Open access peer-reviewed chapter

Salmonella: The Critical Enteric Foodborne Pathogen

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Mohd Afendy Abdul Talib, Son Radu, Cheah Yoke Kqueen and Farinazleen Mohamad Ghazali

Submitted: 08 January 2022 Reviewed: 23 February 2022 Published: 04 July 2022

DOI: 10.5772/intechopen.103900

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Edited by Sonia Bhonchal Bhardwaj

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Persistent cases of Salmonella infection have urged great attention and surveillance on this foodborne pathogen. Salmonella continues to be a significant foodborne disease worldwide for both animals and people in the twenty-first century. It is one of the leading causes of foodborne pathogens infecting animals and humans. Salmonellosis is a principal cause of food poisoning and is, hence, a severe public health problem. The history, classification and nomenclature of Salmonella, as well as its characteristics, clinical manifestations, epidemiology and route of contamination, will be covered in this chapter to help readers gain a better understanding and overview of this microbe.


  • Salmonella
  • foodborne
  • pathogens
  • food poisoning

1. Introduction

Foodborne illnesses are defined by World Health Organization (WHO) as diseases, usually either infectious or toxic in nature, caused by agents that enter the body through the ingestion of food. Foodborne diseases could be caused by a wide range of biological and chemical agents or hazards resulting in varying degrees of severity, ranging from mild indisposition to chronic or life-threatening illness, or both. These agents include bacteria, viruses, protozoa, helminthes, and natural toxins, as well as chemical and environmental contaminants.

Foodborne illness or disease caused by foodborne pathogens occurred every year in both developed and developing countries throughout the world. The incidence of foodborne disease is difficult to be estimated globally but it was reported that an estimate of 600 million or almost 1 in 10 people in the world fall ill after eating contaminated food and 420,000 die every year. Centers for Disease Control & Prevention, US in 2011 [1] estimated that roughly one of six Americans or 48 million people get sick, 128,000 are hospitalized, and 3,000 die of foodborne diseases. Among these, children under 5 years of age carry 40% of the foodborne disease burden, with 125,000 deaths occuring every year [2].


2. History background

Salmonella was a prevalent pathogen that infected the digestive tracts of both human and animals. Salmonella contamination in food, water and the natural environment is mainly caused by faecal contamination in the environment (Figure 1). Some Salmonella serovars are host-specific; for instance, serovars Typhi and Paratyphi A can only be colonised in humans, serovar Abortusovis in sheep and serovar Gallinarum in fowl. Salmonella serovars also induce infectious syndromes distinct to their type; for example, the highly adapted serovar Typhi causes systemic infection called typhoid exclusively in humans. Serovar Typhimurium causes non-typhoidal salmonellosis (NTS) in human, which is one of the most prevalent serotypes responsible for infections, including acute gastroenteritis in humans [1] and animal species like hens [4], pig [5] and mice [6]. Serovar Abortusovis causes high rates of abortion in flocks, ewes, sheep and goat [7, 8], and serovar Dublin originally discovered in cattle, which adapted to infect other animals such as bovines and fox [9, 10, 11]. Infection by serovar Dublin in human is rare but causes rather severe invasive bloodstream infection [10].

Figure 1.

Schematic diagram showing important structural components of Salmonella Typhi (Source: Hu & Kopecko, 2003 [3]).

In 1880, Karl Eberth discovered a bacillus-like pathogen in the spleen and Peyer’s patches of typhoid patients. He was a student of the famous Rudolf Virchow [12]. Four years later (in 1884), Georg Gaffky, a German microbiologist, successfully grew the pure culture of the bacterium [13]. Theobald Smith was the first to discover what would be later known as Salmonella enterica (var. Choleraesuis) while working in the Veterinary Division of the United States Department of Agriculture (USDA) as a research laboratory assistant in a department headed by Daniel Elmer Salmon, the veterinary pathologist. At first, the agent responsible for swine fever or hog cholera was thought to be caused by Salmonella Choleraesuis, prompting both Salmon and Smith to name the bacterium “Hog-cholerabacillus” [14]. In fact, Salmon and Smith were first to discover and isolate S.Choleraesuis from pigs in 1886. Incidentally, it was not until 1900 that the name and genus Salmonella was used when it was proposed by Joseph Leon Lignières and named after Daniel Elmer Salmon as an honorific attribute to the discovery made by his group [15].


