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The risk factors associated with BPF are not well known. However, it has been suggested that children under 5 years of age are more susceptible to BPF since they lack serum bactericidal activity against the infection. Older children and adults have much higher titers of bactericidal antibodies, which serve as a protective measure. Also children residing in warmer geographic areas have been associated with a higher risk of BPF infection.
The eye gnat ("Liohippelates") was thought to be the cause of the conjunctivitis epidemic which occurred in Mato Grosso do Sul in 1991. These gnats were extracted from the conjunctival secretions of the children who were infected with conjunctivitis. 19 of those children developed BPF following the conjunctivitis. Other modes of transmission include contact with the conjunctival discharges of infected people, ophthalmic instruments which have not been properly sterilized, sharing eye makeup applicators or multiple-dose eye medications.
Haemorrhagic septicaemia is one of the most economically important pasteurelloses. Haemorrhagic septicaemia in cattle and buffaloes was previously known to be associated with one of two serotypes of "P. multocida": Asian B:2 and African E:2 according to the Carter-Heddleston system, or 6:B and 6:E using the Namioka-Carter system.
The disease occurs mainly in cattle and buffaloes, but has also been reported in goats ("Capra aegagrus hircus"), African buffalo ("Syncerus nanus"), camels, horses and donkeys ("Equus africanus asinus"), in pigs infected by serogroup B, and in wild elephants ("Elephas maximus"). Serotypes B:1 and B:3,4 have caused a septicaemic disease in antelope ("Antilocapra americana") and elk ("Cervus canadensis"), respectively. Serotype B:4 was associated with the disease in bison ("Bison bison").
Serotypes E:2 and B:2 were associated with HS outbreaks in Africa and Asia respectively. Serotype E:2 was reported in Senegal, Mali, Guinea, Ivory Coast, Nigeria, Cameroon, the Central African Republic and Zambia. However, it is now inaccurate to associate outbreaks in Africa with serotype E:2 as many outbreaks of HS in Africa have now been associated with serogroup B. In the same manner, serogroup E has been associated with outbreaks in Asia. For instance, one record of "Asian serotype" (B:2) was reported in Cameroon. Some reports showed that serotype B:2 may be present in some East African countries. Both serogroups B and E have been reported in Egypt and Sudan.
Natural routes of infection are inhalation and/or ingestion. Experimental transmission has succeeded using intranasal aerosol spray or oral drenching. When subcutaneous inoculation is used experimentally, it results in rapid onset of the disease, a shorter clinical course and less marked pathological lesions compared to the longer course of disease and more profound lesions of oral drenching and the intranasal infection by aerosols.
When HS was introduced for the first time into a geographic area, morbidity and mortality rates were high, approaching 100% unless animals were treated in the very early stages of disease.
The following steps and precautions should be used to avoid infection of the septicemic plague:
- Caregivers of infected patients should wear masks, gloves, goggles and gowns
- Take antibiotics if close contact with infected patient has occurred
- Use insecticides throughout house
- Avoid contact with dead rodents or sick cats
- Set traps if mice or rats are present around the house
- Do not allow family pets to roam in areas where plague is common
- Flea control and treatment for animals (especially rodents)
A wide variety of clinical signs have been described for HS in cattle and buffaloes. The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varies according to the route of infection. The incubation period is 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.
There is variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals. It has also been recorded from field observations that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.
Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by fever, with a rectal temperature of , loss of appetite and depression. Phase two is typified by increased respiration rate (40–50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia. The three phases overlap when the disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with a shorter duration.
Human "Yersinia" infections most commonly result from the bite of an infected flea or occasionally an infected mammal, but like most bacterial systemic diseases, the disease may be transmitted through an opening in the skin or by inhaling infectious droplets of moisture from sneezes or coughs. In both cases septicemic plague need not be the result, and in particular, not the initial result, but it occasionally happens that bubonic plague for example leads to infection of the blood, and septicemic plague results. If the bacteria happen to enter the bloodstream rather than the lymph or lungs, they multiply in the blood, causing bacteremia and severe sepsis. In septicemic plague, bacterial endotoxins cause disseminated intravascular coagulation (DIC), where tiny blood clots form throughout the body, commonly resulting in localised ischemic necrosis, tissue death from lack of circulation and perfusion.
DIC results in depletion of the body's clotting resources, so that it can no longer control bleeding. Consequently, the unclotted blood bleeds into the skin and other organs, leading to red or black patchy rash and to hematemesis (vomiting blood) or hemoptysis (spitting blood). The rash may cause bumps on the skin that look somewhat like insect bites, usually red, sometimes white in the center.
