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User:Reesegroover/Campylobacter jejuni

< User:Reesegroover

Group Assigned (Just Testing) edit

Reese - Disease & Lead

-added treatment section

Simona - Transmission & History

- Adding history after frequency section.

Patrick - Metabolism

Nathaniel - Pathogenesis & Diagnosis & DNA Repair

- Possible inclusion of DNA repair sections under pathogenesis

[Citation needed for last sentence under the possible complication sections]

Lead edit

copied from: Campylobacter

Campylobacter jejuni is a species of pathogenic bacteria that is commonly associated with poultry, and is also often found in animal feces. This species of microbe is one of the most common causes of food poisoning in Europe and in the US, with the vast majority of cases occurring as isolated events rather than mass outbreaks. Active surveillance through the Foodborne Diseases Active Surveillance Network (FoodNet) indicates that about 20 cases are diagnosed each year for each 100,000 people in the US, while many more cases are undiagnosed or unreported; the CDC estimates a total of 1.5 million infections every year. The European Food Safety Authority reported 246,571 cases in 2018, and estimated approximately nine million cases of human campylobacteriosis per year in the European Union.Campylobacter jejuni infections are increasing at an alarming rate in Europe, North America, and Australia. In Africa, Asia, and the Middle East, data indicates that C. jejuni infections are endemic.

Campylobacter is a genus of bacteria that is among the most common causes of bacterial infections in humans worldwide. Campylobacter means "curved rod", deriving from the Greek kampylos (curved) and baktron (rod). Of its many species, C. jejuni is considered one of the most important from both a microbiological and public health perspective.

C. jejuni is commonly associated with poultry, and is also commonly found in animal feces. Campylobacter is a helical-shaped, non-spore-forming, Gram-negative, microaerophilic, nonfermenting motile bacterium with a single flagellum at one or both poles, which are also oxidase-positive and grow optimally at 37 to 42 °C. When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form. This species of pathogenic bacteria is one of the most common causes of human gastroenteritis in the world. Food poisoning caused by Campylobacter species can be severely debilitating, but is rarely life-threatening. It has been linked with subsequent development of Guillain–Barré syndrome, which usually develops two to three weeks after the initial illness. Individuals with recent C. jejuni infections develop Guillain-Barré syndrome at a rate of 0.3 per 1000 infections, about 100 times more often than the general population. Another chronic condition that may be associated with Campylobacter infection is reactive arthritis. Reactive arthritis is a complication strongly associated with a particular genetic make-up. That is, persons who have the human leukocyte antigen B27 (HLA-B27) are most susceptible. Most often, the symptoms of reactive arthritis will occur up to several weeks after infection.

Disease edit

 
Enteritis, a major complication of a Campylobacter jejuni infection, results in inflammation as pictured above, in which eosinophil aggregation occurs.

copied from: Campylobacter jejuni

Campylobacteriosis is an infectious disease caused by bacteria of the genus Campylobacter. In most patients presenting with campylobacteriosis, symptoms develop within two to five days of exposure to the organism and illness typically lasts seven days following onset.[1] Infection with C. jejuni typically results in enteritis, or inflammation of the small intestine, which is characterized by abdominal pain, voluminous diarrhea (often bloody), fever, and malaise. Individuals infected with this bacteria can experience a prodromal phase of symptoms for the first 1 to 3 days, in which the more severe portion of the disease occurs. The prodromal phase presents with symptoms including rigors, high fever, body aches, and dizziness. Other than the prodromal phase, the acute diarrheal phase of enteritis usually lasts around 7 days, however abdominal pain can persist for weeks afterward.[2] The disease is usually self-limiting; however, it does respond to antibiotics. Severe (accompanying fevers, blood in stools) or prolonged cases may require erythromycin, azithromycin, ciprofloxacin, or norfloxacin. Fluid replacement via oral rehydration salts may be needed and intravenous fluid may be required for serious cases.[3] Possible complications of campylobacteriosis include Guillain–Barré syndrome and reactive arthritis.[4]

