4222 salmonella

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Salmonella

Food poisoning, enteric fever

Salmonella infections in humans

• Enteric fever– typhoid and paratyphoid fevers– S. typhi, paratyphi A, B, C– systemic infection – infects only humans– GI symptoms may not be evident

• Salmonella gastroenteritis– non-typhi serovars– zoonosis: predominantly food-borne– can be complicated by septicaemia

• more common with some serovars, e.g. S. dublin (15% mortality rate when septicemic in the elderly)

• Metastatic disease, e.g. osteomyelitis

Bacteriology

• Salmonella enterica– one species, ~2000 serovars– Non standard nomenclature common

• S. enterica serovar Typhimurium• or S. typhimurium

• rod-shaped, non-spore-forming Gram-negative bacterium

• belongs to the family Enterobacteriaceae– close relative of E. coli

• Motile by peritrichous flagella (H antigen).– nonmotile exceptions: S. gallinarum and S. pullorum

Antigenic Structure

• Kauffmann-White antigenic scheme– agglutination reactions with specific antisera against

Salmonella antigens• O antigens– characteristic sequence of repeating polysaccharide units in

LPS. • H antigens– flagellar antigens (protein) and may occur in one of two

phase variations. • Vi antigen– a capsular polysaccharide homopolymer of N-acetyl

galactosamineuronic acid

EpidemiologyEnteric fever

• person-to-person spread – no animal reservoir

• contamination with human faeces – usual vehicle contaminated water.

– occasionally, contaminated food (usually handled by an individual who harbours S. typhi)

EpidemiologyNon-typhoidal serovars

• zoonosis with enormous animal reservoir – common animal reservoirs are chickens, turkeys,

pigs, and cows

• contaminated food is major vehicle, usually: – red and white meats, raw eggs, milk & dairy

products– many other possibilities, from spices or chocolate

to cannabis– can follow direct contact with infected animals

(e.g. farm trip, reptiles as pets)

• outbreaks common

• In food preparation establishments

• In Hospitals– now careful attention to hospital kitchen hygiene

• Food-borne transmission by– contamination of cooked food by raw food

– failing to achieve adequate cooking temperatures.

• secondary cases by person to person spread are common in outbreaks

• food handlers who practice good hygiene very rarely responsible for outbreaks

Salmonella in eggs

• various Salmonella serovars isolated from the outside of egg shells

• S. enteritidis PT4 present inside the egg, in the yolk• vertical transmission– deposition of the organism in the yolk by an infected

layer hen prior to shell deposition.

Infectious dose

• typically about 1,000,000 bacteria

• much lower if the stomach pH is raised

• much lower if the vehicle for infection is chocolate– protects the bacteria in their passage through the

stomach

– an infectious dose of about 100 bacteria

Epidemiologycarrier states

• carrier state may last from many weeks to years with faecal shedding – convalescent carrier

• chronic carrier – ~3% of persons infected with S. typhi

– ~0.1% of those infected with non-typhoidal salmonellae

Clinical FeaturesEnteric Fever

• incubation period 10 to 14 days • septicaemic illness

– myalgia and headache– fever – splenomegaly– leukopenia– abdominal pain – Rose spots (macular rash on abdomen)

• 10% fatal • positive blood, urine, and stool cultures• Sequelae (secondary result ): intestinal haemorrhage and

perforation

Clinical featuresGastroenteritis

• incubation period depends on dose • symptoms usually begin within 6 to 48 hours– Nausea and Vomiting– Diarrhoea – Abdominal pain – Myalgia and headache– Fever

• duration varies, usually 2 to 7 days• seldom fatal, except in elderly or

immunocompromised

Pathogenesis Gastroenteritis

• Pathogenic salmonellae ingested in food survive passage through the gastric acid barrier

• invade intestinal mucosa

• invasion of epithelial cells stimulates the release of proinflammatory cytokines

• induces an inflammatory reaction

• causes diarrhoea and may lead to ulceration and destruction of the mucosa

PathogenesisEnteric Fever

• Bacteria invade mucosa or Peyer's patches of small intestine (?M cells), pass into mesenteric lymph nodes where they multiply and then enter the blood stream via the thoracic duct

• Primary bacteraemia cleared by reticuloendothelial system (RES), bacteria multiply in RES cells and destroy them

• Facultative intracellular parasites

PathogenesisEnteric fever

• Secondary bacteraemia occurs and results in spread to other organs. – Infection of the biliary tract.

• Multiplication in biliary tract leads to seeding the intestine with large numbers of bacteria.

• Involvement of intestinal lymphoid tissue may lead to necrosis and ulceration.

• In untreated nonfatal cases, temperature drops in 3 to 4 weeks (onset on immunity?)

Laboratory Diagnosis

• Biochemical tests and serological tests must be done in parallel– Some other bacteria, e.g. Citrobacter, may have

similar serological profiles– Commercial kits commonly used, e.g. API20

• Phage typing done for epidemiological purposes– E.g. to find source of outbreak– Certain phage types predominate nationally

• S. typhimurium PT4• S. enteritidis DT109

Laboratory diagnosis

Specimens• For the diagnosis of enteric fever, specimens include

blood, urine & feces for culture.• Blood – detected in 75-90% of the patients in the first

10 days of infection, and 30% of the patients in the 3rd week.

• Faeces – can be isolated from 40-50% of patients in the 2nd week of infection &from about 80% of patients in the 3rd week.

• Urine – isolated from about 20% of patients after the 2nd week of infection [esp. pts with schistosomiasis]

• For Salmonella food poisoning, faeces are required for culture and blood during times of fever.