Untreated septicemic plague is almost always fatal. Early treatment with antibiotics reduces the mortality rate to between 4 and 15 percent. Death is almost inevitable if treatment is delayed more than about 24 hours, and some people may even die on the same day they with the disease.
Septicemic plague is caused by horizontal and direct transmission. Horizontal transmission is the transmitting of a disease from one individual to another regardless of blood relation. Direct transmission occurs from close physical contact with individuals, through common air usage, from direct bite from a flea or an infected rodent. Most common rodents may carry the bacteria and so may Leporidae such as rabbits:
Significant carriers of the bacteria in the United States include:
- Rats
- Prairie dogs
- Squirrels
- Chipmunks
- Rabbits
The bacteria are cosmopolitan, mainly in rodents in all continents except Australia and Antarctica. The greatest frequency of human plague infections occur in Africa. The bacteria most commonly appear in rural areas and wherever there is poor sanitation, overcrowding, and high rodent populations in urban areas. Outdoor activities such as hiking, camping, or hunting where plague-infected animals may be found, increase the risk of contracting septicemic plague, and so do certain occupations such as veterinary or other animal-related work.
Carrión's disease, or Oroya fever, or Peruvian wart is a rare infectious disease found only in Peru, Ecuador, and Colombia. It is endemic in some areas of Peru, is caused by infection with the bacterium "Bartonella bacilliformis", and transmitted by sandflies of genus "Lutzomyia".
Cat scratch disease occurs worldwide. Cats are the main reservoir of "Bartonella henselae", and the bacterium is transmitted to cats by the cat flea "Ctenocephalides felis". Infection in cats is very common with a prevalence estimated between 40-60%, younger cats being more commonly infective. Cats usually become immune to the infection, while dogs may be very symptomatic. Humans may also acquire it through flea or tick bites from infected dogs, cats, coyotes, and foxes.
Trench fever, produced by "Bartonella quintana" infection, is transmitted by the human body louse "Pediculus humanus corporis". Humans are the only known reservoir. Thorough washing of clothing may help to interrupt the transmission of infection.
A possible role for ticks in transmission of "Bartonella" species remains to be elucidated; in November 2011, "Bartonella rochalimae", "B. quintana", and "B. elizabethae" DNA was first reported in "Rhipicephalus sanguineus" and "Dermacentor nitens" ticks in Peru.
There are several risk factors that increase the likelihood of developing bacteremia from any type of bacteria. These include:
- HIV infection
- Diabetes Mellitus
- Chronic hemodialysis
- Solid organ transplant
- Stem cell transplant
- Treatment with glucocorticoids
- Liver failure
"Listeria monocytogenes" is ubiquitous in the environment. The main route of acquisition of "Listeria" is through the ingestion of contaminated food products. "Listeria" has been isolated from raw meat, dairy products, vegetables, fruit and seafood. Soft cheeses, unpasteurized milk and unpasteurised pâté are potential dangers; however, some outbreaks involving post-pasteurized milk have been reported.
Rarely listeriosis may present as cutaneous listeriosis. This infection occurs after direct exposure to "L. monocytogenes" by intact skin and is largely confined to veterinarians who are handling diseased animals, most often after a listerial abortion.
Incidence in 2004–2005 was 2.5–3 cases per million population a year in the United States, where pregnant women accounted for 30% of all cases. Of all nonperinatal infections, 70% occur in immunocompromised patients. Incidence in the U.S. has been falling since the 1990s, in contrast to Europe where changes in eating habits have led to an increase during the same time. In the EU, it has stabilized at around 5 cases per annum per million population, although the rate in each country contributing data to EFSA/ECDC varies greatly.
There are four distinct clinical syndromes:
- Infection in pregnancy: "Listeria" can proliferate asymptomatically in the vagina and uterus. If the mother becomes symptomatic, it is usually in the third trimester. Symptoms include fever, myalgias, arthralgias and headache. Miscarriage, stillbirth and preterm labor are complications of this infection. Symptoms last 7–10 days.
- Neonatal infection (granulomatosis infantiseptica): There are two forms. One, an early-onset sepsis, with "Listeria" acquired in utero, results in premature birth. "Listeria" can be isolated in the placenta, blood, meconium, nose, ears, and throat. Another, late-onset meningitis is acquired through vaginal transmission, although it also has been reported with caesarean deliveries.
- Central nervous system (CNS) infection: "Listeria" has a predilection for the brain parenchyma, especially the brain stem, and the meninges. It can cause cranial nerve palsies, encephalitis, meningitis, meningoencephalitis and abscesses. Mental status changes are common. Seizures occur in at least 25% of patients.
