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The mortality of the disease in 1909, as recorded in the British Army and Navy stationed in Malta, was 2%. The most frequent cause of death was endocarditis. Recent advances in antibiotics and surgery have been successful in preventing death due to endocarditis. Prevention of human brucellosis can be achieved by eradication of the disease in animals by vaccination and other veterinary control methods such as testing herds/flocks and slaughtering animals when infection is present. Currently, no effective vaccine is available for humans. Boiling milk before consumption, or before using it to produce other dairy products, is protective against transmission via ingestion. Changing traditional food habits of eating raw meat, liver, or bone marrow is necessary, but difficult to implement. Patients who have had brucellosis should probably be excluded indefinitely from donating blood or organs. Exposure of diagnostic laboratory personnel to "Brucella" organisms remains a problem in both endemic settings and when brucellosis is unknowingly imported by a patient. After appropriate risk assessment, staff with significant exposure should be offered postexposure prophylaxis and followed up serologically for six months. Recently published experience confirms that prolonged and frequent serological follow-up consumes significant resources without yielding much information, and is burdensome for the affected staff, who often fail to comply. The side effects of the usual recommended regimen of rifampicin and doxycycline for three weeks also reduce treatment adherence. As no evidence shows treatment with two drugs is superior to monotherapy, British guidelines now recommend doxycycline alone for three weeks and a less onerous follow-up protocol.
Brucellosis in humans is usually associated with the consumption of unpasteurized milk and soft cheeses made from the milk of infected animals, primarily goats, infected with "Brucella melitensis" and with occupational exposure of laboratory workers, veterinarians, and slaughterhouse workers. Some vaccines used in livestock, most notably "B. abortus" strain 19, also cause disease in humans if accidentally injected. Brucellosis induces inconstant fevers, miscarriage, sweating, weakness, anaemia, headaches, depression, and muscular and bodily pain. The other strains, "B. suis" and "B. canis", cause infection in pigs and dogs, respectively.
The most common way the disease is spread is via arthropod vectors. Ticks involved include "Amblyomma", "Dermacentor", "Haemaphysalis", and "Ixodes". Rodents, rabbits, and hares often serve as reservoir hosts, but waterborne infection accounts for 5 to 10% of all tularemia in the US. Tularemia can also be transmitted by biting flies, particularly the deer fly "Chrysops discalis". Individual flies can remain infectious for 14 days and ticks for over two years.Tularemia may also be spread by direct contact with contaminated animals or material, by ingestion of poorly cooked flesh of infected animals or contaminated water, or by inhalation of contaminated dust.
The bacteria can penetrate into the body through damaged skin, mucous membranes, and inhalation. Humans are most often infected by tick/deer fly bite or through handling an infected animal. Ingesting infected water, soil, or food can also cause infection. Hunters are at a higher risk for this disease because of the potential of inhaling the bacteria during the skinning process. It has been contracted from inhaling particles from an infected rabbit ground up in a lawnmower (see below). Tularemia is not spread directly from person to person. Humans can also be infected through bioterrorism attempts.
Francisella tularensis can live both within and outside the cells of the animal it infections, meaning it is a facultative intracellular bacterium. It primarily infects macrophages, a type of white blood cell, thus is able to evade the immune system. The course of disease involves the spread of the organism to multiple organ systems, including the lungs, liver, spleen, and lymphatic system. The course of disease is different depending on the route of exposure. Mortality in untreated (before the antibiotic era) patients has been as high as 50% in the pneumoniac and typhoidal forms of the disease, which however account for less than 10% of cases.
"B. suis" is a Gram-negative, facultative, intracellular coccobacillus, capable of growing and reproducing inside of host cells, specifically phagocytic cells. They are also not spore-forming, capsulated, or motile. Flagellar genes, however, are present in the "B. suis" genome, but are thought to be cryptic remnants because some were truncated and others were missing crucial components of the flagellar apparatus. Interestingly, in mouse models, the flagellum is essential for a normal infectious cycle, where the inability to assemble a complete flagellum leads to severe attenuation of the bacteria.
"B. suis" is differentiated into five biovars (strains), where biovars 1-3 infect wild boar and domestic pigs, and biovars 1 and 3 may cause severe diseases in humans.
In contrast, biovar 2 found in wild boars in Europe shows mild or no clinical signs and cannot infect healthy humans, but does infect pigs and hares.
