Shigella and salmonella are not found

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Invasive NTS (iNTS) is a particular problem in sub-Saharan Africa where the HIV epidemic coincides with malnutrition and endemic malaria.

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Salmonella

Robert M. Kliegman MD , in Nelson Textbook of Pediatrics , 2020

Pathogenesis

Enteric fever occurs through the ingestion of the organism, and a variety of sources of fecal contamination have been reported, including street foods and contamination of water reservoirs.

Human volunteer experiments established an infecting dose of about 10 5 -10 9 organisms, with an incubation period ranging from 4-14 days, depending on the inoculating dose of viable bacteria. After ingestion,S. Typhi organisms are thought to invade the body through the gut mucosa in the terminal ileum, possibly through specialized antigen-sampling cells known asM cells that overlie GALT, through enterocytes, or via a paracellular route.S. Typhi crosses the intestinal mucosal barrier after attachment to the microvilli by an intricate mechanism involving membrane ruffling, actin rearrangement, and internalization in an intracellular vacuole. In contrast to NTS,S. Typhi expresses virulence factors that allow it to downregulate the pathogen recognition receptor–mediated host inflammatory response. Within the Peyer patches in the terminal ileum,S. Typhi can traverse the intestinal barrier through several mechanisms, including the M cells in the follicle-associated epithelium, epithelial cells, and dendritic cells. At the villi, Salmonella can enter through the M cells or by passage through or between compromised epithelial cells.

On contact with the epithelial cell,S. Typhi assembles type III secretion system encoded on SPI-1 and translocates effectors into the cytoplasm. These effectors activate host Rho guanosine triphosphatases, resulting in the rearrangement of the actin cytoskeleton into membrane ruffles, induction of mitogen-activated protein kinase (MAPK) pathways, and destabilization of tight junctions. Changes in the actin cytoskeleton are further modulated by the actin-binding proteins SipA and SipC and lead to bacterial uptake. MAPK signaling activates the transcription factors activator protein (AP)-1 and nuclear factor (NF)-κB, which turn on production of IL-8. The destabilization of tight junctions allows the transmigration of PMNs from the basolateral surface to the apical surface, paracellular fluid leakage, and access of bacteria to the basolateral surface. Shortly after internalization ofS. Typhi by macropinocytosis, salmonellae are enclosed in a spacious phagosome formed by membrane ruffles. Later, the phagosome fuses with lysosomes, acidifies, and shrinks to become adherent around the bacterium, forming theSalmonella-containing vacuole. A 2nd type III secretion system encoded on SPI-2 is induced within theSalmonella-containing vacuole and translocates effector proteins SifA and PipB2, which contribute toSalmonella-induced filament formation along microtubules.

After passing through the intestinal mucosa,S. Typhi organisms enter the mesenteric lymphoid system and then pass into the bloodstream via the lymphatics. This primary bacteremia is usually asymptomatic, and blood culture results are frequently negative at this stage of the disease. The bloodborne bacteria are disseminated throughout the body and are thought to colonize the organs of the RES, where they may replicate within macrophages. After a period of bacterial replication,S. Typhi organisms are shed back into the blood, causing a secondary bacteremia that coincides with the onset of clinical symptoms and marks the end of the incubation period ( Fig. 225.5 ).

Salmonella

Metabolism and Physiology

Salmonellae are facultative anaerobes and are catalase positive, oxidase negative and ferment glucose, mannitol and sorbotol to produce acid or acid and gas. Whilst S. arizonae is able to ferment lactose, this is the exception rather than the rule. As a group, Salmonella are able to ferment sucrose, but rarely adonitol and overall do not form indole. They also do not hydrolyze urea or deaminate phenylalanine, but usually form H2S on triple sugar iron agar and can use citrate as a sole carbon source. Salmonella form lysine and ornithine decarboxylases, exceptions to this include S. paratyphi A and S. typhi. Salmonellae yield negative Voges-Proskauer and positive methyl red tests and do not produce cytochrome oxide. Salmonellae are also unable to deaminate tryptophan or phenylalanine and are usually urease and indole negative. Based on the biochemical tests above, Salmonella can presumptively be identified. However, for a more detailed identification of Salmonella, isolates are generally serotyped, especially for epidemiological investigations. As mentioned previously, typing of Salmonella is based on the recognition of bacterial surface antigens: the thermostable polysaccharide cell wall or somatic (‘O') antigens and the thermolabile flagella proteins or ‘H' antigens. It is also possible to subtype Salmonella serotypes on the basis of phage typing. Sub-divisions of Salmonella can also be undertaken by plasmid profiling, ribotyping or pulsed field gel electrophoresis (PFGE) of DNA fragments generated from restriction enzyme digestion.