Transmission edit

C. jejuni Is commonly found food animals. It is a zoonotic disease meaning it is more commonly spread from animals to people than in between humans. People most often contract it by touching something that has been in contact with raw or undercooked chicken in addition to eating or touching poultry that is raw or undercooked.[4] Additionally, It can also be obtained form being in contact with animals or eating undercooked seafood. [4] The fecal oral route is the most common way it spreads. [5] C. jejuni seldomly causes disease in animals and Infections are more common in lower income countries who's economies depend on tourism.[6] Deadly Infections are not often seen in young adults but rather among the young and elderly. [6] It can also be found in ice and water making it vital to ensure that you are eating not only properly cooked food but also purified water. It is difficult to know the science behind its transmission due to its sporadic nature.[5][6] The use of antibiotics and other treatments help in slowing and preventing the transmission of C. jejuni. [5] C. jejuni is a fastidious microaerophiles meaning is does need some oxygen to grown, spread, and transmit. However, it is highly adaptable and has adapted to grow in higher concentrations of oxygen.[7] This being said, outside of a host, C. jejuni struggles to survive unless it is an extremely niche environment such as environments containing a lot of moisture and surrounded by many animals that it could use as a host.

Pathogenesis edit

(This should be placed at the beginning of the section)

Campylobacter jejuni is a bacterium that employs unique strategies to breach the intestinal epithelial layer of its host cells. It uses proteases, particularly HtrA, to cleverly disrupt cell junctions and temporarily traverse the cells[8]. The membrane-bound protein Fibronectin is a critical binding site for C. jejuni on the basolateral side of the polarized epithelial cell, facilitating this process. Once inside the cell, C. jejuni leverages dynein to access the perinuclear space within the Clathrin-Coated Vesicle, avoiding lysosomal digestion for up to 72 hours[8].

(This should be placed after the third paragraph)

Campylobacter jejuni, a bacterium known for its flagella-based motility, also employs a highly sophisticated navigation system called chemotaxis [8]. This system is crucial when the bacterium requires guidance through chemical signals. The chemotaxis system utilizes specific chemoattractants that direct the bacterium toward areas with a higher concentration of the attractants. The exact nature of chemoattractants is dependent on the surrounding environmental conditions. Additionally, when the bacterium needs to move away, it uses negative chemotaxis to move in the opposite direction[8].

(This is should be a sub section of the pathogenesis section)

 
A microscopical Image of a gram-stained C. Jejuni isolated from a bird fecal sample. The image was captured by Amy Siceloff, Shariat Graduate Research Assistant in the Vet-Med Population Health department.
Inflammation and Infection edit

Campylobacter jejuni is a bacterium that can invade and destroy host cells upon infection. This releases chemokines that cause inflammation and activate immune response cells. Inflammatory chemokines such as CXCL1, CCL3/CCL4, CCL2, and CXCL10 are upregulated, further triggering the immune response. The immune response activation is primarily driven by the use of ADP-heptoses to activate ALPK1[9] by a C. jejuni infection[8].

Neutrophil granulocytes use phagocytosis to combat C. jejuni infection, releasing antimicrobial proteins and proinflammatory substances. However, C. jejuni can influence the differentiation process of specific types of neutrophil granulocytes, triggering hypersegmentation and increased reactivity, which leads to delayed apoptosis and higher production of reactive oxygen species. In experimental processes, T cells from an immune response only start to grow in number at the inflammation site from the seventh day after infection[8].

After 11 days of having a Campylobacter jejuni infection, the B lymphocytes in the body increase the production of antibodies that specifically fight against C. jejuni flagellin[8]. The persistence of these antibodies in the body can last up to one-year post-infection. In this case, the development of Guillain-Barré syndrome (GBS) is associated with autoimmune IgG1 antibodies[8].

Guillain-Barré syndrome (GBS) is a severe autoimmune neurological disorder that can cause paralysis, respiratory failure, and death. Campylobacter infections often precede GBS, indicating that molecular mimicry between the bacteria and host nervous tissues may be the underlying cause[8]. C. jejuni , the most common causative agent of human campylobacteriosis, can survive in the gut for several days but does not establish a long-term infection due to its low replication rate, which is incompatible with a persistent bacterial presence[8]. The bacteria-induced apoptosis of infected gut cells results in the rapid clearance of the pathogen, which likely contributes to the self-limiting nature of the disease[8].