3. Classification and nomenclature

To characterise and communicate about this bacterial genus, scientists have used comprehensive Salmonella nomenclature. Historically, Salmonella strains were classified based on their epidemiology, host range, clinical symptoms, biochemical reactions and surface antigenic patterns. Previously, the name Salmonella was derived from the geographical location where the first strain is isolated; for example, S. Heidelberg, S. Derby, S. London. Other than that, it was also named according to its clinical conditions or host specificity, such as S. typhimurium, S. enteritidis, S. typhi,‘S. gallinarum’, ‘S. abortusovis’ or S. choleraesuis. However, it was soon realised that these so-called species were ubiquitous [16].

A great number of serovars have been described as a result of O and H antigens analysis initiated by White in 1926 and continued by Kauffmann later in 1941. The species that were defined by Kauffman as ‘a group of related sero-fermentative phage types’ created more than 2000 serovar names according to the species. However, the concept of one serovar one species was discovered to be unsuitable since biochemical test still could not separate most of the serovars. Although the terms serotype and serovar are interchangeable, according to the Bacteriological Code, serovar is now recommended for scientific communication (1990 Revision).

In the early years, Kauffman identified Salmonella serovars in 1966 based on its antigenic composition, and there were multiple species within its genus. He found Salmonella serovars and a variety of species within the genus using the antigenic formula. Some clinically important Salmonella strains were found before 1966, and the majority of serovars were named after the illness and/or the host, such as S. typhi and S. typhimurium, or by the geographical area or origin of the species that were first isolated.

The epidemiologic classification of Salmonella is based on the preferences of the hosts. S.Typhi was the first of the host-restricted serotypes that only infect humans. The second group includes host-adapted serotypes associated with one host species but can cause disease in other hosts. An example of a host-adapted serotype was S. Pullorum, which was discovered in an avian. The remaining serotypes are in the third group. Each year, the three most common serotypes recovered from humans are Salmonella Enteritidis, Salmonella Typhimurium, and Salmonella Heidelberg.

Given the complexities of the various Salmonella species, it was proposed that the genus Salmonella was separated into three species: S. choleraesuis,S. typhosa’ (S. typhi) and ‘S. kauffmannii’. ‘S. kauffmannii’ contains entirely additional serovars. S. enterica, according to Kauffmann and Edwards (1952), should include all salmonellae.S. enterica subsp. enterica(S. enterica subsp. I) are the most frequent Salmonella serovar among the approximately >2600 Salmonella serovars that have been found to date [17]. Human and warm-blooded animal infections with Salmonella infections are virtually always caused by strains belonging to the O-antigen serogroups (bacteria’s surface of their outermost layer), A, B, C1, C2, D, and E [18]. The oligosaccharides associated with lipopolysaccharide determine the O antigen.

Salmonella infections that are typically isolated from cold-blooded animals and the natural environment but uncommonly isolated from human are caused by serovars in the S. enterica subspecies salamae(S. enterica subsp. II), arizonae (S. enterica subsp. IIIa), diarizonae (S. entericasubsp. IIIb), houtenae (S. entericasubsp. IV), indica (S. entericasubsp. VI), and S. bongori.

The White-Kauffmann-Le Minor scheme, previously designated as Kauffman-White scheme, described Salmonella’s characterisation based on antibody recognition with antigens on Salmonella’s surface. Three major antigenic determinants are used to classify Salmonella into three groups in the scheme: flagellar H antigens, somatic O antigens and virulence (Vi) capsular K antigens. This scheme is an established document that lists all identified serovars [19, 20]. The document has been updated by the World Health Organisation (WHO) Collaborating Centre for Reference and Research on Salmonella at the Pasteur Institute, Paris, France, and every newly identified serovar is reported in the journal Research in Microbiology yearly. The WHO Collaborating Centre for Reference and Research on Salmonella, in the Pasteur Institute in Paris, has updated the document. As a result, every newly discovered Salmonella serovar as well as other relevant microorganism is reported in the journal Research in Microbiology every year [21].

