What do pathogenic bacteria cause

The infective dose to get to a Campylobacter enteritis is relatively low. It does not need more than germs to get to an infection. From approximately 15 known Campylobacter species, mainly C. Clostridium species are gram-positive, spore-forming bacteria and are present almost everywhere in the environment. Some Clostridium species are of importance as pathogens, including Clostridium botulinum , Clostridium perfringens and Clostridium estertheticum.

If food is not cooled sufficiently, it can result in a contamination, which can cause serious illnesses. The bacteria are heat-resistant and thus, can also be contained in thoroughly heated food products. Legionella are a genus of gram-negative, rod-shaped bacteria that live in the water. They are considered as potential human pathogens.

The disease is usually transmitted through contaminated drinking water. Listeria can be found in almost all areas of life. It is possible to assess the risk of contamination via quantitative detection to ensure that, if necessary, preventive measures can be taken. Listeria monocytogenes , in particular, is considered a major cause of food poisoning, possibly resulting in the development of sepsis, meningitis and encephalitis. Salmonella is ranked among the most important initiators of cases of food poisoning.

The WHO estimates more than 16 million global infections per year, and more than half a million cases are fatal. Salmonella are found in raw food such as eggs, meat and milk. The hazard potential is high, particularly in food that should only be slightly heated or not at all heated e. Most merozoites continue to reproduce in this way, but some differentiate into sexual forms gametocytes that are taken up by the female mosquito, thus completing the protozoan life cycle.

Disease Watchlist Lyme Disease View full watchlist. What do you know about infectious disease? About how often is someone in the world newly infected with tuberculosis TB?

Every second Every minute Every hour Correct! Infectious Disease Defined Exoskeleton An external skeleton that protects and supports an organism, in contrast to an internal endoskeleton. View our full glossary. Terms of Use and Privacy Statement. History has been shaped not only by pathogens infecting humans, but also those affecting domestic animals and crops.

For example, it has been suggested that the Islamic conquest of the 7 th and 8 th centuries did not extend to Sub-Saharan Africa because the horses and camels of the Islamic armies were dying from trypanosma spread by tsetse flies [ 24 ].

Conversely, pathogens were at other times the drivers of large migration. Around one million Irish people died and another million migrated to the US to escape the famine caused by Phytophthora infestans destroying potato harvests between and [ 25 ].

At least in the developed world, the leading causes of human mortality are no longer infectious diseases but instead age-associated disorders such as cancer, heart disease and diabetes. Numerous countries have undergone an epidemiological transition, starting some years ago in some developed countries and less than 80 years ago for developing countries.

Diseases that once devastated human populations, such as smallpox, are now eradicated. Others, such as the plague or leprosy, are largely under control with the exception of a few hotspots. The current situation is, however, one of new challenges. Globalization and increased mobility, particularly air travel, have facilitated the transmission of diseases not just locally but between continents.

The recent outbreak of Zika in the Americas, for example, has been attributed in part to an increase in air travel from infected areas into Brazilian airports, extending both the incidence and geographic range of the virus [ 26 ]. The outbreak of severe acute respiratory syndrome SARS and recurrent Ebola crises in Central Africa highlight the ability of new and existing diseases rapidly to become significant international health threats. In addition, our ability to combat infectious diseases is also challenged by the widespread emergence of pathogen drug resistance.

The global antimicrobial resistance AMR crisis is increasingly limiting our resources to combat disease through antimicrobial therapy. Thus, in spite of the global health narrative supporting a decline in the number of deaths caused by infectious disease, the complexity of our interactions with disease-causing agents are as significant now as through history. Infectious diseases continue to be a major cause of mortality globally, responsible for between a quarter to a third of all deaths and nearly half of all deaths in people under the age of 45, with most of these in principle avoidable.

Microbiology by numbers. Nat Rev Microbiol. Revised estimates for the number of human and bacteria cells in the body. PLoS Biol. Google Scholar. The role of damselflies Odonata: Ztgoptera as paratenic hosts in the transmission of Halipegus eccentricus Digenea: Hemioridae to Anurans. J Parasitol. Article PubMed Google Scholar. Red squirrels in the British Isles are infected with leprosy bacilli. A single natural nucleotide mutation alters bacterial pathogen host tropism.

Nat Genet. Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis. Insight into the evolution and origin of leprosy bacilli from the genome sequence of Mycobacterium lepromatosis.

Achtman M, Wagner M. Microbial diversity and the genetic nature of microbial species. Immunobiology and pathogenesis of viral hepatitis. Annu Rev Pathol.

The influenza pandemic: insights for the 21st century. J Infect Dis. Infectious diseases of humans. Dynamics and control. Oxford: Oxford University Press; Myxoma virus and the leporipox viruses: an evolutionary paradigm. Emerging fungal threats to animal, plant and ecosystem health. Age of the association between Helicobacter pylori and man. PLoS Pathog. Article Google Scholar. Myths and misconceptions: the origin and evolution of Mycobacterium tuberculosis. Hill AVS. Evolution, revolution and heresy in the genetics of infectious disease susceptibility.

Pathogen-driven selection and worldwide HLA class I diversity. Curr Biol. Genomic signatures of selective pressures and introgression from archaic hominins at human innate immunity genes. Am J Hum Genet. Introgression of Neandertal- and Denisovan-like haplotypes contributes to adaptive variation in human Toll-like receptors. Nat Geosci. Insights from paleomicrobiology into the indigenous peoples of pre-colonial America - a review.