DNA Repair edit

In the intestinal environment, bile functions as a defensive barrier against colonization by C. jejuni[10]. When C. jejuni is grown in a medium containing the bile acid deoxycholic acid, a component of bile, the DNA of C. jejuni is damaged by a process involving oxidative stress[10]. To survive, C. jejuni cells repair this DNA damage by a system employing proteins AddA and AddB that are needed for repair of DNA double-strand breaks[10].

C.jejuni uses homologous recombination to repair its DNA, facilitated by the AddA and AddB proteins[10]. These proteins replace RecBCD, which is used in other bacteria like E.Coli. AddA and AddB are crucial for nuclease, helicase, and Chi recognition[11], which allow for successful homologous recombination[10].

When AddA and AddB are introduced into a wild C.jejuni variant, an added deletion mutant gene addAB gene is formed, which repairs DNA damaged by oxidative stress[10]. This inclusion protects C.jejuni from deoxycholate found in bile, allowing for survival[10]. However, the added gene is absent during growth in deoxycholate from 10 to 16 hours and may be upregulated in response to environmental conditions[10]. Additionally, AddAB proteins enhance C.jejuni colonization of chicken intestines[10].


Metabolism edit

C. jejuni is unable to utilize sugars as a carbon source, primarily using amino acids for growth instead. The main reason C. jejuni lacks glycolytic capabilities is a lack of glucokinase and a lack of the 6-phosphofructokinase enzyme to employ the EMP pathway. The four main amino acids C. jejuni takes in are serine, aspartate, asparagine, and glutamate, which are listed in order of preference. If all of these are depleted, some strains can use proline as well. Either the host or metabolic activity of other gut microbes can supply these amino acids.

The metabolic pathways C. jejuni is capable of include the TCA cycle, a non-oxidative pentose phosphate pathway, gluconeogenesis, and fatty acid synthesis. Serine is the most important amino acid used for growth, brought into the cell by SdaC transport proteins and further broken down into pyruvate by the SdaA dehydratase. Though this pyruvate cannot directly be converted into phosphoenolpyruvic acid (as C. jejuni lacks this synthetase), the pyruvate can enter the TCA cycle to form oxaloacetic acid intermediates that can be converted to phosphoenolpyruvic acid for gluconeogenesis. This production of carbohydrates is important for the virulence factors of C. jejuni . The pyruvate created from serine can also be converted to acetyl CoA and be applied to fatty acid synthesis or continue into the TCA cycle to create precursors for other biosynthetic pathways. Aspartate and glutamate are both brought into the cell via Peb1A transport proteins. Glutamate can be transaminated into aspartate, and aspartate can be deaminated to make fumerate that feeds into the TCA cycle as well. Asparagine is also able to be deaminated into aspartate (which follows the process into the TCA cycle mentioned above). While the amino acids listed above are able to be metabolized, C. jejuni is capable of taking in many of the other amino acids which helps to lower the anabolic cost of de novo synthesis.

If other sources of carbon are exhausted, C. jejuni can also utilize acetate and lactate as carbon sources. Acetate is a normal secreted byproduct of C. jejuni metabolism stemming from the recycling of CoA, and the absence of other carbon sources can cause C. jejuni to "switch" this reaction to take in acetate for the conversion to acetyl-CoA (catalyzed by phosphate acetyltransferase and acetate kinase enzymes). Lactate is a normal byproduct of many fermentative bacteria in the gut, and C. jejuni can take in and oxidize this lactate to supply pyruvate through the activity of dehydrogenase iron-sulfur enzyme complexes.

The energetic needs of these anabolic pathways are met in multiple ways. The cytochrome c and quinol terminal oxidases allow for C. jejuni to use oxygen as a terminal electron acceptor for the reduced carriers produced through the TCA cycle (hence why C. jejuni is considered an obligate microaerophile). The conversion of acetyl-CoA to acetate mentioned above has substrate-level phosphorylation take place, giving another form of energy production without the use of microaerophilic respiration.

Electron Donors and Acceptors edit

C. jejuni can utilize many different electron donors for its metabolic processes, using NADH and FADH most commonly - though C. jejuni utilizes NADH poorly compared to FADH due to a replacement of genes encoding subunits for NADH dehydrogenases for genes contributing to processes relating to FADH electron donation[12]. Aside from these donors, C. jejuni can turn to products from the host gut microbiota including hydrogen, lactate, succinate, and formate to contribute electrons; formate, for example, is generated through intestinal mixed-acid fermentation[12]. Unlike almost all other Campylobacter or Helicobacter species, C. jejuni can also accept electrons from sulfite and metabisulfite through its cytochrome c oxidoreductase system[12].