On the recommendation of the WHO collaborating centre, the current nomenclature used by the Centers for Disease Control and Prevention (CDC), Department of Health and Human Services, USA, is widely recognised. It is based on a two-species system (S. enterica and S. bongori), with multiple serovars in each species [22]. Microbiologists in clinical and public health have praised the system for meeting their needs [23]. Salmonella nomenclature is currently divided into two species, S. enterica and S. bongori, which has six subspecies and one subspecies, respectively. The nomenclature is summarised in Table 1. In addition, the relationship of phylogenetic tree among Salmonella subspecies is demonstrated in Figure 2.

Genus (capitalised, italic)Species (not capitalised, italic)Subspecies (symbol) (not capitalised, italic)Serovar name (with examples) (capitalised, Roman)
Salmonellaentericaenterica (subspecies I)Choleraesuis, Enteritidis, Paratyphi, Typhi, Typhimurium
salamae (subspecies II)9,46:z:z39
arizonae (subspecies IIIa)43:z29:-
diarizonae (subspecies IIIb)6,7:l,v:1,5,7
houtenae (subspecies IV)21:m,t:-
indica (subspecies VI)59:z36:-
Salmonellabongori(subspecies V)13,22:z39:-

Table 1.

Salmonella nomenclature.

Adapted from Su and Chiu [24].

Figure 2.

Summary of relationship of phylogenetic tree among Salmonella subspecies and other bacterial species (adapted from reference [1]).

Serovar names should not be printed in italics because they are no longer considered species names. For example, S. enteritidis becomes S. enterica subsp. enterica serovar Enteritidis, or simply written as Salmonella serovar Enteritidis and can be shortened to S. Enteritidis. Only serovars of S. enterica subsp. enterica are given names associated with disease syndrome or host habitat, while others represent the geographical origin of the first isolate found. On the other hand, other subspecies’ serovars are identified by their antigenic formula O:H.

Serovars designated by antigenic formulae include the following: (i) subspecies designation (subspecies I through VI); (ii) O (somatic) antigens separated by a comma if needed, followed by colon: (iii) H (flagellar) antigens (phase 1) separated by a colon and (iv) H antigens (phase 2, if present) (for example, Salmonella serotype II 39:z10:-) [25].


4. Characteristic

Salmonella belongs to the family Enterobacteriaceae, a gram-negative, facultative anaerobic and rod-shaped bacterium. The bacteria are 3–5 μm long and 0.7–1.5 μm wide. They are commonly motile with peritrichous flagella that help the bacteria to move, aerogenic, grow on nutrient agar, glucose-fermenting, non-lactose fermenting, often gas producer, urease-negative, citrate-utilising, oxidase-negative, potassium cyanide-negative and acetylmethyl carbinol-negative [26, 27].

Some serovars have peculiarities that are a mutant of normal motile serovars and can change to non-motile. The majority of isolates expressing H antigen exist in two phases: a motile phase I and a non-motile phase II. A Cragie tube can be used to switch non-motile cultures into the motile phase after they have been established in the primary culture [28]. Most Salmonella strains are prototrophic and can grow in a minimal medium utilising glucose as the sole carbon energy source and ammonium ion as a nitrogen source. Some host-adapted serovars (e.g., Typhi, Paratyphi A, Gallinarum, Sendai and Abortusovis) are auxotrophic and require one or more growth factors. The biochemical characteristic of Salmonella is shown in Table 2. Most species produce hydrogen sulphide, which can be detected by growing them on media containing ferrous sulphate, such as triple sugar iron (TSI). However, certain serovars, such as S. Typhi, never produce gas from glucose.

CharacteristicsSalmonella enterica subsp.Salmonellabongori
Subspecies groupIIIIIIaIIIbIVVIV
Hydrogen sulfide+++++++
Indole test
Lysine decarboxylase+++++++
Methyl red test+++++++
Ortho-nitrophenyl-β-D-Galactopyranoside test++d+
Phage O1 susceptible++++D
Potassium cyanide broth
Voger-Proskauer test

Table 2.

Biochemical characteristics of Salmonella species and subspecies.

Note: +: more than 90% positive reactions; −: less than 10% positive reactions; d: 10–90% strains positive; ONPG: ortho-nitrophenyl-β-D-galactopyranoside.