Bacterial, Parasitic, and Fungal Infections of the Liver, Including Liver Abscesses

Mark Feldman MD , in Sleisenger and Fordtran's Gastrointestinal and Liver Disease , 2021

Shigella and Salmonella

Several case reports have described cholestatic hepatitis attributable to enteric infection withShigella spp. 14 , 15 Histologic findings in the liver have included portal and periportal infiltration with polymorphonuclear leukocytes (neutrophils), hepatocyte necrosis, and cholestasis. Severe hepatic dysfunction associated withShigella spp. infection has been reported. 16

Typhoid fever, caused by Salmonella Typhi, is a systemic infection that frequently involves the liver. Elevation of serum aminotransferase levels is common, whereas the serum bilirubin level may rise in a minority of cases. 17 Some patients may present with an acute hepatitis-like picture, characterized by fever and tender hepatomegaly. 18 Cholecystitis and liver abscess may complicate hepatic involvement withS. Typhi infection. 19

Hepatic damage byS. Typhi appears to be mediated by bacterial endotoxin, although organisms can be visualized within the liver tissue. Endotoxin may produce focal necrosis, a periportal mononuclear infiltrate, and Kupffer cell hyperplasia in the liver. These changes resemble those seen in Gram-negative sepsis. Characteristic typhoid nodules scattered throughout the liver are the result of profound hypertrophy and proliferation of Kupffer cells. The clinical course can be severe, with a mortality rate approaching 20%, particularly with delayed treatment or in patients with other complications ofSalmonella infection. Severe typhoid fever with jaundice and encephalopathy may be differentiated from ALF by the presence of an elevated serum alkaline phosphatase level, mild hypoprothrombinemia, thrombocytopenia, hepatomegaly, and an AST level greater than the ALT level. 20 Ceftriaxone is the first-line agent for the treatment of typhoid fever, with ciprofloxacin as an alternative in areas where resistance is uncommon.

S. Paratyphi A and B (Salmonella enterica serotypes paratyphi A and B) are the predominant causes of paratyphoid fever. As in typhoid fever, abnormalities in liver biochemical test results, particularly elevated serum aminotransferase levels, with or without hepatomegaly, are common. 21 Liver abscess is a rare complication. 22 Treatment is with a third-generation cephalosporin or, where prevalence of resistance is low, a fluoroquinolone.

Salmonella

General Description and Nomenclature

Salmonella are a group of Gram-negative, nonspore forming prokaryotic rods. They are motile through the use of multiple flagella, but can switch to be nonmotile in culture. They make up a core group of the Enterobacteriaceae family and are believed to have evolved from the same ancestor as Escherichia coli 160–180 million years ago with E. coli and certain serovars of Salmonella adapting to mammals while other Salmonella serovars having adapted to reptiles.

According to the Centers for Disease Control and Prevention, there are only two species within the genus Salmonella: Salmonella enterica and Salmonella bongori. However, while only two species of Salmonella are recognized, their significance should not be underestimated given that S. enterica itself consists of six subspecies with over 2500 serovars.