Mem Inst Oswaldo Cruz. Webb Jr JLA. One mechanism relies on effector proteins secreted by the pathogen; these effector proteins trigger entry into the host cell. This is the method that Salmonella and Shigella use when invading intestinal epithelial cells. When these pathogens come in contact with epithelial cells in the intestine, they secrete effector molecules that cause protrusions of membrane ruffles that bring the bacterial cell in.

This process is called membrane ruffling. The second mechanism relies on surface proteins expressed on the pathogen that bind to receptors on the host cell, resulting in entry.

For example, Yersinia pseudotuberculosis produces a surface protein known as invasin that binds to beta-1 integrins expressed on the surface of host cells. Some host cells, such as white blood cells and other phagocytes of the immune system, actively endocytose pathogens in a process called phagocytosis. Although phagocytosis allows the pathogen to gain entry to the host cell, in most cases, the host cell kills and degrades the pathogen by using digestive enzymes.

Normally, when a pathogen is ingested by a phagocyte, it is enclosed within a phagosome in the cytoplasm; the phagosome fuses with a lysosome to form a phagolysosome, where digestive enzymes kill the pathogen see Pathogen Recognition and Phagocytosis.

However, some intracellular pathogens have the ability to survive and multiply within phagocytes. Bacteria such as Mycobacterium tuberculosis , Legionella pneumophila , and Salmonella species use a slightly different mechanism to evade being digested by the phagocyte.

These bacteria prevent the fusion of the phagosome with the lysosome, thus remaining alive and dividing within the phagosome. Following invasion, successful multiplication of the pathogen leads to infection. Infections can be described as local, focal, or systemic, depending on the extent of the infection. A local infection is confined to a small area of the body, typically near the portal of entry.

For example, a hair follicle infected by Staphylococcus aureus infection may result in a boil around the site of infection, but the bacterium is largely contained to this small location. Other examples of local infections that involve more extensive tissue involvement include urinary tract infections confined to the bladder or pneumonia confined to the lungs.

In a focal infection , a localized pathogen, or the toxins it produces, can spread to a secondary location. For example, a dental hygienist nicking the gum with a sharp tool can lead to a local infection in the gum by Streptococcus bacteria of the normal oral microbiota. These Streptococcus spp. When an infection becomes disseminated throughout the body, we call it a systemic infection. For example, infection by the varicella-zoster virus typically gains entry through a mucous membrane of the upper respiratory system.

It then spreads throughout the body, resulting in the classic red skin lesions associated with chickenpox. Since these lesions are not sites of initial infection, they are signs of a systemic infection. Sometimes a primary infection , the initial infection caused by one pathogen, can lead to a secondary infection by another pathogen. For example, the immune system of a patient with a primary infection by HIV becomes compromised, making the patient more susceptible to secondary diseases like oral thrush and others caused by opportunistic pathogens.

Similarly, a primary infection by Influenzavirus damages and decreases the defense mechanisms of the lungs, making patients more susceptible to a secondary pneumonia by a bacterial pathogen like Haemophilus influenzae or Streptococcus pneumoniae.

Some secondary infections can even develop as a result of treatment for a primary infection. Antibiotic therapy targeting the primary pathogen can cause collateral damage to the normal microbiota, creating an opening for opportunistic pathogens. Anita, a year-old mother of three, goes to an urgent care center complaining of pelvic pressure, frequent and painful urination, abdominal cramps, and occasional blood-tinged urine. Suspecting a urinary tract infection UTI , the physician requests a urine sample and sends it to the lab for a urinalysis.

Since it will take approximately 24 hours to get the results of the culturing, the physician immediately starts Anita on the antibiotic ciprofloxacin. The next day, the microbiology lab confirms the presence of E. After taking her antibiotics for 1 week, Anita returns to the clinic complaining that the prescription is not working.

Although the painful urination has subsided, she is now experiencing vaginal itching, burning, and discharge. After a brief examination, the physician explains to Anita that the antibiotics were likely successful in killing the E. The new symptoms that Anita has reported are consistent with a secondary yeast infection by Candida albicans , an opportunistic fungus that normally resides in the vagina but is inhibited by the bacteria that normally reside in the same environment.

To confirm this diagnosis, a microscope slide of a direct vaginal smear is prepared from the discharge to check for the presence of yeast.

A sample of the discharge accompanies this slide to the microbiology lab to determine if there has been an increase in the population of yeast causing vaginitis. After the microbiology lab confirms the diagnosis, the physician prescribes an antifungal drug for Anita to use to eliminate her secondary yeast infection. For a pathogen to persist, it must put itself in a position to be transmitted to a new host, leaving the infected host through a portal of exit Figure 6.

As with portals of entry, many pathogens are adapted to use a particular portal of exit. Similar to portals of entry, the most common portals of exit include the skin and the respiratory, urogenital, and gastrointestinal tracts. Coughing and sneezing can expel pathogens from the respiratory tract.

A single sneeze can send thousands of virus particles into the air. Secretions and excretions can transport pathogens out of other portals of exit. Feces, urine, semen, vaginal secretions, tears, sweat, and shed skin cells can all serve as vehicles for a pathogen to leave the body. Pathogens that rely on insect vectors for transmission exit the body in the blood extracted by a biting insect.

Similarly, some pathogens exit the body in blood extracted by needles. Figure 6. Pathogens leave the body of an infected host through various portals of exit to infect new hosts. Which pathogen is most virulent? Skip to main content. Microbial Mechanisms of Pathogenicity.