Salmonella lives predominantly in the intestines of animals and have adapted to live with their hosts [29]. Salmonella enterica subsp. enterica inhabits warm-blooded animals, whereas all other S. enterica subspecies and S. bongori live in cold-blooded animals and rarely infect humans. In terms of the types of hosts infected, S. entericasubsp. enterica serovars can be clustered to host-adapted, host-restricted and general-host [30]. Table 3 lists out the host range of Salmonella. The host-adapted Salmonella infects habitually a single host but is capable of causing disease in another animal. Host-restricted Salmonella infects only a single host, while general-host Salmonellahas the capability of infecting a variety of animals. However, the disease’s progression may vary depending on the host [31].

ClassificationSerovarNatural hostRare hosts
Host restrictedTyphiHumansNone
Paratyphi A and CHumansNone
GallinarumPoultry, birdsNone
PullorumPoultry, birdsNone
Host adaptedCholeraesuisSwineHumans
DublinBovinesHuman and bovines
General-hostTyphimuriumHumans, poultry, swine, bovines, and rodentsNone
EnteritidisHumans, poultry, and rodentsSwine and bovines

Table 3.

Host range of Salmonella enterica subsp. enterica serovars.

Adapted from references [30, 31].

Most Salmonella grows at a temperature of 7–48°C with the optimal growth at 37°C. However, some strains are capable of withstanding extremely low temperature, 2°C, or high temperature, 54°C [32]. Unfortunately, they are not commonly heat resistant and usually die within 1–10 min at 60°C and less than 1 min at 70°C.

The water activity (aw) of foods influences the time and temperature needed to kill Salmonella and reduces the effectiveness of the heat treatment. Salmonella needs high water activity (aw) between 0.94 and 0.99, optimally at 0.995 but can survive in foods with low aw [33]. Low-aw foods, such as nuts, flour, butter and chocolate, can extend the time and temperature required to kill the bacteria [34]. Some rare serotypes, such as S. Senftenberg strain 775 W, has 10–30 times more heat resistant than S. Typhimurium in low-aw food products with high carbohydrate or high fat [35]. Salmonella grows at a pH value of 4–9 with the optimum growth at a pH value of 6.5–7.5 [36].


5. Clinical manifestation

Salmonellosis is a type of food infection that can occur when you eat foods that contain Salmonella bacteria. Once ingested, the bacteria may initiate infection and cause illness. The illness’s possibility and severity depend largely on the dose, the host’s resistance and the specific Salmonella strain causing the disease. The bacteria are disseminated by direct contact with the animal or human excrement through faecal to the oral pathway or spread out indirectly by ingesting food contaminated with Salmonella from faeces or raw food through cross-contamination. Clinical manifestation in human can be classified into four syndromes: gastroenteritis, enteric fever, septicaemia and asymptomatic chronic carriage.

5.1 Gastroenteritis

Non-typhoidal salmonellosis caused gastroenteritis, a condition commonly called as food poisoning. It is a condition resulted from the inflammation of the gastrointestinal tract spread by faecal to an oral route such as enteric fever. Frequently related serovars reported caused gastroenteritis related to outbreaks are Enteritidis, Typhimurium and Heidelberg [37]. Non-typhoidal salmonellosis is the leading cause of death and hospitalisations among other foodborne pathogens in the USA [1], and the estimated cases of non-typhoidal salmonellosis worldwide massively exceed the enteric fever cases.

The incubation period is 12–72 hours as a result of ingesting tainted food or drinking tainted water and dose-dependent on bacteria that infect the intestines [38]. Symptomatic disease in healthy adults occurs if they are being infected with 106–108 CFU/mL Salmonella. Common symptoms are diarrhoea, vomiting, abdominal pain, nausea, myalgia and headache. In addition, chills and fever within 38–39°C can also occur to the patient. In severe cases, it can lead to severe dehydration and bloody diarrhoea in rare cases. The duration of the symptoms varied from 2 to 7 days but generally resolved by itself without the need for treatment within a week.

5.2 Enteric fever

Enteric fevers are severe systemic forms of salmonellosis and occasionally life-threatening illness. Enteric fever that is caused by S. Typhi and S. Paratyphi A, B or C infections is called as typhoid fever and paratyphoid fever, respectively [39, 40, 41] . Paratyphoid fever is a similar illness causing a milder form of enteric fever compared to the typhoid fever. S. Typhi is responsible for causing the most endemic and epidemic cases of enteric fever worldwide with 200,000 deaths and 23 million illness cases per year [42].

