Can Lyme disease and chronic infections cause cancer?
Numerous studies have demonstrated a negative correlation between acute infections and the emergence of cancer, however, on the other hand, there is mounting proof that persistent infections may have a considerable impact on the development of cancer.
Modifications to the body's regular defence systems or host immunity degradation brought on by changed immunological function, genetic polymorphisms, ageing, and malnutrition are examples of factors that can increase susceptibility to infections.
Studies have shown that whereas common acute infections in adults are linked to decreased risks for melanoma, glioma, meningioma, and other cancers, exposure to febrile infectious disorders in children is related with a reduced risk for ovarian cancer, melanoma, and many other cancers.
Tumor formation has been linked to chronic inflammation that is linked to a number of infectious illnesses. The mitogen-activated protein kinase pathway, the creation of toxins that alter the cell cycle and result in aberrant cell development, and the prevention of apoptosis are all mechanisms of carcinogenesis caused by infections.
How acute chronic infections can cause cancer
Since the beginning of the twentieth century, there has been much discussion on the complex relationship between cancer and infectious diseases. The cause of 2.2 million newly diagnosed instances of cancer in 2012 was carcinogenic infections. Helicobacter pylori (HP) (770,000 cases), human papillomavirus (HPV) (640,000), hepatitis B virus (HBV) (420,000), hepatitis C virus (HCV) (170,000), and Epstein-Barr virus (EBV) (120,000) have been identified as the most significant infectious agents involved in the development and progression of cancer.
A wide variety of host immunological responses can be modulated by infectious pathogens and related biochemical species, which in turn may have an impact on the initiation and progression of tumours. The mechanisms that influence carcinogenesis that are connected to infection-mediated immunity are still not fully known.
Acute and chronic infections may have various effects in the development of cancer; epidemiological research has indicated that acute infections inhibit the development of cancer while chronic infections may promote it. Rapid onset and brief duration are the hallmarks of acute infections, which are typically accompanied by fever, the release of cytokines and other inflammatory mediators, and the creation of liver acute-phase proteins.
Chronic infections may occasionally result from a weak or ineffective immune response. Alterations to normal defence systems or host immunity impairment, aberrant immunological function, genetic polymorphisms, ageing, and malnutrition are among the factors that enhance susceptibility to infections. The biological traits of viruses, bacteria, and parasites, such as pathogenicity, virulence, invasiveness, infectious load, toxinogenesis, contagiousness, tenacity, and vitality, may also affect whether infections happen.
People with higher socioeconomic level (SES) are more likely to get certain tumours, such as melanoma, colorectal, breast, kidney, testicular, and prostate cancers, whereas those with lower SES are more likely to develop lung, liver, cervical, and stomach cancers. In low SES groups, there is a higher frequency of chronic infections such HPV, HP, HBV, and HCV, which have been linked to uterine cervix, stomach, and liver cancers.
There is also a higher concurrent use of tobacco and alcohol, which causes lung and liver cancers. The decline in the incidence and mortality of infectious diseases and the rise in the death rates from cancer may be inversely related. Mastrangelo et al. reported that in Italy, infections were declining and tumours were expanding at the same time.
A decrease in the activation of immune defences against altered cells during the early stages of carcinogenesis could account for this trend. There is proof that certain viruses, including the West Nile virus, the mumps virus, the reovirus, the Newcastle disease virus, and others, may behave as oncolytic viruses, triggering the lysis of infected cells and activating antitumor immunity. The production of mucin 1 (MUC1), a cell surface glycoprotein and tumor-associated antigen, which is able to establish immune surveillance of ovarian cancer cells, may be the preventive mechanism, according to epidemiological research, in preventing ovarian cancer.
According to a study by Mink et al., White females had a higher risk of ovarian cancer, which is caused by anti-MUC1 antibodies. These findings were in line with the theory that ovarian cancer prevalence was rising and mumps parotitis infections were declining as a result of vaccination. Poliovirus infection in colon epithelial cells may offer protection from the onset of colon cancer, according to Lehrer and Rheinstein. Polio virus cellular receptor 13 and CD155 appear to act as mediators in the decrease in colon cancer mortality rate caused by polio virus infection.
Here, we provide a summary of the research on the connection between chronic infections and cancer formation and progression as well as the use of acute infections to prevent cancer.
Some microbes have the capacity to produce DNA alterations and cause chronic infections, both of which have been linked to the growth of tumours. Immunological mechanisms, such as the induction of regulatory T-cells, the production of anti-inflammatory cytokines, and the expression of immune checkpoint regulators [cytotoxic T-lymphocyte antigen 4 (CTLA-4) and programmed cell death protein-1 (PD-1)], can be linked to the development of chronic infections and cancer. T-cells that express CTLA-4 can interact with CD80 and CD86 to prevent T-cell activation, which can result in anergy. The programmed death ligands 1 and 2, which are mostly expressed on T-cells but can also be found on tumour cells and antigen-presenting cells (APCs), can interact with PD-1 to limit T-cell activity. The "initiated cells" that collect over the course of life may use inflammation as a promoter to accelerate the development of cancer. DNA and other biomolecules may be harmed by the biosynthesis of biochemical and metabolic intermediates during the development of tumours and inflammatory processes, which can result in the formation of malignant lesions.
