Colibacillosis

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Colibacillosis in a broiler chicken [13].

Introduction

Colibacillosis (ko″lĭbas″ĭ-lo´sis) [1] is a broad term that refers to any infection or disease caused by the bacteria Escherichia coli [6]. These infections include colisepticemia, coligranuloma, veneral colibacillosis, coliform cellulitis, peritonitis, salpingitis, orchitis and enteritis, among others [2][5]. In mammals, colibacillosis is usually a primary intestinal or urinary tract infection. While colibacillosis in poultry is usually a secondary disease that occurs when the host’s immune system has become overwhelmed with virulent E. coli strains [2].

Colibacillosis is a common disease that is seen worldwide and is of significant economic importance concerning the loss of livestock [2][4][5]. It is the most common infectious bacterial disease of poultry [2] and is seen in cattle [12], pigs [9], goats [3], and other mammals. Current research is being done to determine if colibacillosis is a public health concern for humans and how antibiotic resistance is affecting the development of a widespread treatment [2].

Description

Cause

Colibacillosis is caused by infection with the bacteria Escherichia coli (E. coli) [2]. It is associated with many different kinds of diseases ranging from respiratory tract infection to swollen head syndrome in poultry to urinary tract infections [5]. E. coli can infect hosts as either a primary or secondary pathogen [5].

Signs

Colibacillosis can be detected in livestock by severe diarrhea caused by enteritis [7], lameness, stunted growth, inactivity, lack of appetite and water consumption, and unresponsiveness [2]. These factors are common signs of the infections listed above, and are all possible indicators of colibacillosis. It is important to note that one infected animal might not express all of these characteristics, or even most of them. If an animal possesses one or more of these factors, it does necessarily have colibacillosis either. These are simply common symptoms of the disease. Colibacillosis signs are nonspecific and vary widely among different hosts [4]. Morbidity and mortality are very variable depending on which infection/infections the E. coli strain causes in a particular flock of animals [2]. However, almost all flocks exhibit some degree of mortality due to an outbreak of colibacillosis [2]. Highly virulent strains of E. coli cause the hosts to become sick and die within a few hours, while mildly affected flocks can take days to show morbidity [2].

Diagnosis

There are several ways to diagnose colibacillosis. Typical macroscopic lesions in the carcass of an animal are the predominant signs of colibacillosis [2][5]. Also, a pure colony of E. coli isolated from an animal’s heart blood, liver or typical visceral lesions is needed for diagnosis [4]. Isolates are then determined to be pathogenic via multiplex PCR panels for plasmid-mediated virulence genes [4]. If the isolate contains virulence genes, then it is certain the animal died of colibacillosis [4]. Inoculation of the allantoic sac of 12-day-old chicken embryos can also determine pathogenicity, if virulent E. coli is found to be present [4]. Another way colibacillosis could be detected is through Iss sequences, which are possible indicators of a particular isolate’s ability to cause disease [11]. This could potentially lead to a new form of colibacillosis treatment, but this field still needs more research [11].

Significance

E. coli infections are the cause of substantial economic losses, and colibacillosis is one of the most highly reported E. coli related diseases [2]. These losses are usually the result of mortality and decreased production of commodities such as milk or eggs in infected animals [5]. Colibacillosis is also found worldwide [2] in places ranging from Egypt [7], Bangladesh [10], Malaysia [3] to America [2][9].

Public Health Issues

Colibacillosis primarily affects livestock including poultry [2], cattle [12], pigs [9] and goats [3]. It infects most, if not all, avian species [2]. There have been studies done on the ability of colibacillosis to infect humans, but many of them point to the disease being fairly harmless to humans [2][8]. One study discovered that, while there is a large overlap in genes, including transmissible plasmids, between APEC (avian pathogenic E. coli, which cause colibacillosis in birds) and UPEC (uropathegenic E. coli, which cause urinary tract infections in humans), there are also many differences between the two groups [8]. These differences suggest that, while APEC might be able to cause disease in humans, it may only be involved in urinary tract infections [8]. However, more research is needed to determine if and in what capacity colibacillosis is able to infect humans [8].