The incubation period varied from 6 to 30 days after infection [43] giving rise to symptoms such as gradual fever (38–40°C) over several days, headache, hepatosplenomegaly, myalgias, diarrhoea and constipation when the onset of the systemic disease takes place. Some people develop a transient skin rash with rose-coloured spots, which can be confused with malaria. Therefore, typhoid fever should be suspected in a traveller who is unresponsive to anti-malarial treatment. If left untreated, the symptoms can last for weeks or months. Without treatment, symptoms may last from weeks or months, and it can be deadly [44]. The fatality rate was reported to be at 10–30% if left without treatment but improved to 1–4% fatality in treated patients [45, 46].

5.3 Bacteraemia/septicaemia

Bacteraemia is the presence of viable bacteria in the bloodstream that may occur through a wound, injection or a surgical procedure. Septicaemia is referred to the presence and proliferation of germs in the blood. Septicaemia is a medical term that refers to blood poisoning. Salmonella bacteraemia is a condition in which the presence of Salmonella bacteraemia in the blood elicits a systematic inflammatory response that can be fatal. It is an intermediate stage of infection in which the patient is not showing any symptom and the bacteria cannot be isolated from faecal specimens. Bacteraemia can further progress to septicaemia whereby the bacteria multiply in the blood and giving symptoms such as chills, fever, high respiration rate or very fast heart rate.

Bacteraemia can be caused by all Salmonella subspecies but is more commonly associated with S. Choleraesuis, S. Paratyphi, S. Typhi and S. Dublin. The increased risk is seen in old, young and immunocompromised persons. The severity of the infection depends on the bacterial dose, immune response of the patient and the virulence of the Salmonella strain [47]. The severe development of septicaemia was reported higher to occur in cancer patients and immunecompromised individual infected with human immunodeficiency virus (HIV) [48, 49].

5.4 Chronic carrier

After treatment for salmonellosis, some patients become Salmonella carriers and shed faeces with Salmonella for an extended time, making them a reservoir or carrier for the pathogen, thus making them a chronic carrier. Salmonella can continue to be excreted in stool for many weeks following resolution of an initial diarrheal episode without symptoms exhibited by the patients. The factors of the host and pathogen that influence the occurrence of carrier state study are limited; hence, the condition is poorly understood [48]. Chronic carrier state occurred higher in patients infected with S. Typhi compared to non-Typhi. About 1–4% of patients that recovered from typhoid fever become chronic carriers, while only 0.2–0.6% of patients infected with non-typhoidal salmonellosis progress into the chronic carrier [50]. The chronic carrier state is associated with carcinoma of the gallbladder, which the host could form into the chronic carriage [51].


6. Epidemiology

Epidemiology is the study of the distribution and causative agents of disease and the application of the study to the control of diseases. The epidemiology of salmonellosis cases differs extensively on the type of Salmonella spp. implicated. Annually, enteric fever was estimated to cause 200,000 deaths in 22 million illness cases, which mainly occurred in non-developed countries [45] and is low in developed countries. Enteric fever is endemic in many places on the African and Asian continents, as well as in countries throughout Europe, Central and South America and the Middle East. The prevalence and fatality rate caused by the enteric fever may vary greatly from one location to another. Enteric fever is uncommon in the USA and certain European nations, with less than 10 Salmonella cases reported per 100,000 people annually. The majority of cases reported in these nations are linked to travel, with foreigners or travellers returning from Pakistan, Africa or India, bringing the disease with them [45].

Contrary, non-typhoidal salmonellosis (NTS) incidence is increasing and continues to lead the gastroenteritis cases worldwide affecting 155,000 deaths from 93.8 million cases estimated every year [37]. Epidemiology data are well documented in developed countries, such as the USA and the countries of Europe, but are poorly compiled in less-developed countries like Asian and African countries. Owing to less effective monitoring systems, statistics on salmonellosis incidence are limited in countries of Asia, Africa and South and Central America, where only 1–10% of cases are reported [52, 53, 54, 55]. It was reported that the most frequent serotype in Asia and Africa was Salmonella Enteriditis, accounting for 38% and 26% of the clinical isolates, respectively. NTS disease is an extremely serious infection in Vietnam, and the high death rate (26%) is comparable to the incidence in sub-Saharan Africa, which is a significant risk factor for both infection and mortality in HIV-infected individuals [54].