Microscopy

• Gram negative motile rods except for S. pullorum-gallinarum

• Faeces may contain blood in the late stages of infection and few pus cells and red blood cells in Salmonella food poisoning cases

Culture• Enrichment and selective media for

Salmonella in faeces is Selenite broth.• Differential media is XLD and SSA• XLD-pink colonies with black centers• SSA- black colonies with silver metallic

sheen.

No Species Glu Lac/Suc H2S Gas

1 P. aeruginosa K/K - - - -

2 E. coli A/A + + - +

3 Salmonella Typhimurium K/A + - + +

Shigella flexneri K/A + - - -

1 2 3 4

Serology• The Kaufmann-White system used to classify

Salmonella based on identifying the O and H antigens possessed by different serovars.

• The detection of Vi antigen is also used in the detection of Salmonella typhi and other species.

O Antigens• Cell wall heat stable antigens.• Groups are designed A- Z, 51-61 AND 64-66• Medically important Salmonella belong to groups A

to G.• Each group has a group factor, which is an O antigen

common to all members of the group and not possessed by Salmonella belonging to other groups.

H Antigens• Flagella, heat-stable antigens• Serotyped by their H antigens• Many Salmonella are diphasic, i.e. occur in 2 antigen

forms referred to as phase l and phase ll.• Phase l antigens are given in alphabetical letters and

phase ll are either numbered or given a letter if known to occur in both phases.

Vi Antigens• Surface or capsule K antigen can be found in S. typhi, S.

paratyphi C and a few other Salmonella.• It is associated with virulence and can be detected using

Vi antiserum.• It can interfere with O antigen testing• If an isolate agglutinates the Vi antiserum but not an O

antiserum, interference from Vi antigen should be suspected.

• Saline suspension of organism should be heated in water bath for 20 mins and after being allowed to cool, the bacterial cells should be retested with the O antiserum.

Grouping and serotyping of Salmonella• Antisera are costly, there laboratories need to stock up their

polyvalent O antisera w/c covers locally important groups of Salmonella. Specific O, H and Vi antisera to identify the S. typhi.

• The following sera are required to identify S. typhi: Salmonella O antiserum Factor 9 [Group D] Salmonella H antiserum d Salmonella Vi antiserum

Widal Test

• This tests for O & H antibodies in the patients serum and comes in handy when culturing facilities are not available.

Treatment

• Gastroenteritis– replace fluid loss by oral and intravenous routes– antibiotics are not recommended for uncomplicated

gastroenteritis • do not shorten illness • prolong excretion.

– antibiotic therapy reserved for the septicaemic and metastatic disease

• Typhoid fever and enteric fevers should be treated with antibiotics– usually ciprofloxacin– rise of resistance

Prevention

• Remove source– Salmonella free life-stock– Vaccinate chicks

• Interrupt transmission– Good food hygiene

• Cook food properly• Keep raw and cooked foods apart

– Public Health: clean water

• Strengthen host– vaccination

Salmonella vaccines

• Vaccination of travellers against typhoid recommended, but does not remove need for good hygiene

• Three licensed vaccines– Traditional heat-killed

• very reactogenic

– Vi subunit vaccine– live oral vaccine, S. typhi Ty21A

• Salmonellas can act as live attenuated carriers for other antigens– So far only experimental

• No vaccines for gastroenteritis

Shigella

Bacillary dysentery

Shigella

Species

• S. dysenteriae [Subgroup A, serovars 1-10]

• S. flexneri [Subgroup B, serovars 1-6, & X and Y variants]

• S. boydii [Subgroup C, serovars 1-15]

• S. sonnei [Subgroup D, only 1 serovar]

Normal habitat• Found only in the human intestinal tract.• Carriers of the pathogenic strain can excrete

the organisms upto 2 wks after the infection &occasionally for longer periods.

• Killed by drying

Transmission• Transmitted by fecal-oral route• High incidence of shigellosis occur in areas of poor sanitation

and where water supplies are polluted.• Lack of personal hygiene• Young children are more frequently affected than adults [> 6

months]• Horseflies are also thought to be important in transferring

Shigella from faeces to food.• Epidemics can be caused by ingestion of contaminated milk

and milk products.

Pathogenecity• Shigella species cause bacillary dysentery

[shigellosis]• Deaths in young children are caused by S. dysenteriae• Clinical features include toxemia, sometimes

bacteremia, and severe dysentery leading to marked dehydration &protein loss, inflammation & ulceration of LI, hemorrhage, abdominal pain & high fever.

• Death can occur from circulatory collapse or kidney failure.

• Total WBCs is raised with neutrophilia

• Infection with S. dysenteriae can lead to leukemoid reaction developing 5-10 days after infection caused by an endotoxin.

• S. sonnei is not very pathogenic, therefore infections are rarely serious.

Laboratory diagnosisSpecimen• Faeces• Specimen may be watery and contain little blood and

mucus in the early stages of infection but consist mostly of pus and blood mixed with mucus in the later stages of infection.

• Specimens have an alkaline pH whereas faeces of amoebic dysentery are acidic.

Microscopy

• Gram negative non-motile rods

• Fecal microscopy will have red cells and large numbers of pus cells

• Faeces of amoebic dysentery contain red cells but very few pus cells

Culture

• SSA or XLD are required to isolate Shigella.

• XLD- colonies are pink

• Aerobic organism growing at 35-37ºC/24hrs

Serology

• Shigella are serotyped by their O antigens using polyvalent S. dysenteriae, S. flexneri, S. boydii & S. sonnei antisera using slide agglutination method.

• Some Shigella strains [S. dysenteriae and S. sonnei] possess surface or K antigens that can hide the O antigens being tested.

Antibiotic sensitivity• Patient with severe bacillary dysentery require

antibiotic therapy.• Antimicrobials against Shigella species

include A, D, C, cephalothin, nalidixic acid, SXT.

• Multidrug resistant strains have also been reported.

4222 salmonella

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