Rat Bite Fever (RBF) & Exposure Risks
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In early 2014, the family of a San Diego County boy who died from rat-bite fever, believed to have been contracted from his pet rat the previous year, filed a lawsuit against the company that sold the rat. News of the 10 year old child’s death and subsequent lawsuit made national headlines.
Rat-bite fever (RBF) is an infectious disease that can be caused by two different types of bacteria. Streptobacillary RBF is caused by Streptobacillus moniliformis in North America while Spirillary RBF is caused by Spirillum minus and occurs mostly in Asia.
Both types of bacteria are part of the normal respiratory flora of rodents. Either organism may be transmitted to humans through bites or scratches. Infection can also result from handling an infected rodent (even with no reported bite or scratch), or ingestion of a contaminated food or drink. Although rats are considered the natural reservoir of RBF, the bacteria that cause the condition have also been found in other rodent species, such as mice and gerbils.
If not treated, RBF can be a serious or even fatal disease.
People who may be at increased risk of contracting RBF include those who:
• Live in rat-infested buildings
• Have pet rats in their home
• Work with rats in laboratories or pet stores
People can protect themselves from RBF by:
• Avoiding contact with rodents or places where rodents may be present
• Avoiding drinking or eating foods that may have come in contact with rodents
People who handle rats or clean their cages should:
• Wear protective gloves
• Practice regular hand washing
• Avoid touching their mouth with their hands
These are just a few things to know about RBF and exposure risks. To learn more about this or other health & safety, environmental or IAQ issues, please visit the websites shown in the video.
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Chapters
0:00 Introduction
0.59 Causes and Risk Factors of Leptospirosis
1:46 Symptoms of Leptospirosis
3:23 Diagnosis of Leptospirosis
3:47 Treatment of Leptospirosis
Leptospirosis is a blood infection caused by the bacteria Leptospira.[8] Signs and symptoms can range from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs or meningitis).[5] Weil’s disease, the acute, severe form of leptospirosis, causes the infected individual to become jaundiced (skin and eyes become yellow), develop kidney failure, and bleed.[6] Bleeding from the lungs associated with leptospirosis is known as severe pulmonary haemorrhage syndrome.[5]
More than ten genetic types of Leptospira cause disease in humans.[12] Both wild and domestic animals can spread the disease, most commonly rodents.[8] The bacteria are spread to humans through animal urine, or water and soil contaminated with animal urine, coming into contact with the eyes, mouth, nose or breaks in the skin.[8] In developing countries, the disease occurs most commonly in farmers and low-income people who live in areas with poor sanitation.[5] In developed countries, it occurs during heavy downpours and is a risk to sewage workers[13] and those involved in outdoor activities in warm and wet areas.[5] Diagnosis is typically by testing for antibodies against the bacteria or finding bacterial DNA in the blood.[5]
Efforts to prevent the disease include protective equipment to block contact when working with potentially infected animals, washing after contact, and reducing rodents in areas where people live and work.[7] The antibiotic doxycycline is effective in preventing leptospirosis infection.[7] Human vaccines are of limited usefulness;[14] vaccines for other animals are more widely available.[15] Treatment when infected is with antibiotics such as doxycycline, penicillin, or ceftriaxone.[8] The overall risk of death is 5–10%.[10] However, when the lungs are involved, the risk of death increases to the range of 50–70%.[8]
It is estimated that one million severe cases of leptospirosis occur every year, causing about 58,900 deaths.[11] The disease is most common in tropical areas of the world but may occur anywhere.[7] Outbreaks may arise after heavy rainfall.[7] The disease was first described by physician Adolf Weil in 1886 in Germany.[16][17]
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