuclear cell, monocytes fail to control the infection and carry these organisms
into the mesenteric lymph nodes.
Organisms then reach blood stream thru the thoracic duct
Organism then spread thru to the reticuloendothelial system such as liver, spleen
bone marrow and may seed other organisms such as the kidney
Gall bladder is susceptible to being infected and organisms multiply in such large
numbers that they then reach the intestines through the bile
IMMUNOLOGY
Cell mediate immunity is important in controlling the infection so that patients
acutely ill with typhoid fever have been found to have low levels of T-lymphocytes
Carrier show impaired cellular activity against salmonella typhi antigens in the
leucocyte migration inhibition test.
Large numbers of virulent bacilli pass in the intestines and are excreted in the stool
without entering the epithelium of the host.
CLINICAL MANIFESTATION
Differs with age the commonest we see being the preschool aged children and adolescents;
Fever which increases in a stepwise fashion to become unremitting within 1 week
Headache
Abdominal pain which can worsen with development of perforation
Diarrhoe with a pea soup consistency, early in the disease. More prominent in the infants and young
children below 5 years
Constipation later becomes more prominent
Nausea, vomiting
Cough
Epistaxis
Rose spot rash in the lower part of chest and abdomen appreciated in white skin,
macular or maculopapular, erythematous, discrete, appears on day 7-10, lasts 2-3
days leaving a brownish discolouration.
Culture of lesions have 60% yield for the organism
Sever lethargy which can persist for upto 1-2 months
Myalgia
Malaise
Can occur in neonates and presents within 3 days of delivery
Hepatomegaly
Splenomegaly
Relative bradycardia
Altered mental state: delirium, stupor, disorientation
COMPLICATIONS
Perforation in the distal ileum
Overt hepatitis
Cholecystitis
Pancreatitis
Toxic cardiomyopathy with fatty infiltration causing arrhythmias, sinoatrial block,
cardiogenic shock, ST-T changes in EEG
Meningitis
Cerebral thrombosis
Acute cerebral ataxia
Chorea
Aphasia
Deafness
Psychosis
Transverse myelitis
Fatal bone marrow necrosis
Pyelonephritis
Nephrotic syndrome
Endocarditis
Parotitis
Orchitis
Suppurative adenitis
Osteomyelitis
Suppurative arthritis
Leukopenia
Thrombocytopenia
Proteinuria
DIFFERENTIAL DIAGNOSIS
Tuberculosis
Septicemia from other bacterial infections
Infectious mononucleosis
Hepatitis
Leukemia
lymphoma
DIAGNOSIS
Blood culture (Deoxychocolate citrate agar [DCA], Bismuth sulphate agar [BSA],
Selenite F Broth, XID))
Stool and urine culture are positive after the first week of infection
Bone marrow is the most sensitive method as it is not influenced by antribiotic
therapy
Widals test measures antibodies against the O and H antigens-lots of false positives
and negatives thus not reliable on its own. A four fold increase in titres in two tests
done 10-14 days apart may be relied on.
TREATMENT
Ciprofloxacin is the drug of choice in our set up-treat for 7-10 days
Cipro at 750mg BD per day for 28 days or norfloxacin 400mg BD per days has been
reported to treat carriers in 80-90% of cases
Other drugs used are Chlorammphenical, Ampicilin, Amoxycilin, Cefotaxime,
Ceftrioxone, cefixime, TMP-SMX
PROGNOSIS
Relapse can occur in 4-8% of patients without antibiotic therapy
Those that have received therapy can relapse within 2 weeks
Numerous relapse can occur-mild and shorter in duration
1-5% become chronic carries
Those with biliary tract disease more prone to chronic carrier state than the general
population
Those with schistosomiasis or kidney stones are prone to urinary carrier state
Middle aged and women more prone to chronic carrier state which is less common in
children.
PREVENTION
Good hygiene
Good water supply
Good sanitation
Vaccination. 2 vaccines available
Ty21a oral live attenuated vaccine given from >or = 6years, 4 enteric-coated
capsules given twice on alternate days, repeated after 5 years
Vi capsular polysaccharide vaccine can be give to those >or = 2yr and repeated every
2 years
Vaccine given to travelers to endemic areas, individuals with intimate contact and
household members of known chronic carriers, high risk populations, school-aged
children in endemic areas
Chronic carriers can only be certified to handle food after 3 consecutive negative
authenticated stool/urine sample test done 1 month apart and one of the 3 samples to
be collected by purging.
Prevention
And
Treatment

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