While oxygen is mainly used as a terminal electron acceptor, C. jejuni can use nitrate, nitrite, sulfur oxides (such as dimethyl sulfoxide or trimethylamine N-oxide), or fumerate as terminal electron acceptors as well to survive as a microaerophilic bacterium[12]. Due to oxygen-limited conditions in the common areas of colonization, C. jejuni possesses two separate terminal oxidases with different affinities for oxygen, where the low affinity oxidase can directly retrieve electrons from the menaquinones[12]. The adaptations allowing for multiple electron acceptors help to combat the problem with reactive oxygen species arising from the sole use of oxygen as well; C. jejuni cannot grow under strictly aerobic conditions. Enzymes C. jejuni carries to impede the effects of reactive oxygen species include: superoxide dismutase SodB, alkyl hydroxide reductase AhpC, catalase KatA, and thiolperoxidases Tpx and Bcp[12].

(added links directly to the wiki page; sources also disappeared from sandbox? included in the live article as well)

Frequency edit

Europe edit

In 2020, there were around 120,000 cases of C. jejuni infection, which showed a decline of about 25.4% compared to the previous year. However, it's important to note that the COVID-19 pandemic may have influenced this decrease, and its statistical significance is yet to be determined[8]. Notably, C. jejuni infections tend to peak in July, which could be linked to the rise in temperature worldwide. This pattern is associated with an increased reflection rate of the bacteria, which needs further investigation to establish any potential correlations[8].

Globally edit

C. jejuni infection is a significant global health issue, with infection rates ranging from 0.3 to 2.9%. It is a widespread infection that affects individuals of all ages but is more prevalent in developing countries[8]. In these areas, diarrhea is the most common clinical presentation, and it has a severe impact on children[8]. Given that C. jejuni infection is more prevalent in developing countries and has a more significant effect on children, public health officials must urgently address this alarming global health concern.

History edit

In 1886, Dr. Escherich found organisms that may have resembled Campylobacter while he was observing the stool samples of some children.[13] C. jejuni was first discovered in the small intestines of humans since the 1970s, however, symptoms have existed since the early 20th century.[14] Veterinarians were able to extract it from a human stool sample an the cause of these symptoms was discovered. recognize Campylobacter as being the cause of abortions in sheep and cattle in the early 20th century. in the late 1940s and early 1950s, it was causing abortions in women however, the cause was not yet discovered. it was not until the 1970's when C. jejuni was finally isolated. Although it was isolated in the 1970's, C. jejuni was not recognized until the 1980's. It was previously though that C. jejuni was isolated to animals. Once it was discovered to exist in humans as well, it was and still is a wide spread belief that most diarrhea cases were caused by Campylobacter. The CDC, USDA and FDA worked together and discovered that C. jejuni is responsible for over 40% of bacterial gastroenteritis found in laboratories as of 1996.

Diagnosis edit

A complete rewriting of the diagnosis section is necessary for a better description of the diagnosis methods and clear information.

Various diagnostic tools are available to identify Campylobacter infections, including C.jejuni[15]. The Stool Culture is considered the gold standard for diagnosing C.jejuni[16], with selective culture techniques now being used to distinguish it from other variants[15]. Stool cultures are typically grown at 42 degrees Celsius with 5% - 10% oxygen, as C.jejuni requires these conditions due to being thermophilic and microaerophilic [15]. A final diagnosis from a stool sample requires a gram stain or contrast microscopy[16].

Aside from stool cultures, C.jejuni can be detected using enzyme immunoassay (EIA) or polymerase chain reaction (PCR)[15]. These methods are more sensitive than stool cultures, but PCR tends to be the most sensitive especially in children and developing countries[17].

Advanced technologies such as reverse transcription-polymerase chain reaction (RT-PCR) and Real-time PCR are highly effective in accurately and sensitively diagnosing C. jejuni from diarrheal stool samples[15].