Alimentary system

Simon S. Cross MD FRCPath , in Underwood's Pathology , 2019

Salmonella

Food poisoning by Salmonella organisms (salmonellosis) is a relatively common problem in many countries. In the USA, Salmonella infections occur in 1 million individuals per year of which nearly 20,000 need to be treated in a hospital and approx. 400 patients die of Salmonella foodborne disease. In some patients, Salmonella infection results in vomiting and profuse watery diarrhoea, usually with colicky, periumbilical pain suggesting predominantly gastric and small intestinal involvement. In others, the symptoms relate to the large intestine, with frequent, small volume, bloody motions, and tenderness over the sigmoid colon. The histological appearances are varied. Some biopsies show oedema, focal interstitial haemorrhage and a mild increase in neutrophil polymorphs; more severe cases show a marked increase in polymorphs, with occasional crypts distended by polymorphs and mucus in the lumen (‘mucoid crypt abscesses’). The crypt architecture, however, remains normal. Uncomplicated disease usually resolves within 10 days.

Typhoid fever is caused bySalmonella enterica serotype Typhi (S. typhi), and remains a major public health problem with over 16 million cases reported each year worldwide. In contrast to the gastroenteritis caused by most other Salmonella species, typhoid fever is not a typical diarrhoeal disease and the intestinal histopathology is characterised by a macrophage predominant, not a polymorph, infiltrate. Patients usually present with prolonged fever, headache, abdominal discomfort and general debility. Around 10% of patients develop severe complicated disease and without specific treatment 5% to 30% of all patients may die.S. typhi is ingested in contaminated food or water, passes through the stomach and then invades the gut epithelium, possibly in the distal ileum. After penetration through the epithelium, Salmonella are ingested by macrophages which probably facilitate the systemic spread of the bacteria as Salmonella-infected macrophages can survive for several hours. In this way, infected cells pass into the liver and spleen and can be found also in bone marrow and blood. Some find their way back to the intestine. Shedding ofS. typhi in the faeces of an infected individual is an essential step in the transmission of typhoid fever.

Salmonella

Salmonella spp. remains a major cause of morbidity and mortality worldwide. Outbreaks of enteric fever remain commonplace in developing countries, whereas nontyphoidal salmonellas are significant in developed countries, with the main presentation that of gastroenteritis. The primary method for identification is serotyping, with over 2400 serovars identified. Methods for discrimination within serovars of clinical and epidemiological importance include phenotypic tests such as phage typing, and the gold standard molecular method is that of pulsed field gel electrophoresis. Antimicrobial drug resistance is increasing in incidence worldwide, with considerable implications for treatment of infected individuals and for public health. For nontyphoidal serovars, those commonplace in developing countries appear more virulent than those common in developed countries. Control of salmonella may be exercised by vaccination (typhoid, Salmonella Enteritidis in poultry), eradication, hygiene, and proper cooking practices.

Salmonella

Virulence Aspects of Salmonella

Host Adaptation

Salmonella virulence is a highly complex phenomenon and is probably driven by source-sink dynamics (see Sokurenko EV in Further Reading ). Some Salmonella serovars such as Typhi, Pullorum, Gallinarum, Dublin, Choleraesuis, and Enteritidis are highly host specific, with a source habitat (one in which the population expands) which we think of as reservoirs of infection in humans (Typhi), poultry (Pullorum, Gallinarum, Enteritidis), swine (Choleraesuis), and cattle (Dublin). Some of these serovars, such as Typhi, Gallinarum, and Pullorum, cause disease almost exclusively in their reservoir, while others, such as Choleraesuis and Dublin, also cause disease in a sink habitat (one which would not support the population alone) which is outside of their normal reservoir (e.g., in humans). Population growth, of the serovars in the two hosts, follows source-sink population dynamics and this in turn influences the development of virulence. The symptoms in hosts representing sink habitats can be very severe, often resulting in septicemia with subsequent mortality whereas the host-adapted serovars growing in their source habitat (e.g., Enteritidis) cause little overt disease but when transmitted to humans can be a major cause of salmonellosis. Still other serovars (e.g., Typhimurium) have a wide host range and cause disease both in their food animal reservoir (e.g., cattle) and in humans.