Swine brucellosis is a zoonosis affecting pigs, caused by the bacterium "Brucella suis". The disease typically causes chronic inflammatory lesions in the reproductive organs of susceptible animals or orchitis, and may even affect joints and other organs. The most common symptom is abortion in pregnant susceptible sows at any stage of gestation. Other manifestations are temporary or permanent sterility, lameness, posterior paralysis, spondylitis, and abscess formation. It is transmitted mainly by ingestion of infected tissues or fluids, semen during breeding, and suckling infected animals.
Since brucellosis threatens the food supply and causes undulant fever, "Brucella suis" and other "Brucella" species ("B. melitensis, B. abortis, B. ovis, B. canis") are recognized as potential agricultural, civilian, and military bioterrorism agents.
The U.S. Centers for Disease Control and Prevention (CDC) publishes a journal "Emerging Infectious Diseases" that identifies the following factors contributing to disease emergence:
- Microbial adaption; e.g. genetic drift and genetic shift in Influenza A
- Changing human susceptibility; e.g. mass immunocompromisation with HIV/AIDS
- Climate and weather; e.g. diseases with zoonotic vectors such as West Nile Disease (transmitted by mosquitoes) are moving further from the tropics as the climate warms
- Change in human demographics and trade; e.g. rapid travel enabled SARS to rapidly propagate around the globe
- Economic development; e.g. use of antibiotics to increase meat yield of farmed cows leads to antibiotic resistance
- Breakdown of public health; e.g. the current situation in Zimbabwe
- Poverty and social inequality; e.g. tuberculosis is primarily a problem in low-income areas
- War and famine
- Bioterrorism; e.g. 2001 Anthrax attacks
- Dam and irrigation system construction; e.g. malaria and other mosquito borne diseases
Several species of rickettsia bacteria cause anaplasmosis in ruminants:
- Cattle:
- "Anaplasma marginale" - found worldwide.
- "Anaplasma centrale" - found mainly in South America, Africa and the Middle East.
- Sheep and goats:
- "Anaplasma ovis" - found worldwide.
Vaccines against anaplasmosis are available. Carrier animals should be eliminated from flocks. Tick control may also be useful although it can be difficult to implement.
Methicillin-resistant Staphylococcus aureus (MRSA) evolved from Methicillin-susceptible Staphylococcus aureus (MSSA) otherwise known as common "S. aureus". Many people are natural carriers of "S. aureus", without being affected in any way. MSSA was treatable with the antibiotic methicillin until it acquired the gene for antibiotic resistance. Though genetic mapping of various strains of MRSA, scientists have found that MSSA acquired the mecA gene in the 1960s, which accounts for its pathogenicity, before this it had a predominantly commensal relationship with humans. It is theorized that when this "S. aureus" strain that had acquired the mecA gene was introduced into hospitals, it came into contact with other hospital bacteria that had already been exposed to high levels of antibiotics. When exposed to such high levels of antibiotics, the hospital bacteria suddenly found themselves in an environment that had a high level of selection for antibiotic resistance, and thus resistance to multiple antibiotics formed within these hospital populations. When "S. aureus" came into contact with these populations, the multiple genes that code for antibiotic resistance to different drugs were then acquired by MRSA, making it nearly impossible to control. It is thought that MSSA acquired the resistance gene through the horizontal gene transfer, a method in which genetic information can be passed within a generation, and spread rapidly through its own population as was illustrated in multiple studies. Horizontal gene transfer speeds the process of genetic transfer since there is no need to wait an entire generation time for gene to be passed on. Since most antibiotics do not work on MRSA, physicians have to turn to alternative methods based in Darwinian medicine. However prevention is the most preferred method of avoiding antibiotic resistance. By reducing unnecessary antibiotic use in human and animal populations, antibiotics resistance can be slowed.
Estimates of the rate of HCV vertical transmission range from 2–8%; a 2014 systematic review and meta-analysis found the risk to be 5.8% in HCV-positive, HIV-negative women. The same study found the risk of vertical transmission to be 10.8% in HCV-positive, HIV-positive women. Other studies have found the risk of vertical transmission to be as high as 44% among HIV-positive women. The risk of vertical transmission is higher when the virus is detectable in the mother's blood.
Evidence does not indicate that mode of delivery (i.e. vaginal vs. cesarean) has an effect on vertical transmission.
