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The common routes of transmission for the disease-causing bacteria are fecal-oral, person-to-person sexual contact, ingestion of contaminated food (generally unpasteurized (raw) milk and undercooked or poorly handled poultry), and waterborne (i.e., through contaminated drinking water). Contact with contaminated poultry, livestock, or household pets, especially puppies, can also cause disease.
Animals farmed for meat are the main source of campylobacteriosis. A study published in PLoS Genetics (September 26, 2008) by researchers from Lancashire, England, and Chicago, Illinois, found that 97 percent of campylobacteriosis cases sampled in Lancashire were caused by bacteria typically found in chicken and livestock. In 57 percent of cases, the bacteria could be traced to chicken, and in 35 percent to cattle. Wild animal and environmental sources were accountable for just three percent of disease.
The infectious dose is 1000–10,000 bacteria (although ten to five hundred bacteria can be enough to infect humans). "Campylobacter" species are sensitive to hydrochloric acid in the stomach, and acid reduction treatment can reduce the amount of needed to cause disease.
Exposure to bacteria is often more common during travelling, and therefore campylobacteriosis is a common form of travelers' diarrhea.
The World Health Organization recommends the following:
- Food should be properly cooked and hot when served.
- Consume only pasteurized or boiled milk and milk products, never raw milk products.
- Make sure that ice is from safe water.
- If you are not sure of the safety of drinking water, boil it, or disinfect it with chemical disinfectant.
- Wash hands thoroughly and frequently with soap, especially after using the toilet and after contact with pets and farm animals.
- Wash fruits and vegetables thoroughly, especially if they are to be eaten raw. Peel fruits and vegetables whenever possible.
- Food handlers, professionals and at home, should observe hygienic rules during food preparation.
- Professional food handlers should immediately report to their employer any fever, diarrhea, vomiting or visible infected skin lesions.
Measures to reduce contact between the vesper mouse and humans may have contributed to limiting the number of outbreaks, with no cases identified between 1973 and 1994. Although there are no cures or vaccine for the disease, a vaccine developed for the genetically related Junín virus which causes Argentine hemorrhagic fever has shown evidence of cross-reactivity to Machupo virus, and may therefore be an effective prophylactic measure for people at high risk of infection. Post infection (and providing that the person survives the infection), those that have contracted BHF are usually immune to further infection of the disease.
Investigational vaccines exist for Argentine hemorrhagic fever and RVF; however, neither is approved by FDA or commonly available in the United States.
The structure of the attachment glycoprotein has been determined by X-ray crystallography and this glycoprotein is likely to be an essential component of any successful vaccine.
Fowl cholera is also called avian cholera, avian pasteurellosis, avian hemorrhagic septicemia.
It is the most common pasteurellosis of poultry. As the causative agent is "Pasteurella multocida", it is considered as a zoonosis.
Adult birds and old chickens are more susceptible. In parental flocks, cocks are far more susceptible than hens.
Besides chickens, the disease also concerns turkeys, ducks, geese, raptors, and canaries. Turkeys are particularly sensitive, with mortality ranging to 65%.
The recognition of this pathological condition is of ever increasing importance for differential diagnosis with avian influenza.
In birds, "Chlamydia psittaci" infection is referred to as avian chlamydiosis (AC). Infected birds shed the bacteria through feces and nasal discharges, which can remain infectious for several months. Many strains remain quiescent in birds until activated under stress. Birds are excellent, highly mobile vectors for the distribution of chlamydial infection because they feed on, and have access to, the detritus of infected animals of all sorts.
The most efficient treatment in breeding flocks or laying hens is individual intramuscular injections of a long-acting tetracycline, with the same antibiotic in drinking water, simultaneously. The mortality and clinical signs will stop within one week, but the bacteria might remain present in the flock.
Rodent control in and around the home remains the primary prevention strategy, as well as eliminating contact with rodents in the workplace and campsite. Closed storage sheds and cabins are often ideal sites for rodent infestations. Airing out of such spaces prior to use is recommended. Avoid direct contact with rodent droppings and wear a mask to avoid inhalation of aerosolized rodent secretions.
HFRS is primarily a Eurasian disease, whereas HPS appears to be confined to the Americas. The geography is directly related to the indigenous rodent hosts and the viruses that coevolved with them.
Infection is usually via the droppings of another infected bird, though it can also be transmitted via feathers and eggs, and is typically either inhaled or ingested.
"C. psittaci" strains in birds infect mucosal epithelial cells and macrophages of the respiratory tract. Septicaemia eventually develops and the bacteria become localized in epithelial cells and macrophages of most organs, conjunctiva, and gastrointestinal tract. It can also be passed in the eggs. Stress will commonly trigger onset of severe symptoms, resulting in rapid deterioration and death. "C. psittaci" strains are similar in virulence, grow readily in cell culture, have 16S-rRNA genes that differ by <0.8%, and belong to eight known serovars. All should be considered to be readily transmissible to humans.