Salmonella Pathogenicity Islands

Many of the major components required by S. enterica to cause infections are chromosomally encoded. The regions responsible for the virulence functions are termed Salmonella pathogenicity islands (SPI). Fourteen such islands have now been identified, termed SPI-1–SPI-14. It is noteworthy that not all serovars possess all the islands, and that differential pathogenicity in different hosts may be related to the presence or absence of such islands as part of the balance between gene acquisition and functional gene loss seen in the genomes of host-adapted Salmonella serovars ( Langridge et al., 2015 ).

Salmonella enterica Virulence Plasmids

In addition to chromosomal hallmarks of host adaptation, certain serovars of subspecies I harbor serovar-specific plasmids ranging from 40 to 90 kb, which poses a gene cluster promoting virulence in mice. This gene cluster, termed the Salmonella plasmid virulence (spv) cluster has been identified in the epidemiologically important Salmonella serovars such as Enteritidis, Typhimurium, Dublin, and Gallinarum. The biology of the spv cluster indicates involvement in serum resistance and invasion, but not in the initial phase of the disease in human salmonellosis.

Salmonella are a group of bacteria that can be divided into typhoid Salmonella (Salmonella typhi) which causes typhoid fever and non-typhoid Salmonella. The latter is commonly known for causing salmenollosis which is a type of foodborne intestinal infection contracted after eating food contaminated with the Salmonella bacteria. These types of intestinal infections are more likely in children or the elderly.

What is Shigella?

Shigella are a family of bacteria that cause an infectious intestinal disease known as shigellosis. It is mainly transmitted through contact with an infected person and contaminated food and water. Shigellosis can occur in any age group but is more commonly seen in children. It is one of the common causes of outbreaks of bacillary dysentry.

Differences and Similarities

  • Salmonella and Shigella are different groups of Gram-negative bacteria.
  • There are about 2,200 serotypes of Salmonella bacteria compared to about 40 serotypes of Shigella bacteria.
  • Both Salmonella and Shigella can be transmitted through contaminated food and water, personal contact or even from animals and objects (fomites).
  • The most common way Shigella is transmitted is through direct person-to-person contact whereas ingesting contaminated raw food is the most common route of transmission of Salmonella.
  • Salmonella infection requires a larger infective dose than for Shigella infection. This means that more bacterial cells need to be ingested for salmonellosis than for shigellosis.
  • Salmonellosis and shigellosis are more likely to occur in children under 5 years of age and the elderly.
  • Salmonella infection affects the small and large intestine (enterocolitis) where as Shigella infection affects the colon (colitis).
  • Diarrhea, abdominal pain and fever are the main symptoms in both diseases.
  • Bloody and mucoid diarrhea is more likely in shigellosis than salmonellosis.
  • The symptoms of both diseases resolve within 7 days or less in most people.
  • Death in both diseases are uncommon but is more likely to occur in children with shigellosis.

Causes

Salmonellosis

The most common type of Salmonella bacteria responsible for salmonellosis are Salmonella enteritidis and Salmonella typhimurium. These bacteria tend to live and thrive in the intestines of mammals. Common ways in which fecal matter containing the bacteria is ingested includes :

  • Raw meat and poultry that is contaminated during the slaughtering process.
  • Raw seafood that are harvested from contaminated water.
  • Raw eggs that are infected before the shell forms.
  • Contaminated fruit, vegetables and milk.
  • Contact with a person who is infected or a carrier.
  • Contact with domestic animals and reptiles.

Only about 1,000,000 (one million) bacterial cells are needed to cause an infection. This is known as the infective dose and most of these bacterial cells are destroyed by the stomach acid. Only a few cells survive to pass into the small and large intestine where it causes enterocolitis. Infection can occur with as little as 1,000 (one thousand) bacterial cells in a person with one or more of the following risk factors :

  • Low stomach acid seen in the elderly, people with conditions like atrophic gastritis or using antacids or acid suppressing medication.
  • Weakened immune system in conditions such as HIV/AIDS or with the use of drugs like corticosteroids.