For women who are HCV-positive and HIV-negative, breastfeeding is safe; however, CDC guidelines suggest avoiding breastfeeding if a woman's nipples are "cracked or bleeding" to reduce the risk of transmission.
Vertical transmission is a significant contributor of new HBV cases each year, with 35–50% of transmission from mother to neonate in endemic countries. Vertical transmission occurs largely via a neonate's exposure to maternal blood and vaginal secretions during birth. While the risk of progression to chronic infection is approximately 5% among adults who contract the virus, it is as high as 95% among neonates subject to vertical transmission. The risk of viral transmission is approximately 10–20% when maternal blood is positive for HBsAg, and up to 90% when also positive for HBeAg.
Given the high risk of perinatal transmission, the CDC recommends screening all pregnant women for HBV at their first prenatal visit. It is safe for non-immune pregnant women to receive the HBV vaccine. Based on the limited available evidence, the American Association for the Study of Liver Diseases (AASLD) recommends antiviral therapy in pregnant women whose viral load exceeds 200,000 IU/mL. A growing body of evidence shows that antiviral therapy initiated in the third trimester significantly reduces transmission to the neonate. A systematic review of the Antiretroviral Pregnancy Registry database found that there was no increased risk of congenital anomalies with Tenofovir; for this reason, along with its potency and low risk of resistance, the AASLD recommends this drug. A 2010 systematic review and meta-analysis found that Lamivudine initiated early in the third trimester also significantly reduced mother-to-child transmission of HBV, without any known adverse effects.
The ACOG states that the evidence available does not suggest any particular mode of delivery (i.e. vaginal vs. cesarean) is better at reducing vertical transmission in mothers with HBV.
The WHO and CDC recommend that neonates born to mothers with HBV should receive hepatitis B immune globulin (HBIG) as well as the HBV vaccine within 12 hours of birth. For infants who have received HBIG and the HBV vaccine, breastfeeding is safe.
Although it is very uncommon, women undergoing surgical abortion after 18 weeks gestation sometimes give birth to a fetus that may survive briefly. Longer term survival is possible after 22 weeks.
If medical staff observe signs of life, they may be required to provide care: emergency medical care if the child has a good chance of survival and palliative care if not. Induced fetal demise before termination of pregnancy after 20–21 weeks gestation is recommended to avoid this.
Death following live birth caused by abortion is given the ; data are identified as either fetus or newborn. Between 1999 and 2013, in the U.S., the CDC recorded 531 such deaths for newborns, approximately 4 per 100,000 abortions.
The rate of cancer during pregnancy is 0.02–1%, and in many cases, cancer of the mother leads to consideration of abortion to protect the life of the mother, or in response to the potential damage that may occur to the fetus during treatment. This is particularly true for cervical cancer, the most common type of which occurs in 1 of every 2,000–13,000 pregnancies, for which initiation of treatment "cannot co-exist with preservation of fetal life (unless neoadjuvant chemotherapy is chosen)". Very early stage cervical cancers (I and IIa) may be treated by radical hysterectomy and pelvic lymph node dissection, radiation therapy, or both, while later stages are treated by radiotherapy. Chemotherapy may be used simultaneously. Treatment of breast cancer during pregnancy also involves fetal considerations, because lumpectomy is discouraged in favor of modified radical mastectomy unless late-term pregnancy allows follow-up radiation therapy to be administered after the birth.
Exposure to a single chemotherapy drug is estimated to cause a 7.5–17% risk of teratogenic effects on the fetus, with higher risks for multiple drug treatments. Treatment with more than 40 Gy of radiation usually causes spontaneous abortion. Exposure to much lower doses during the first trimester, especially 8 to 15 weeks of development, can cause intellectual disability or microcephaly, and exposure at this or subsequent stages can cause reduced intrauterine growth and birth weight. Exposures above 0.005–0.025 Gy cause a dose-dependent reduction in IQ. It is possible to greatly reduce exposure to radiation with abdominal shielding, depending on how far the area to be irradiated is from the fetus.
The process of birth itself may also put the mother at risk. "Vaginal delivery may result in dissemination of neoplastic cells into lymphovascular channels, haemorrhage, cervical laceration and implantation of malignant cells in the episiotomy site, while abdominal delivery may delay the initiation of non-surgical treatment."