"C. psittaci" serovar A is endemic among psittacine birds and has caused sporadic zoonotic disease in humans, other mammals, and tortoises. Serovar B is endemic among pigeons, has been isolated from turkeys, and has also been identified as the cause of abortion in a dairy herd. Serovars C and D are occupational hazards for slaughterhouse workers and for people in contact with birds. Serovar E isolates (known as Cal-10, MP or MN) have been obtained from a variety of avian hosts worldwide and, although they were associated with the 1920s–1930s outbreak in humans, a specific reservoir for serovar E has not been identified. The M56 and WC serovars were isolated during outbreaks in mammals.
In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".
"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.
Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.
Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.
AHF is a grave acute disease which may progress to recovery or death in 1 to 2 weeks. The incubation time of the disease is between 10 and 12 days, after which the first symptoms appear: fever, headaches, weakness, loss of appetite and will. These intensify less than a week later, forcing the infected to lie down, and producing stronger symptoms such as vascular, renal, hematological and neurological alterations. This stage lasts about 3 weeks.
If untreated, the mortality of AHF reaches 15–30%. The specific treatment includes plasma of recovered patients, which, if started early, is extremely effective and reduces mortality to 1%.
Ribavirin also has shown some promise in treating arenaviral diseases.
The disease was first detected in the 1950s in the Junín Partido in Buenos Aires, after which its agent, the Junín virus, was named upon its identification in 1958. In the early years, about 1,000 cases per year were recorded, with a high mortality rate (more than 30%). The initial introduction of treatment serums in the 1970s reduced this lethality.
Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.
Among the causal agents of acute enterocolitis are:
- bacteria: "Salmonella", "Shigella", "Escherichia coli", "Campylobacter" etc.;
- viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses;
- fungi: candidiasis, especially in immunosuppressed patients or who have previously received prolonged antibiotic treatment;
- parasites: "Giardia lamblia" (with high frequency of infestation in the population, but not always with clinical manifestations), "Balantidium coli", "Blastocystis homnis", "Cryptosporidium" (diarrhea in people with immunosuppression), "Entamoeba histolytica" (produces the amebian dysentery, common in tropical areas).
Streptococcus species are the cause of opportunistic infections in poultry leading to acute and chronic conditions in affected birds. Disease varies according to the Streptococcal species but common presentations include septicaemia, peritonitis, salpingitis and endocarditis.
Common species affecting poultry include:
- "S. gallinaceus" in broiler chickens
- "S. gallolyticus" which is a pathogen of racing pigeons and turkey poults
- "S. dysgalactiae" in broiler chickens
- "S. mutans" in geese
- "S. pluranimalium" in broiler chickens
- "S. equi subsp. zooepidemicus" in chickens and turkeys
- "S. suis" in psittacine birds
Preventing Omsk Hemorrhagic Fever consists primarily in avoiding being exposed to tick. Persons engaged in camping, farming, forestry, hunting (especially the Siberian muskrat) are at greater risk and should wear protective clothing or use insect repellent for protection. The same is generally recommended for persons at sheltered locations.
Omsk hemorrhagic fever is caused by the Omsk hemorrhagic fever virus (OHFV), a member of the Flavivirus family. The virus was discovered by Mikhail Chumakov and his colleagues between 1945 and 1947 in Omsk, Russia. The infection is found in western Siberia, in places including Omsk, Novosibirsk, Kurgan, and Tyumen. The virus survives in water and is transferred to humans via contaminated water or an infected tick.
The disease was first reported in the town of in Buenos Aires province, Argentina in 1958, giving it one of the names by which it is known. Various theories about its nature were proposed: it was Weil's disease, leptospirosis, caused by chemical pollution. It was associated with fields containing stubble after the harvest, giving it another of its names.
The endemic area of AHF covers approximately 150,000 km², compromising the provinces of Buenos Aires, Córdoba, Santa Fe and La Pampa, with an estimated risk population of 5 million.
The vector, a small rodent known locally as "ratón maicero" ("maize mouse"; "Calomys musculinus"), suffers from chronic asymptomatic infection, and spreads the virus through its saliva and urine. Infection is produced through contact of skin or mucous membranes, or through inhalation of infected particles. It is found mostly in people who reside or work in rural areas; 80% of those infected are males between 15 and 60 years of age.
Specific types of enterocolitis include:
- necrotizing enterocolitis (most common in premature infants)
- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")
Crohn's disease – also known as regional enteritis, it can occur along any surface of the gastrointestinal tract. In 40% of cases it is limited to the small intestine.
Coeliac disease – caused by an autoimmune reaction to gluten by genetically predisposed individuals.
Eosinophilic enteropathy – a condition where eosinophils build up in the gastrointestinal tract and blood vessels, leading to polyp formation, necrosis, inflammation and ulcers. It is most commonly seen in patients with a history of atopy, however is overall relatively uncommon.
The organism should be cultured and antibiotic sensitivity should be determined before treatment is started. Amoxycillin is usually effective in treating streptococcal infections.
Biosecurity protocols and good hygiene are important in preventing the disease.
Vaccination is available against "S. gallolyticus" and can also protect pigeons.
Five families of RNA viruses have been recognised as being able to cause hemorrhagic fevers.