A person is also more likely to be exposed to an infective dose in one or more of the following situations :

  • Regular exposure to pets – mammals and reptiles.
  • International travel particularly to countries with poor sanitation and hygiene procedures.
  • Close contact with many people as in medical institutions, day care centers and crowded residential buildings.
  • Frequent use of antibiotics.
  • Inflammatory bowel disease (IBD).

Shigellosis

Most cases of shigellosis are caused by Shigella sonnei and Shigella flexneri species which are also known as group D and group B Shigella. These bacteria are mainly found in the feces of an infected person and can be spread through the following routes :

  • Touching the hands of an infected person who does not practice good hygiene. Contact with the mouth then transfers fecal particles into the gut.
  • Mothers and nannies who touch soiled diapers of infants with shigellosis or shortly after having the infection.
  • Sexual contact with an infected person particularly with certain practices that may allow fecal particles to reach the mouth.
  • Food contaminated with fecal particles transmitted by infected food workers who do not practice proper hygiene.
  • Contaminated water which may be ingested or used to irrigate and wash fruit and vegetables.
  • Swimming or playing in contaminated water.

The infective dose of shigellosis is as low as 200 bacterial cells – the number of cells that can cause shigellosis when ingested. During the acute disease a person passes out 100,000,000 (100 million) cells per gram of stool. Therefore even a minute amount of fecal matter from an infected person is sufficient to cause shigellosis. The chances of developing shigellosis is higher in the following people and situations :

  • Children under 5 years of age, particularly within the 2 to 4 years group.
  • Facilities such as nursing homes and day care centers.
  • Poor sanitary facilities particularly in developing countries.
  • Endemic areas particularly where there is an infestation of flies and in rural communities where contaminated water may be used for irrigation.
  • Homosexual men are at greater risk due certain sexual practices.

Symptoms

The incubation period is typically between 1 to 3 days in salmonellosis and 2 to 4 days in shigellosis. This is the time from when the bacterial cells enter the gut to cause symptoms. The incubation can be as short as 12 hours in both diseases. Salmonella causes inflammation of the small and large intestine – enterocolitis. Shigella causes inflammation of the colon – colitis. The signs and symptoms of salmonellosis and shigellosis are largely the same and usually indistinguishable.

  • Watery diarrhea which may be bloody with mucus in shigellosis but is typically non-bloody in salmonellosis.
  • Abdominal pain is seen in both diseases and is more cramping-like in shigellosis.
  • Fever
  • Malaise

Other symptoms that may be seen particularly in salmonellosis includes :

  • Headache
  • Muscle aches
  • Nausea
  • Vomiting

Bacteremia is a serious complication where the bacteria, particularly with Salmonella infection, enters the bloodstream and travels to different sites. Here it causes infections of other organs like the lining around the brain and spinal cord (meningitis), bones (osteomyelitis) and inner heart lining (endocarditis).

Treatment

The treatment for both salmonellosis and shigellosis is largely supportive. This includes :

  • Plenty of fluids – oral rehydration solution.
  • Bed rest while signs and symptoms like fever and abdominal pain are intense.
  • Practice good hygiene so as not to infect others.
  • Eat bland but balanced meals if there is no vomiting despite the presence of diarrhea.

Salmonellosis resolves within 4 to 7 days and shigellosis within 5 to 7 days even without medication provided that a person does not have underlying diseases or weakened immune systems and are properly nourished. The following medication can be used :

Что такое сальмонеллез? Причины возникновения, диагностику и методы лечения разберем в статье доктора Александрова Павла Андреевича, инфекциониста со стажем в 14 лет.

Над статьей доктора Александрова Павла Андреевича работали литературный редактор Маргарита Тихонова , научный редактор Сергей Федосов и шеф-редактор Лада Родчанина

Александров Павел Андреевич, инфекционист, гепатолог, паразитолог, детский инфекционист - Санкт-Петербург

Определение болезни. Причины заболевания

Сальмонеллёз — это острое инфекционное заболевание желудочно-кишечного тракта с возможностью дальнейшей генерализации процесса (распространением заболевания по всему организму). Причина развития сальмонеллёза — различные серотипы бактерий рода Salmonella. К клиническим характеристикам сальмонеллёза относят синдром общей инфекционной интоксикации, синдром поражения желудочно-кишечного тракта (гастрит, энтерит), синдром обезвоживания, гепатолиенальный синдром (увелечение печени и/или селезёнки) и иногда синдром экзантемы (высыпания).