7. Pathogenicity

Pathogenicity of Salmonella is dependent on the serovar and the host. However, factors that influencing serovar–host specificity are not well known [56]. The basic of Salmonella virulence mechanism is associated with the invasion of intestinal mucosa and multiplication in gut-associated lymphoid tissue (GALT). Salmonella will invade non-phagocytic cells in the intestine by promoting their self-uptake in a complicated and dynamic process similar to phagocytosis [57].

Salmonella infection in human can cause either systemic disease with rare association with food poisoning or one that can cause enteritis or localised disease. In oral infection, Salmonella must go through a variety of host defence mechanisms and different environments in the stomach during the progression of infection before successfully entering the intestinal tract. Salmonella adapted to these settings by using a broad variety of genes that may be reflected as virulence determinants, including Salmonella-specific virulence genes, housekeeping genes and regulatory genes. Virulence genes involved in invasion and critical for intracellular survival are grouped in large chromosomal DNA regions termed as Salmonella pathogenicity islands (SPIs). SPIs often exist in huge clusters of genes that are found in the vast chromosomal DNA regions that contribute to a certain virulence phenotype that manifests at a given period during infection [58].

Significant pathogenicity islands in Salmonella are SPI-1 and SPI-2. SPI-1 being the most well-defined SPI and required for virulence encodes the type III protein secretion system (T3SS), which injects effector proteins into host cells and provides the essential mechanism for intestinal invasion and enteritis formation [59]. The T3SS is the most significant Salmonella virulence factor. SPI-1 genes are involved in host cell invasion, immune cell recruitment, apoptosis, and biofilm formation, while other transcription factors encoded outside SPI-1 engage in the expression of SPI-1-encoded genes. SPI-1’s regulatory network is intricate and extremely important [37]. SPI-1’s ubiquity is conserved and essential for Salmonella pathogenicity, as shown by its direct role in invasion. The T3SS of SPI-1 and SPI-2 has been suggested to be inversely regulated [52, 53].

This is an appealing hypothesis as Salmonella systemic infection to a host must first infiltrate M cells, where SPI-1 expression is required, and then replicate within macrophages, where SPI-2 expression is required. Mutations in SPI-2 genes encoding the type III secretion apparatus, on the other hand, diminish the expression of genes encoding a transcriptional activator of SPI-1 (sipC, prgK and hilA), suggesting the interaction between SPI-1 and SPI-2 [60]. Over the previous decade, around 30 SPI-2 T3SS effectors have been discovered. Thirteen of them are involved in the regulation of Salmonella-containing vacuole (SCV) membrane dynamics, the location of Salmonella-containing vacuole (SCV) inside host cells, immunological modulation, cytoskeletal changes and the motility of infected cells, among other things [61].


8. Route of contamination by Salmonella

Salmonella is broadly spread in various food types and extensively distributed in the environment. The most common vehicle for Salmonella includes poultry, eggs, livestock animal and dairy products [62, 63, 64]. The contamination of Salmonella can occur at various points along the food chain route, as described in the diagram in Figure 3.

Figure 3.

Various points in food chain where Salmonella contamination could occur.

Food that is based on poultry forms the key reservoir of Salmonella and poses a risk to be transferred to other medium [65]. The host that the bacteria colonise ranges from wild birds to domestic animals [66, 67]. In most scenarios, Salmonella bacteria multiply in chicken and poultry, in which they then become the reservoir for the pathogen (EFSA, 2010). Colonisation in the intestines of the animal becomes the key source of contamination in many points and is typically widespread in the abattoir and poultry processing facilities [68].


9. Conclusion

Salmonella is a gastrointestinal microorganism with numerous abilities to infect and survive in human and animal hosts. This chapter optimistically gives a better insight of Salmonella’s history background, nomenclature, characteristic, clinical manifestation, epidemiology, pathogenicity and the possible route of contamination. It is worth noting that, despite the advancement in sanitary procedures and quality control in food processing and manufacturing, the infection of these gram-negative bacteria still triggers increase in morbidity and mortality in humans worldwide. Therefore, increased attention and surveillance of this dangerous pathogen should be emphasised and strengthened for the better management of the disease.


Conflict of interest

The authors declare no conflict of interest.


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Written By

Mohd Afendy Abdul Talib, Son Radu, Cheah Yoke Kqueen and Farinazleen Mohamad Ghazali

Submitted: 08 January 2022 Reviewed: 23 February 2022 Published: 04 July 2022