Treatment edit

Campylobacter infections tend to be mild, requiring only hydration and electrolyte repletion while diarrhea lasts. Depending on the degree of dehydration, alternate measures may be taken including parenteral methods of hydration.[2][18]

Antibiotic Treatment edit

 
Kirby-Bauer Disk Diffusion utilizing the macrolide Ciprofloxacin to inhibit bacillus growth on Mueller-Hinton agar.

Antibiotic treatment for Campylobacter infections is usually not required nor recommended. Antibiotics are limited for treating high-risk patients including immunocompromised and older individuals. Severe cases exhibiting symptoms such as bloody stools, fever, and severe abdominal pain may also require treatment by antibiotics.[2] It is advisable to treat these infections with macrolide antibiotics, such as erythromycin or azithromycin. Erythromycin is inexpensive and limits toxic exposure to patients, however resistance rates are reportedly increasing; its use is continued however, as resistance rates remain below 5%.[19] Azithromycin usage is increasing due to various drug characteristics, including its once-a-day dosage, tolerability by patients, decreased relation to Infantile Hypertrophic Pyloric Stenosis (IHPS), and less negative symptoms; this is comparative to erythromycin. Fluoroquinolones are another source of treatment, however resistance rates of bacteria to this type of antibiotic are greatly increasing.

Antibiotic Resistance edit

Fluoroquinolones were first approved as a treatment for Campylobacter infections in 1986, and were later U.S. Food and Drug Administration (FDA) approved in 1996, so as to control infections in poultry flocks. The CDC began monitoring Campylobacter in 1997 in the National Antimicrobial Resistance Monitoring System (NARMS). Data from NARMS indicated ciprofloxacin, a fluoroquinolone, had microbial resistance rates of 17% in 1997-1999, which further increased to 27% in 2015-2017.[19] On September 12, 2005, the FDA suspended the use of all fluoroquinolones in poultry production, and the prevalence of Campylobacter strains that are fluoroquinolone resistant in poultry flocks, poultry products, production facilities, and human infections became vital to monitor; this was in an effort to determine if the fluoroquinolone ban led to a reduction in the antibiotic-resistant strains.[20] A presence of drug-resistance to ciprofloxacin has been observed in isolate studies, as well as significant drug-resistance amongst Campylobacter to the antibiotics nalidixic acid and tetracyclines. There is a low rate of resistance to erythromycin, the preferred source of antibiotic treatment for Campylobacter infections, however resistant strains have been detected in many countries amongst sources of the origin of food from farm animals.[21]