Заболевание, вызываемое различными серотипами бактерий рода Salmonella

Возбудитель

семейство — кишечные бактерии (Enterobacteriaceae)

род — Сальмонелла (Salmonella)

Существует 7 подвидов (более 2500 сероваров). Наиболее актуальные серовары: typhimurium, enteritidis, panama, london.

Представлены следующей антигенной структурой:

  • О-антиген (соматический, термостабильный);
  • H-антиген (жгутиковый, термолабильный);
  • К-антиген (поверхностный, капсульный);
  • Vi-антиген (антиген вирулентности — степень способности штамма вызвать заболевание; является компонентом О антигена);
  • М-антиген (слизистый).

К факторам патогенности (механизмам приспособления бактерий) относятся:

  • холероподобный энтротоксин — интенсивная секреция жидкости в просвет кишки;
  • эндотоксин (липополисахарид) — общее проявление интоксикации;
  • инвазия — заражение.

Тинкториальные свойства: разлагают глюкозу и маннит, образовывая кислоту и газ, продуцируют сероводород. Грамм-отрицательные палочки подвижны, спор и капсул не образуют. Растут на обычных питательных средах, образуя прозрачные колонии, на мясо-пептонном агаре с образованием колоний голубоватого цвета, на среде Эндо образуют прозрачные розовые колонии, на среде Плоскирева — бесцветные мутные, на висмут-сульфитном агаре — чёрные с металлическим блеском.

Бактерии в агаре Эндо

Высокоустойчивы во внешней среде (без агрессивных воздействий), активно размножаются в мясе и молоке (до 20 суток), в воде сохраняют жизнесособность до 5 мес., в почве — до 9 мес., в комнатной пыли — до 6 мес., в колбасе — до 1 мес., в яйцах — до 3 мес., в фекалиях сохраняются до 4 лет. При 56 °C погибают через 3 минуты, при кипячении мгновенно. Сальмонеллы, которые находятся в куске мяса массой 400 гр и толщиной до 9 см, погибают при его варке за 3,5 часа. Соление и копчение оставляет сальмонелл в живых. Воздействие кислот и хлорсодержащих дезинфицирующих средств вызывает их гибель. В последнее десятилетие появились штаммы сальмонелл, устойчивые ко многим антимикробным препаратам. [2] [5]

Эпидемиология

Зооантропоноз, распространённый повсеместно.

Источники инфекции: домашние животные (сами не болеют), птицы, человек (больной и носитель).

Резервуары инфекции и причина эпидемических вспышек сальмонеллеза: грызуны, дикие птицы, тараканы, улитки, лягушки, змеи.

Источники заражения сальмонеллой

Механизм передачи: фекально-оральный (пути — алиментарный, т. е. через органы ЖКТ, водный, контактно-бытовой). В основном источниками заражения являются птицы, яйца и молочные продукты. Инфицирующая доза 10*5-10*8 микробных тел.

Факторы риска

  • детский возраст до 5 лет;
  • возраст до 12 месяцев, особенно высока вероятность заболеть без грудного вскармливания;
  • иммунодефицит (в основном у младенцев и лиц старше 65 лет, а так же у пациентов с ВИЧ в стадии СПИДа, принимающих иммунодепрессивные препараты);
  • регулярный приём препаратов, снижающих кислотность желудка;
  • употребление сырого и недостаточно термически обработанного мяса, молочных продуктов и яиц;
  • частый контакт с животными с несоблюдением правил гигиены;
  • посещение стран с низким уровнем жизни.