- The family "Arenaviridae" include the viruses responsible for Lassa fever (Lassa virus), Lujo virus, Argentine (Junin virus), Bolivian (Machupo virus), Brazilian (Sabiá virus), Chapare hemorrhagic fever (Chapare virus) and Venezuelan (Guanarito virus) hemorrhagic fevers.
- The family "Bunyaviridae" include the members of the "Hantavirus" genus that cause hemorrhagic fever with renal syndrome (HFRS), the Crimean-Congo hemorrhagic fever (CCHF) virus from the "Nairovirus" genus, Garissa virus and Ilesha virus from the "Orthobunyavirus" and the Rift Valley fever (RVF) virus from the "Phlebovirus" genus.
- The family "Filoviridae" include Ebola virus and Marburg virus.
- The family "Flaviviridae" include dengue, yellow fever, and two viruses in the tick-borne encephalitis group that cause VHF: Omsk hemorrhagic fever virus and Kyasanur Forest disease virus.
- In September 2012 scientists writing in the journal PLOS Pathogens reported the isolation of a member of the "Rhabdoviridae" responsible for 2 fatal and 2 non-fatal cases of hemorrhagic fever in the Bas-Congo district of the Democratic Republic of Congo. The non-fatal cases occurred in healthcare workers involved in the treatment of the other two, suggesting the possibility of person-to-person transmission. This virus appears to be unrelated to previously known Rhabdoviruses.
The pathogen that caused the cocoliztli epidemics in Mexico of 1545 and 1576 is still unknown.
Venezuelan hemorrhagic fever (VHF) is a zoonotic human illness first identified in 1989. The disease is most prevalent in several rural areas of central Venezuela and is caused by the Guanarito virus (GTOV) which belongs to the Arenaviridae family. The short-tailed cane mouse ("Zygodontomys brevicauda") is the main host for GTOV which is spread mostly by inhalation of aerosolized droplets of saliva, respiratory secretions, urine, or blood from infected rodents. Person-to-person spread is possible, but uncommon.
Brazilian hemorrhagic fever (BzHF) is an infectious disease caused by the Sabiá virus, an Arenavirus. The Sabiá virus is one of the arenoviruses from South America to cause hemorrhagic fever. It shares a common progenitor with the Junin virus, Machupo virus, Tacaribe virus, and Guanarito virus. It is an enveloped RNA virus and is highly infectious and lethal. Very little is known about this disease, but it is thought to be transmitted by the excreta of rodents.
There have only been three documented infections of the Sabiá virus, only one of which occurred naturally and the other two cases occurred in the clinical setting. The only naturally occurring case was in 1990, when a female agricultural engineer who was staying in the neighborhood of Jardim Sabiá near São Paulo, Brazil contracted the disease. She presented with hemorrhagic fever and died. Her autopsy showed liver necrosis. A virologist who was studying the woman's disease contracted the virus but survived. Ribavirin was not given in these first two cases. Four years later, in 1994, a researcher was exposed to the virus in a level 3 biohazard facility at Yale University when a centrifuge bottle cracked, leaked, and released aerosolized virus particle. He was successfully treated with ribavirin.
Ribavirin is thought to be effective in treating the illness, similar to other arenaviruses. Compared to the patients who did not receive ribavirin, the patient who was treated with it had a shorter and less severe clinical course. Symptomatic control such as fluids to address dehydration and bleeding may also be required.
The Sabiá virus is a Biosafety Level 4 pathogen.
This virus has also been implicated as a means for bioterrorism, as it can be spread through aerosols.
The VHF viruses are spread in a variety of ways. Some may be transmitted to humans through a respiratory route. According to Soviet defector Ken Alibek, Soviet scientists concluded China may have tried to weaponise a VHF virus during the late 1980's but discontinued to do so after an outbreak . The virus is considered by military medical planners to have a potential for aerosol dissemination, weaponizaton, or likelihood for confusion with similar agents that might be weaponized.
Amphistomiasis in farm and wild mammals is due to infection of paramphistomes, such as the species of "Paramphistomum", "Calicophoron", "Cotylophoron", "Pseudophisthodiscus", etc. These are essentially rumen flukes, of which "Paramphistomum cervi" is the most notorious in terms of prevalence and pathogenicity. Infection occurs through ingestion of contaminated vegetables and raw meat, in which the viable infective metacercaria are deposited from snails, which are the intermediate hosts. The immature flukes are responsible for destroying the mucosal walls of the alimentary tract on their way to growing into adults. It is by this fervent tissue obliteration that the clinical symptoms are manifested. The adult flukes, on the other hand, are quite harmless, as they merely prepare for reproduction.
The zoonotic infection in human is caused by "G. discoides" and "W. watsoni" which are essentially intestinal flukes. The disease due to "G. discoides" is more specifically termed gastrodiscoidiasis. In their natural hosts such as pigs and monkeys, their infection in asymptomatic, but human infection is prevalent, by which they cause serious health problems, characterised by diarrhoea, fever, abdominal pain, colic, and an increased mucous production. In extreme situations such as in Assam, India, a number of mortality among children is attributed to this disease.