These terms can apply to any species of mammal. Amongst domestic animals, metritis and endometritis are most common in cattle after parturition, and the diseases are often called postpartum metritis or postpartum endometritis. These diseases in cattle are caused by bacteria and occasionally viruses. The most common bacteria that cause postpartum metritis and endometritis in cattle are "Escherichia coli", "Trueperella" (previously "Arcanobacterium") "pyogenes" and anaerobic bacteria such as "Prevotella" species and "Fusobacterium necrophorum". The virus most consistently associated with postpartum uterine disease in cattle is Bovine Herpesvirus 4 (BoHV-4). In addition, "Several specific diseases are associated with metritis or endometritis. These include brucellosis, leptospirosis, campylobacteriosis, and trichomoniasis"
In cattle, bacterial infection of the uterus affects almost all animals after parturition. Of course this doesn't mean they will get disease. In fact beef cattle rarely have disease unless they have a predisposing factor such as retained placenta or difficult parturition. However, uterine disease is common in dairy cattle - particularly high-milk-yield cows such as Holstein-Friesian cows.
Contagious equine metritis is a sexually transmitted infection in horses, recognized since 1977.
In 2014 a study reported about the first successful vaccination trials in cattle. The infection rate declined significantly.Vinícius Silva Machado, Marcela Luccas de Souza Bicalho u. a.: "Subcutaneous Immunization with Inactivated Bacterial Components and Purified Protein of Escherichia coli, Fusobacterium necrophorum and Trueperella pyogenes Prevents Puerperal Metritis in Holstein Dairy Cows." In: "PLoS ONE." 9, 2014, S. e91734, .
Globally, infants are a population that are especially vulnerable to foodborne disease. The World Health Organization has issued recommendations for the preparation, use and storage of prepared formulas. Breastfeeding remains the best preventative measure for protection of foodborne infections in infants.
In addition to disease caused by direct bacterial infection, some foodborne illnesses are caused by enterotoxins (exotoxins targeting the intestines). Enterotoxins can produce illness even when the microbes that produced them have been killed. Symptom appearance varies with the toxin but may be rapid in onset, as in the case of enterotoxins of "Staphylococcus aureus" in which symptoms appear in one to six hours. This causes intense vomiting including or not including diarrhea (resulting in staphylococcal enteritis), and staphylococcal enterotoxins (most commonly staphylococcal enterotoxin A but also including staphylococcal enterotoxin B) are the most commonly reported enterotoxins although cases of poisoning are likely underestimated. It occurs mainly in cooked and processed foods due to competition with other biota in raw foods, and humans are the main cause of contamination as a substantial percentage of humans are persistent carriers of "S. aureus". The CDC has estimated about 240,000 cases per year in the United States.
- "Clostridium botulinum"
- "Clostridium perfringens"
- "Bacillus cereus"
The rare but potentially deadly disease botulism occurs when the anaerobic bacterium "Clostridium botulinum" grows in improperly canned low-acid foods and produces botulin, a powerful paralytic toxin.
"Pseudoalteromonas tetraodonis", certain species of Pseudomonas and Vibrio, and some other bacteria, produce the lethal tetrodotoxin, which is present in the tissues of some living animal species rather than being a product of decomposition.
Tobacco (cigarette) smokers have an increased risk of miscarriage. There is an increased risk regardless of which parent smokes, though the risk is higher when the gestational mother smokes.
Several intercurrent diseases in pregnancy can potentially increase the risk of miscarriage, including diabetes, polycystic ovary syndrome (PCOS), hypothyroidism, certain infectious diseases, and autoimmune diseases. PCOS may increases the risk of miscarriage. Two studies suggested treatment with the drug metformin significantly lowers the rate of miscarriage in women with PCOS, but the quality of these studies has been questioned. The use metformin treatment in pregnancy has not been shown to be safe. In 2007 the Royal College of Obstetricians and Gynaecologists also recommended against use of the drug to prevent miscarriage. Thrombophilias or defects in coagulation and bleeding were once thought to be a risk in miscarriage but have been subsequently questioned.
Severe cases of hypothyroidism increase the risk of miscarriage. The effect of milder cases of hypothyroidism on miscarriage rates has not been established. A condition called luteal phase defect (LPD) is a failure of the uterine lining to be fully prepared for pregnancy. This can keep a fertilized egg from implanting or result in miscarriage.