- Gastroenteritis: "L. monocytogenes" can produce food-borne diarrheal disease, which typically is noninvasive. The median incubation period is 21 days, with diarrhea lasting anywhere from 1–3 days. Patients present with fever, muscle aches, gastrointestinal nausea or diarrhea, headache, stiff neck, confusion, loss of balance, or convulsions.
"Listeria" has also been reported to colonize the hearts of some patients. The overall incidence of cardiac infections caused by "Listeria" is relatively low, with 7-10% of case reports indicating some form of heart involvement. There is some evidence that small subpopulations of clinical isolates are more capable of colonizing the heart throughout the course of infection, but cardiac manifestations are usually sporadic and may rely on a combination of bacterial factors and host predispositions, as they do with other strains of cardiotropic bacteria.
Gram negative bacterial species are responsible for approximately 24% of all cases of healthcare-associated bacteremia and 45% of all cases of community-acquired bacteremia. In general, gram negative bacteria enter the bloodstream from infections in the respiratory tract, genitourinary tract, gastrointestinal tract, or hepatobiliary system. Gram-negative bacteremia occurs more frequently in elderly populations (65 years or older) and is associated with higher morbidity and mortality in this population.
"E.coli" is the most common cause of community-acquired bacteremia accounting for approximately 75% of cases. E.coli bacteremia is usually the result of a urinary tract infection. Other organisms that can cause community-acquired bacteremia include "pseudomonas aeruginosa", "klebsiella pneumoniae", and "proteus mirabilis". "Salmonella" infection, despite mainly only resulting in gastroenteritis in the developed world, is a common cause of bacteremia in Africa. It principally affects children who lack antibodies to Salmonella and HIV+ patients of all ages.
Among healthcare-associated cases of bacteremia, gram negative organisms are an important cause of bacteremia in the ICU. Catheters in the veins, arteries, or urinary tract can all create a way for gram negative bacteria to enter the bloodstream. Surgical procedures of the genitourinary tract, intestinal tract, or hepatobiliary tract can also lead to gram negative bacteremia. "Pseudomonas" and "enterobacter" species are the most important causes of gram negative bacteremia in the ICU.
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.
Treatment of infections caused by "Bartonella" species include:
Some authorities recommend the use of azithromycin.
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.
Some strains of group A streptococci (GAS) cause severe infection. Severe infections are usually invasive, meaning that the bacteria has entered parts of the body where bacteria are not usually found, such as the blood, lungs, deep muscle or fat tissue. Those at greatest risk include children with chickenpox; persons with suppressed immune systems; burn victims; elderly persons with cellulitis, diabetes, vascular disease, or cancer; and persons taking steroid treatments or chemotherapy. Intravenous drug users also are at high risk. GAS is an important cause of puerperal fever worldwide, causing serious infection and, if not promptly diagnosed and treated, death in newly delivered mothers. Severe GAS disease may also occur in healthy persons with no known risk factors.
All severe GAS infections may lead to shock, multisystem organ failure, and death. Early recognition and treatment are critical. Diagnostic tests include blood counts and urinalysis as well as cultures of blood or fluid from a wound site.
Severe Group A streptococcal infections often occur sporadically but can be spread by person-to-person contact.
Public Health policies internationally reflect differing views of how the close contacts of people affected by severe Group A streptococcal infections should be treated. Health Canada and the US CDC recommend close contacts see their doctor for full evaluation and may require antibiotics; current UK Health Protection Agency guidance is that, for a number of reasons, close contacts should not receive antibiotics unless they are symptomatic but that they should receive information and advice to seek immediate medical attention if they develop symptoms. However, guidance is clearer in the case of mother-baby pairs: both mother and baby should be treated if either develops an invasive GAS infection within the first 28 days following birth (though some evidence suggests that this guidance is not routinely followed in the UK).
Treatment for gastroenteritis due to "Y. enterocolitica" is not needed in the majority of cases. Severe infections with systemic involvement (sepsis or bacteremia) often requires aggressive antibiotic therapy; the drugs of choice are doxycycline and an aminoglycoside. Alternatives include cefotaxime, fluoroquinolones, and co-trimoxazole.