Macrophages make up a significant portion of the tumour microenvironment and often support tumour survival, angiogenesis, proliferation, and dissemination. By activating certain genes involved in cell proliferation, survival, and invasion while inhibiting growth regulators such the tumour suppressor p5328, NF-B may initiate and advance cancer in people with persistent infections.
Low-grade mucosa-associated lymphoid tissue (MALT) lymphomas, as well as lymphomas of the stomach, intestine, bladder, larynx, lung, salivary glands, spleen, and thyroid, have all been shown to regress with antibiotic therapy. The first therapeutic strategy for low-grade stomach MALT lymphoma is HP eradication therapy.
Some lymphoma forms may be linked to HP, Campylobacter jejuni, HCV, or other bacteria. After receiving antiviral medication, the remission of benign and malignant lesions brought on by HPV has been documented3132. Anogenital warts and high-grade vulvar intraepithelial neoplasia have both been treated topically with imiquimod, an immune response modifier, or cidofovir, an inhibitor of viral replication, and the results have been positive (50–60%).
Topical application of the antiviral medication AV2® demonstrated good outcomes in lowering the size of cervical lesions linked to HPV31 in a phase II randomised controlled trial. These results must be verified in other well-designed trials, though.
Cancer and Viral infections
Viruses have the power to alter the physiological processes that control growth arrest and apoptosis in the host cell. Oncogenes from biological genes involved in mitogenic signalling, cell proliferation, and programmed cell death are carried by transforming viruses.
The numerous stages of carcinogenesis may involve shared pathways between cancer-causing viruses including HBV, HPV, and EBV, including the functional inactivation of p53 by virally encoded oncoproteins.
As several years may pass between the initiation of an infection and the development of cancer, host immunity may affect tumour growth. The carcinogenesis process can also be influenced by direct and indirect processes, such as potential synergy between viruses and environmental cofactors35.
Seven viruses have so far been identified as being linked to various types of human cancer. EBV, Kaposi's sarcoma-associated human herpes virus (KSHV), HPV, MCPV, HBV, HCV, and human T-cell leukaemia virus type 1.
Cancer and bacterial infections
Numerous factors, including the host immune response, stimulation of cell growth, inhibition of apoptosis, and generation of bacterial toxins, may affect how bacterial infections affect carcinogenesis. Reactive oxygen and nitrogen intermediates are released during some bacterial infections that increase inflammation or hyperplasia, and these intermediates can directly result in DNA damage.
Bacterial infections may affect how carefully host cells' signal pathways are regulated, which is important for the initiation or suppression of cancer. Numerous effector chemicals produced by bacteria interact with host cells to control adhesion, alter cytoskeletal or junctional function, and activate particular eukaryotic signalling pathways.
These virulence factors can promote cancer by directly affecting cellular functions. An essential step in the growth of cancerous cells is the suppression of apoptosis, particularly when intracellular microorganisms are the cause of infections. This is typically brought on by a variety of extracellular stimuli, which are reflected by the release of TNF- and the serine protease granzyme B by CD8+ T-cells. High NF-B concentrations can prevent TNF-induced apoptosis.
Bacteria may enhance the escape of altered cells from the destruction mechanisms by blocking apoptosis, favouring carcinogenesis96. Rho family proteins can be activated by Escherichia coli cytotoxic necrotizing factor, and cyclooxygenase-2 (COX-2) can be activated by Pasteurella multocida toxin, a potent mitogen for quiescent cells and an inducer of anchorage-independent growth. COX-2 is also involved in various stages of carcinogenesis, including the suppression of apoptosis. In people with HP infection, histological changes (such metaplasia) have been seen prior to the development of stomach cancer.
High salivary levels of Capnocytophaga gingivalis, Prevotella melaninogenica, and Streptococcus mitis have been found in cases of oral squamous cell carcinoma, showing diagnostic sensitivity and specificity of 80%-90%. This suggests that the presence of bacteria may be used as a diagnostic marker for cancer. The reduction of lesions following antibiotic therapy, as seen after HP eradication in patients with gastric cancer, may provide additional insight into the relationship between bacteria and cancer.
Lyme Disease and Risk of Leukemia
Leukemias are malignancies that affect certain immunological, bone marrow, or blood cells in the body. People can contract the bacterial illness Lyme disease from tick bites. Despite the stark differences between these illnesses, there may be some correlations.
Leukemias are tumours that arise from certain cells called leukocytes. Some of a person's leukocytes develop and divide erratically when they have leukaemia. These tumours can be categorised by medical professionals based on whether they impact lymphoid or myeloid cells. These cells belong to the leukocyte class.
Leukemia may have a wide range of genetic and environmental causes.