"Mycoplasma genitalium" infection is associated with increased risk of preterm birth and miscarriage.
Infections can increase the risk of a miscarriage: rubella (German measles), cytomegalovirus, bacterial vaginosis, HIV, chlamydia, gonorrhoea, syphilis, and malaria.
Metritis is inflammation of the wall of the uterus, whereas endometritis is inflammation of the functional lining of the uterus, called the endometrium The term pelvic inflammatory disease (PID) is often used for metritis.
In developed countries, the annual incidence of infective endocarditis is 3 to 9 cases per 100,000 persons. The male to female case ratio is over 2:1. There is an increased incidence of infective endocarditis in persons 65 years of age and older, which is probably because people in this age group have a larger number of risk factors for infective endocarditis. In recent years, over one third of infective endocarditis cases in the United States were healthcare-associated. Another trend observed in developed countries is that chronic rheumatic heart disease accounts for <10% of cases. Although a history of valve disease has a significant association with infective endocarditis, 50% of all cases develop in people with no known history of valvular disease.
Risk factors for infective endocarditis are based on the premise that in a healthy individual, bacteremia (bacteria entering the blood stream) is cleared quickly with no adverse consequences. However, if a heart valve is damaged, the bacteria can attach themselves to the valve, resulting in infective endocarditis. Additionally, in individuals with weakened immune systems, the concentration of bacteria in the blood can reach levels high enough to increase the probability that some will attach to the valve. Some significant risk factors are listed here:
1. Artificial heart valves
2. Intracardiac devices, such as Implantable cardioverter-defibrillators
3. Unrepaired cyanotic congenital heart defects
4. History of infective endocarditis
5. Chronic rheumatic heart disease, which is an autoimmune response to repeated "Streptococcus pyogenes" infection
6. Age-related degenerative valvular lesions
7. Hemodialysis, a medical procedure that filters the blood of individuals with kidney failure
8. Coexisting conditions, especially ones that suppress immunity. Diabetes mellitus, alcohol abuse, HIV/AIDS, and intravenous drug use all fall in this category
More detailed descriptions of these and other risk factors are provided below.
Other conditions that result in high number of bacteria entering into the bloodstream include colorectal cancer (mostly "Streptococcus bovis"), serious urinary tract infections (mostly enterococci), and drug injection ("Staphylococcus aureus"). With a large number of bacteria, even a normal heart valve may become infected.
A more virulent organism (such as "Staphylococcus aureus") can cause infective endocarditis by infecting even a normal heart valve.
Intravenous drug users tend to get their right-sided heart valves infected because the veins that are injected drain into the right side of the heart. In rheumatic heart disease, infection occurs on the aortic and the mitral valves on the left side of the heart.
Other factors that increase the risk of developing infective endocarditis are low levels of white blood cells, immunodeficiency or immunosuppression, malignancy, diabetes mellitus, and alcohol abuse.
The Great Imitator (also The Great Masquerader) is a phrase used for medical conditions that feature nonspecific symptoms and may be confused with a number of other diseases. Most great imitators are systemic in nature. Diseases sometimes referred to with this name include:
- Various cancers
- Intravascular large B-cell lymphoma
- Various rheumatic conditions, including:
- Fibromyalgia
- Psoriatic arthritis
- Lupus erythematosus
- Systemic lupus erythematosus
- Sarcoidosis
- Multiple sclerosis
- Celiac disease
- Addison's Disease
- Pulmonary embolism
- Various infectious diseases, including:
- Syphilis
- Lyme disease
- Nocardiosis
- Tuberculosis
- Brucellosis
- Malaria
- Breathing-related sleep disorders (chiefly sleep apnea/hypopnea and upper-airway resistance syndrome).
The Jarisch–Herxheimer reaction is traditionally associated with antimicrobial treatment of syphilis. The reaction is also seen in the other diseases caused by spirochetes: Lyme disease, relapsing fever, and leptospirosis. There have been case reports of the Jarisch-Herxheimer reaction accompanying treatment of other infections, including Q fever, bartonellosis, brucellosis, trichinellosis, and African trypanosomiasis.
Lipoproteins released from treatment of "Treponema pallidum" infections are believed to induce the Jarisch-Herxheimer reaction. The Herxheimer reaction has shown an increase in inflammatory cytokines during the period of exacerbation, including tumor necrosis factor alpha, interleukin-6 and interleukin-8.