В России в 2016 г. заболеваемость была – 26 на 100 тыс. населения, у детей в до 14 лет – 71 на 100 тыс. Для сравнения в США среднегодовая заболеваемость — 15 на 100 тыс. (1,35 миллиона заболеваний, 26 500 госпитализаций и 420 смертей ежегодно). Иммунитет строго типоспецифичен (возможно многократное инфицирование различными штаммами) и непродолжителен [2] [6] [9] [10] .

При обнаружении схожих симптомов проконсультируйтесь у врача. Не занимайтесь самолечением - это опасно для вашего здоровья!

Симптомы сальмонеллеза

Инкубационный период — от 6 часов (при алиментарном заражении) до 3 суток. При внутрибрюшном заражении (искусственно) — до 8 дней.

Начало заболевания острое (т. е. развитие основных синдромов происходит в первые сутки заболевания).


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Salmonella-Shigella (SS) agar is used for selective isolation and differentiation of Salmonella and Shigella. It is used for the isolation, cultivation and differentiation of gram-negative enteric microorganisms from both clinical and non-clinical specimens such as from feces, urine, and suspected food items (fresh and canned foods). This medium is not recommended for the primary isolation of Shigella as some Shigella strains may not grow on SS agar due to relatively high level of selectivity.

    ,,
  1. Eosin Methylene Blue (EMB) Agar,
  2. Xylose Lysine Deoxycholate (XLD Agar), and

Despite its name, Salmonella-Shigella (SS) agar is not suitable for isolating shigellae as it is inhibitory to most strains.

Table of Contents

Composition of Salmonella-Shigella (SS) Agar and their function:

  1. Lactose: fermentable carbohydrate
  2. Beef extract, proteose peptone: provides the nitrogen, vitamins, and amino acids in SS Agar
  3. Ferric citrate: Sodium Thiosulfate is also a sulfur source, and acts with Ferric Citrate as an indicator to detect hydrogen sulfide production.
  4. Sodium thiosulphate &Sodium citrate: selective agents, providing an alkaline pH to inhibit Gram-positive organisms and suppress coliforms
  5. Bile salts : The bile salts inhibit growth of gram-positive microorganisms
  6. Brilliant Green/Neutral Red: pH indicator.
  7. Agar: Solidifying agent.

Final pH: 7.0 +/- 0.2 at 25ºC

Principle

The presence of bile salts mixture and dyes (brilliant green) inhibits the growth of gram-positive species to a varying degree. Differentiation of enteric organisms is achieved by the incorporation of lactose in the medium. Organisms which ferment lactose produce acid which, in the presence of the neutral red indicator, results in the formation of red/pink colonies. Lactose non-fermenters form colorless colonies. The latter group contains the majority of the intestinal pathogens, including Salmonella and Shigella.

The sodium thiosulfate and ferric citrate enable the detection of hydrogen sulfide production as evidenced by colonies with black centers.

E coli Shigella Salmonella

Colony morphology of E.coli, Salmonella and Shigella in Salmonella-Shigella Agar

Preparation of the media

  1. Suspend 60 g of the medium in one liter of deionized or distilled water.
  2. Mix well.
  3. Heat with frequent agitation and boil for one minute.
  4. Sterilization in autoclave is not necessary.
  5. Pour into plates
  6. Let the agar solidify and store in the refrigerator (avoid freezing). Prepared culture media can be kept for at least a week in refrigeration.
    Note: Various commercial suppliers now supplies ready-to-use culture plates.

Culturing the sample

Results

  1. Lactose fermenter: If lactose fermentation occurs, the medium will turn red due to the acidic pH. e.g. Escherichia coli, Klebsiella pneumoniae gives red colonies.
  2. Non-Lactose fermenter: Salmonella, Shigella, and other non-lactose fermenters appear as transparent or translucent colorless colonies. Colonies of Salmonella spp. may appear with or without black centers (depending on the species isolated).

Precautions:

As SS Agar media contains components of animal origin (absence of transmissible pathogenic agents cannot be ruled out) so treat it as potentially infectious, and handle observing the usual universal blood precautions. Do not ingest, inhale, or allow the media to come into contact with skin.

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Acharya Tankeshwar

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