History

Deaths in birds caused by a bacteria consistent with E. coli was first reported in 1894 [2]. Experiential inoculations of different animals showed the bacteria’s diverse number of hosts between 1894 and 1922 [2]. Colisepticemia was first described in 1907 as a virulent E. coli infection that was killing chickens [2]. In 1923, E. coli was isolated from birds with infectious enteritis and paralysis, which lead to more descriptions of colibacillosis [2]. Between 1938 and 1965, E. coli was discovered as the cause of coligranuloma, plantar abscesses, omphalitis, and peritonitis, among other infections in chickens [2]. The bacteria was also seen to possess resistance to vaccinations around this time [2]. These discoveries provided the basis of colibacillosis knowledge, but there is still much to learn about the disease.

Epidemiology, Pathology, and Virulence

Escherichia coli is a normal and beneficial component of the intestine microflora of many animals. However, certain strains such as APEC can spread to different internal organs and cause infection [2][5]. Therefore, the largest reservoir of E. coli is in the intestinal tract of most animals [2][5].

The specific serotypes most associated with colibacillosis are O78:K80, O1:K1, and O2:K1 [2]. However, there is a high percentage of APEC isolates that are untypeable [4]. The virulence factors associated with colibacillosis include the possession of large transmissible virulence plasmids, as well as the ability to resist phagocytosis and serum killing [4]. They also include the ability to uptake iron at low extracellular concentrations and, most importantly, the ability to attach and adhere to the host’s structures [4].

Age of the host also plays a role in the pathogenicity of E. coli types. Younger birds that do not have an established microflora are more susceptible to infection [2]. There are other risk factors that increase the likelihood of a colibacillosis infection as well. The E. coli strain, the strength of the host’s immune system and exposure time all play a role [5].

Thorough cleaning, the prevention of overcrowding, and good ventilation are all important steps to prevent the spread of the illness [2][5]. Fecal contamination of eggs is the most common form of transmission [2]. The bacteria contaminates the egg’s surfaces and is able to penetrate the shell and membrane [2], killing the animal inside. Dusty and dry conditions allow the bacteria to survive on surface for long periods of time, and to combat this, water and moisture can be pumped into the houses [2]. This results in an 84-97% reduction of E. coli in 7 days [2]. Contaminated water and rodent dropping are other ways the disease is transmitted [2].

Mechanism of Infection

Pathogenic strains of E. coli such as APEC and UPEC have the ability to cause disease and infections. These strains have acquired virulence factors through horizontal gene transfer and some are also opportunists that infect already immunocompromised mammals [2]. The virulent factors they have acquired are genes that are iron-related, toxin-related, and adhesion-related [2]. Iron-related genes encode for iron acquisition mechanisms which are significantly less common in commensal E. coli [2]. The reason for this is not entirely understood, but it is believed that iron acquisition is an important part of pathogenesis in E. coli [2]. Toxin-related genes include the gene stx1 which encodes for shiga toxins that inhibit protein synthesis and the gene cdtB which encodes for a toxin that blocks mitosis [2]. Adhesion-related genes allow the pathogenic E. coli to attach itself to the host [2]. These genes include the pap pilus and s fimbrial operons which both encode for pilus tip adhesion [2].

Treatment

Treatment is still an emerging field in colibacillosis studies. Most treatments do not focus on already occurring colibacillosis infections, rather in the prevention of the disease. This can be done by preventing fecal contamination in newly hatched eggs and ventilating the incubators/houses where the animals are kept [5]. Competitive exclusion is also being studied [5]. This involves inoculating newly hatched chicks with normal bacterial flora and determining if they are better able to fight off colibacillosis infections [5].

Other treatments include antibiotics and attempts to control the resulting infections [4]. Experimental vaccines have been shown to protect against some colibacillosis causing serogroups [4], but this is still an active area of study. The large diversity among APEC strains pose limits on the potential of an overarching vaccination [5]. Growing concern about antibiotic resistance has also affected the way colibacillosis is being treated [2]. Tetracylcines have been show to combat colibacillosis, but now 90% of the strains are resistant and 60% are resistant to five or more antibiotics [4]. This increasing rate of resistance poses a real threat to clinicians and famers around the world [10].