User:Reesegroover/Campylobacter jejuni

References edit

  1. ^ "Campylobacter: Questions and Answers". U.S. Centers for Disease Control and Prevention. 2019-12-20. Retrieved 2020-01-02.
  2. ^ a b c Fischer, Greg H.; Hashmi, Muhammad F.; Paterek, Elizabeth (2024), "Campylobacter Infection", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 30725718, retrieved 2024-02-29
  3. ^ "Campylobacter: Questions and Answers". U.S. Centers for Disease Control and Prevention. 2019-12-20. Retrieved 2020-01-02.
  4. ^ a b c "Questions and Answers | Campylobacter | CDC". www.cdc.gov. 2023-02-16. Retrieved 2024-02-28.
  5. ^ a b c Facciolà, A.; Riso, R.; Avventuroso, E.; Visalli, G.; Delia, S.A.; Laganà, P. (June 2017). "Campylobacter: from microbiology to prevention". J Prev Med Hyg.: 1.
  6. ^ a b c "Campylobacter". www.who.int. Retrieved 2024-02-28.
  7. ^ Bronowski, Christina; James, Chloe E.; Winstanley, Craig (2014-07). "Role of environmental survival in transmission of Campylobacter jejuni". FEMS Microbiology Letters. 356 (1): 8–19. doi:10.1111/1574-6968.12488. {{cite journal}}: Check date values in: |date= (help)
  8. ^ a b c d e f g h i j k l m n o Kemper, Leon; Hensel, Andreas (2023). "Campylobacter jejuni: targeting host cells, adhesion, invasion, and survival". Applied Microbiology and Biotechnology. 107 (9): 2725–2754. doi:10.1007/s00253-023-12456-w. ISSN 0175-7598. PMID 36941439.
  9. ^ Sidor, Karolina; Skirecki, Tomasz (2023-05-17). "A Bittersweet Kiss of Gram-Negative Bacteria: The Role of ADP-Heptose in the Pathogenesis of Infection". Microorganisms. 11 (5): 1316. doi:10.3390/microorganisms11051316. ISSN 2076-2607. PMC 10221265. PMID 37317291.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  10. ^ a b c d e f g h i Gourley, Christopher R.; Negretti, Nicholas M.; Konkel, Michael E. (2017-10-31). "The food-borne pathogen Campylobacter jejuni depends on the AddAB DNA repair system to defend against bile in the intestinal environment". Scientific Reports. 7 (1). doi:10.1038/s41598-017-14646-9. ISSN 2045-2322. PMC 5665897. PMID 29089630.{{cite journal}}: CS1 maint: PMC format (link)
  11. ^ Smith, Gerald R. (2012-06). "How RecBCD Enzyme and Chi Promote DNA Break Repair and Recombination: a Molecular Biologist's View". Microbiology and Molecular Biology Reviews. 76 (2): 217–228. doi:10.1128/MMBR.05026-11. ISSN 1092-2172. PMC 3372252. PMID 22688812. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  12. ^ a b c d e f Hofreuter, Dirk (2014). "Defining the metabolic requirements for the growth and colonization capacity of Campylobacter jejuni". Frontiers in Cellular and Infection Microbiology. 4. doi:10.3389/fcimb.2014.00137. ISSN 2235-2988. PMC 4178425. PMID 25325018.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  13. ^ Altekruse, Sean F.; Stern, Norman J.; Fields, Patricia I.; Swerdlow, David L. (1999-02). "Campylobacter jejuni— An Emerging Foodborne Pathogen". Emerging Infectious Diseases. 5 (1): 28–35. doi:10.3201/eid0501.990104. ISSN 1080-6040. PMC 2627687. PMID 10081669. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  14. ^ Acheson, D.; Allos, B. M. (2001-04-15). "Campylobacter jejuni Infections: Update on Emerging Issues and Trends". Clinical Infectious Diseases. 32 (8): 1201–1206. doi:10.1086/319760. ISSN 1058-4838.
  15. ^ a b c d e Fischer, Greg H.; Hashmi, Muhammad F.; Paterek, Elizabeth (2024), "Campylobacter Infection", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 30725718, retrieved 2024-04-08
  16. ^ a b "Diagnosis of a Campylobacter Infection". Marler Clark. Retrieved 2024-04-08.
  17. ^ Platts-Mills, James A.; Liu, Jie; Gratz, Jean; Mduma, Esto; Amour, Caroline; Swai, Ndealilia; Taniuchi, Mami; Begum, Sharmin; Peñataro Yori, Pablo; Tilley, Drake H.; Lee, Gwenyth; Shen, Zeli; Whary, Mark T.; Fox, James G.; McGrath, Monica (2014-04). Diekema, D. J. (ed.). "Detection of Campylobacter in Stool and Determination of Significance by Culture, Enzyme Immunoassay, and PCR in Developing Countries". Journal of Clinical Microbiology. 52 (4): 1074–1080. doi:10.1128/JCM.02935-13. ISSN 0095-1137. PMC 3993515. PMID 24452175. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  18. ^ "Antibiotic Resistance | Campylobacter | CDC". www.cdc.gov. 2022-06-27. Retrieved 2024-04-11.
  19. ^ a b Eiland, Lea S.; Jenkins, Lauren S. (Jul–Sep 2008). "Optimal Treatment of Campylobacter Dysentery". National Library of Medicine. Retrieved April 11, 2024.{{cite web}}: CS1 maint: date format (link)
  20. ^ Price, Lance; Lackey, Leila; Vailes, Rocio; Silbergeld, Ellen (March 19, 2007). "The Persistence of Fluoroquinolone-Resistant Campylobacter in Poultry Production". National Library of Medicine. Retrieved April 18, 2024.
  21. ^ Portes, Ana; Panzenhagen, Pedro; Pereira dos Santos, Anamaria; Conte, Carlos (March 9, 2023). "Antibiotic Resistance in Campylobacter: A Systematic Review of South American Isolates". National Library of Medicine. Retrieved April 18, 2024.
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