Small blood-feeding arthropods known as ticks have the potential to spread the B. burgdorferi bacteria. Borrelia burgdorferi bacteria causes Lyme disease which occurs following a tick bites, through which the bacteria can enter a person's body.
Leukemia and Lyme disease do notparticularly share a direct link. However, some data suggests that Lyme disease may raise a person's chance for lymphoma, a different type of blood cancer. This could be as a result of the body's inflammation brought on by Lyme disease.
Lyme Disease and Lymphoma
There is some proof that Lyme disease increases the risk of lymphomas. However, this danger is minimal, and the connection is unclear.
Cancers that affect a person's lymphoid cells are known as lymphomas. These cells are a part of the immune system, and lymphomas are among the immune system's most prevalent tumours.
According to the American Cancer Society (ACS), some Europeans who contracted the Lyme disease-causing B. burgdorferi infection also acquired cutaneous lymphomas. But the ACS cautions that cutaneous lymphomas are uncommon in people with Lyme disease.
Cancer as a result of Lyme disease Inflammation
Scientists have proven bacterial infections like Lyme disease may raise a person's risk of developing cancer by creating inflammation in the body. Infections and inflammation may account for up to 25% of cancer-causing factors. Although scientists are unsure of the exact mechanism at play in this process, one theory holds that DNA damage is caused by inflammation. This might result in genetic alterations that cause cancer.
Leukemia and Lyme disease occurring together
Leukemia and Lyme disease can both strike a person at the same time. Then, this person can start showing signs of both diseases. Leukemia and Lyme disease symptoms may overlap and be unique to each individual, so not everyone will have the same symptoms.
Common signs and symptoms of leukemia
Depending on the type of leukaemia a person has, leukaemia symptoms might change. Common signs and symptoms of leukaemia include:
- Easy bleeding
- Easy bruising
- Persistent lethargy, tiredness and weakness
- Shedding pounds without trying
- swollen lymph nodes, the liver, or the spleen
- Simple bruising or bleeding
- Frequent nosebleeds
- Skin lesions that appear as red spots called petechiae
- Excessive perspiration, especially at nighttime, called night swears
- Muscle aches
- Pain and/ or tenderness in the bones
Common Lyme disease signs and symptoms
- The tick bite site developing a "bull's-eye" rash, fever, and other flu-like symptoms malaise, headache, dizziness
- Chest pain
- Heart flutters
- Aching or swollen joints
- Enlarged lymph nodes
- Neurological deficits
- Brain fog
Treating leukemia and Lyme disease
The most common therapy for Lyme disease is antibiotics. For a period of 10 to 14 days, a doctor may advise taking the antibiotics against Lyme disease.
This therapy is thought to be equally effective for those with and without leukaemia, according to scientists. In leukaemia patients, it does not increase the risk of problems.
Can Lyme disease mask Leukemia resulting in misdiagnosis?
It is unlikely that Lyme disease could conceal leukaemia since the common symptoms of both illnesses differ. Some leukaemia patients experience skin rashes. Under the skin blood vessels burst, causing this to occur. When a leukaemia rash appears, some people worry that Lyme disease is the cause. But the "bull's-eye" rash that occasionally occurs with Lyme disease can be easily recognised. About 70–80% of Lyme disease patients have a rash.
It is also highly unlikely and doubtful that medical personnel would confuse Lyme disease for leukaemia because the two conditions have different symptoms and operate in very different ways.
If a person has a new rash and is worried about it, they should see their doctor.
What you should talk about with your physician
A person should consult their doctor if they have any concerns about having Lyme disease. When diagnosing Lyme disease, clinicians must take into account a number of variables, according to the Centers for Disease Control and Prevention (CDC). These consist of:
- relevant symptoms or signs
- the likelihood that a person came into contact with a tick that was carrying B. burgdorferi and the possibility of another illness with comparable symptoms
- laboratory test findings
Even in the absence of a certain diagnosis, treatment for Lyme disease might begin.
Leukemia and Lyme disease patients may also want to talk about the medical implications of having both diseases. Typically, antibiotics are used to treat Lyme disease, which is normally safe for a person with leukaemia to consume.
It is important to note that Lyme disease is not contagious – it does not spread from person to person and the bacteria can only be transmitted through tick bites.
Infection by bacteria, parasites or viruses and tissue inflammation such as gastritis, hepatitis and colitis are recognized risk factors for human cancers at various sites.
Nitric oxide (NO) and other oxygen radicals produced in infected and inflamed tissues could contribute to the process of carcinogenesis by different mechanisms, which are discussed on the basis of authors' studies on liver fluke infection and cholangiocarcinoma development.
A similar mechanism could apply to other suspected and known cancer-causing agents including Helicobacter pylori infection (causing stomach cancer) or in the case of Lyme disease or asbestos exposure (lung mesothelioma).
Studies on the type of tissue and DNA damage produced by NO and by other reactive oxygen species are shedding new light on the molecular mechanisms by which chronic inflammatory processes may initiate or enhance carcinogenesis in humans.