A study performed at Strong Memorial Hospital in Rochester, New York, showed that infants ≤ 60 days old meeting the following criteria were at low-risk for having a serious bacterial illness:
- generally well-appearing
- previously healthy
- full term (at ≥37 weeks gestation)
- no antibiotics perinatally
- no unexplained hyperbilirubinemia that required treatment
- no antibiotics since discharge
- no hospitalizations
- no chronic illness
- discharged at the same time or before the mother
- no evidence of skin, soft tissue, bone, joint, or ear infection
- White blood cells (WBCs) count 5,000-15,000/mm
- absolute band count ≤ 1,500/mm
- urine WBC count ≤ 10 per high power field (hpf)
- stool WBC count ≤ 5 per high power field (hpf) "only in infants with diarrhea"
Those meeting these criteria likely do not require a lumbar puncture, and are felt to be safe for discharge home without antibiotic treatment, or with a single dose of intramuscular antibiotics, but will still require close outpatient follow-up.
One risk for Group B streptococcal infection (GBS) is Preterm rupture of membranes. Screening women for GBS (via vaginal and rectal swabbing) and treating culture positive women with intrapartum chemoprophylaxis is reducing the number of neonatal sepsis caused by GBS.
Late-onset meningitis is most likely infection from the community. Late onset meningitis may be caused by other Gram-negative bacteria and "staphylococcal" species. In developing countries "Streptococcus pneumoniae" accounts for most cases of late onset.
Nephropathia epidemica ("NE" or epidemic nephropathy) is a type of viral haemorrhagic fever with renal syndrome (HFRS) caused by the Puumala virus. The incubation period is three weeks. Nephropathia epidemica has a sudden onset with fever, abdominal pain, headache, back pain and gastrointestinal symptoms. More severe symptoms include internal hemorrhaging. Although fatal in a small percentage of cases, nephropathia epidemica is generally milder than the HFRS that is caused by hantaviruses in other parts of the world. The bank vole is the reservoir for the virus, which humans contract through inhalation of aerosolised vole droppings.
The majority of infected individuals are asymptomatic or develop only mild symptoms, and the disease is not known to spread from human to human.
This infection is known as "sorkfeber" in Swedish and "myyräkuume" in Finnish (vole fever). In Norway, it is called "musepest" (mouse plague).
Yersiniosis is an infectious disease caused by a bacterium of the genus "Yersinia". In the United States, most yersiniosis infections among humans are caused by "Yersinia enterocolitica". The infection by "Y. enterocolitica" is also known as pseudotuberculosis. Yersiniosis is mentioned as a specific zoonotic disease to prevent outbreaks in European Council Directive 92/117/EEC.
Infection with " Y . enterocolitica" occurs most often in young children. The infection is thought to be contracted through the consumption of undercooked meat products, unpasteurized milk, or water contaminated by the bacteria. It has been also sometimes associated with handling raw chitterlings.
Another bacterium of the same genus, "Yersinia pestis", is the cause of Plague.
A subset of children with acute, rapid-onset of tic disorders and obsessive compulsive disorder (OCD) are hypothesized to be due to an autoimmune response to group A beta-hemolytic streptococcal infection (PANDAS).
In early-onset neonatal meningitis, acquisition of the bacteria is from the mother before the baby is born or during birth. The most common bacteria found in early-onset are group B "Streptococcus" (GBS), "Escherichia coli", and "Listeria monocytogenes". In developing countries, Gram-negative enteric (gut) bacteria are responsible for the majority of early onset meningitis.
Braxy is an disease which causes sudden death in sheep. It is caused by the bacterium "Clostridium septicum".
Braxy generallly occurs in winter, when sheep eat frosted root crops, or frosted grass. The frozen feed damages the mucosa (lining) of the abomasum, allowing "C. septicum" to enter, causing abomasitis and a fatal bacteremia.
Young sheep not protected with a vaccine are most commonly affected. If sheep are not found dead, signs include abdominal pain and recumbency. There is no treatment, and sheep usually die within 36 hours of the onset of signs. The carcass of sheep which died of braxy will often decompose more rapidly than expected.
Historically, the mutton of affected sheep was also referred to as braxy.
A vaccine against braxy was developed at the Moredun Research Institute in Scotland.
Braxy has been reported in Europe (particularly in Iceland, Norway and the UK), Australia and the United States.
In humans, "Erysipelothrix rhusiopathiae" infections most commonly present in a mild cutaneous form known as erysipeloid or fish poisoning. "E. rhusiopathiae" can cause an indolent cellulitis, more commonly in individuals who handle fish and raw meat. It gains entry typically by abrasions in the hand. Bacteremia and endocarditis are uncommon but serious sequelae. Due to the rarity of reported human cases, "E. rhusiopathiae" infections are frequently misidentified at presentation.
Yersinia pseudotuberculosis is a Gram-negative bacterium that causes Far East scarlet-like fever in humans, who occasionally get infected zoonotically, most often through the food-borne route. Animals are also infected by "Y. pseudotuberculosis". The bacterium is urease positive.