Current Research

The declining use of antibiotics for colibacillosis prevention has left the field of treatment open to new studies [2]. Alternative methods for treatment such as prebiotics, probiotics, enzymes and anti-inflammatory drugs are being investigated [2]. Prebiotics and probiotics are widely available and used on poultry, but the effect they could potentially have on colibacillosis has yet to be published [2]. Essential oils have been shown to significantly inhibit E. coli colonization in vitro and in the lower intestines of chickens, but no studies have investigated this effect on colibacillosis [2]. Different dietary components such as protein and non-starch polysaccharides could have an effect on E. coli growth in animals as well, but more research needs to be done on this treatment [9]. Also, bacteriophages have the potential to be a new form of colibacillosis treatment [2]. New research has shown that a combination of enrofloxacin and bacteriophage treatment has a synergistic, helpful effect on the host animal [2]. However, more must be done before a commercial product of any colibacillosis treatment is ready to be distributed [2].

References

[1] “Colibacillosis.” Dorland’s Medical Dictionary for Health Consumers. 2007. Saunders, an imprint of Elsevier, Inc. 30 Oct. 2014 <http://medical-dictionary.thefreedictionary.com/ colibacillosis>

[2] Barnes J, Nolan L, Vaillancourt J. 2008. Colibacillosis. Diseases of Poultry. Saif YM. Iowa, Blackwell Publishing Professional. 12: 716-762.

[3] Salisi MS, Saad MZ, Kasim A. 2012. Implementation of herd health program to improve survival of Boer goats in Malaysia. Trop Anim Health Prod. 44 (2): 207-11.

[4] Nolan L. “Overview of Colibacillosis in Poultry.” The Merck Veterinary Manual. 2013. Merck Manuals. 2014. <http://www.merckmanuals.com/vet/poultry/colibacillosis/overview_of_colibacillosis_in_poultry.html >

[5] Lutful Kabir SM. 2010. Avian Colibacillosis and Salmonellosis: A Closer Look at Epidemiology, Pathogenesis, Diagnosis, Control and Public Health Concerns. Int J Environ Res Public Health. 7 (1): 89-114.

[6] “Colibacillosis.”2014. Merriam-Webster. <http://www.merriam-webster.com/medical/colibacillosis>

[7] Ahmed M, Youssef F, Rahman, A. 2013. Differentiation between E. colis strains causing diarrhea in broiler chicken by using multiplex PCR. Proc. 6th Inter Conf. Vet. Res. Div., NRC, Cairo, Egypt: 33-47.

[8] Rodriguez-Siek K, Giddings C, Doetkott C, Johnson T, Fakhr M, Nolan L. 2005. Comparison of Escherichia coli isolates implicated in human urinary tract infection and avian colibacillosis. Microbiology. 151 (6): 2097-2110.

[9] Kim, J.C., Hansen C.F., Mullan, B.P. and Pluske, J.R. 2012. Nutrition and pathology of weaner pigs: Nutritional strategies to support barrier function in the gastrointestinal tract. Animal Feed Science and Technology. 173 (1-2): 3-16.

[10] Rahman MA, Samad M, Rahman MB, Kabir M. 2004. In Vitro Antibiotic Sensitivity And Therapeutic Efficacy Of Experimental Salmonellosis, Colibacillosis And Pasteurellosis In Broiler Chickens. Bangl. J. Vet. Med. 2 (2): 99-102.

[11] Pfaff-McDonough S, Horne S, Giddings J, Ebert O, Doetkott C, Smith M, Nolan L. 2000. Complement Resistance-Related Traits among Escherichia coli Isolates from Apparently Healthy Birds and Birds with Colibacillosis. Avian Diseases. 44 (1): 23-33.

[12] Besser TE, Gay CC. 1985. Septicemic colibacillosis and failure of passive transfer of colostral immunoglobulin in calves. Vet Clin North Am Food Anim Pract. 1 (3): 445-59.

[13] Lucyin. 2014. "Pathogenic Escherichia coli." Wikipedia, The Free Encyclopedia.<http://en.wikipedia.org/wiki/Pathogenic_Escherichia_coli>


Created by [Alyssa Bunce], student of Jennifer Talbot for BI 311 General Microbiology, 2014, Boston University.