Leptospirosis – Infection

Leptospirosis is a bacterial infection caused by long, thin, motile spirochetes belonging to the genus Leptospira, family Leptospiraceae, and order Spirochaetales. These spirochetes are finely coiled, thin, motile, obligate, slow-growing anaerobes. Their flagella allow them to burrow into tissue. More recent work has identified 7 distinct species of pathogenic leptospires, which appear as more than 250 serologic variants (serovars). They may be free-living or associated with animal hosts and survive well in freshwater, soil, and mud areas where they can live for weeks or months.

They can thrive in hot, humid environments but not in acidic environments. They are primarily contained in the genital and urinary tract. The disease is known as the most common zoonosis in the world, that is, it is the most common disease carried by animals and affects animals, including humans. The incidence varies from sporadic in temperate zones to endemic in a few tropical countries. The disease is often referred to as swineherd’s disease, or swamp fever, mud fever, Icterohemorrhagic fever, Rice-field fever, Cane-cutter fever, Hemorrhagic jaundice, Stuttgart disease, or Canicola fever.

Wild mammals are known to be the main reservoir of the leptospiral serovars. About 160 mammals including fats, skunks, raccoon, and cattle, have been termed as vectors or carriers of the disease. Rats are considered to be the most important reservoir. Transmission occurs by contamination of soil, water, or vegetation by urine excreted from infected animals. Humans can become infected upon contact of the contaminated material with abraded skin, mucous membranes such as conjunctiva or alimentrary tract, or ingestion of the contaminated material.

Occasionally, the organism may even enter the body through intact skin. Infection has occurred after animal and rodent bites, after contact with abortion products of infected animals, and after ingestion of contaminated food and water. The latter route of infection is believed to occur via the mucosa of the mouth and the esophagus because leptospires cannot survive in an acidic environment. Leptospires may persist for long periods in the renal tubules of animals by establishing a symbiotic relationship with no evidence of disease or pathological changes in the kidney.

Important source – What are Kidney Infections?

As a result, animals that serve as reservoirs of host-adapted serovars can shed high concentrations of the organism in their urine without showing clinical evidence of disease. Leptospiruria in humans is more transient, rarely lasting more than 60 days. Humans and nonadapted animals are incidental hosts. With rare exceptions, man represents a dead end in the chain of infection because person-to-person spread of the disease is rare. Most cases occur in the warm season and in rural areas because leptospires can persist in water for many months.

The leptospires from infected animals contaminate the warm lake water. They survive best in freshwater, damp alkaline soil, vegetation, and mud with temperatures higher than 22°C. Mucous surfaces of the mouth, pharynx, and esophagus may be crossed easily by pathogenic leptospires, as are mucous membranes of the bronchial tree and lung alveoli. Transmission via laboratory accidents may occur but is rare. The bacterium usually invades through the mucosa, multiplies in the blood and tissue. The resulting leptospiremia can spread to any part of the body but particularly affects the liver and kidney.

After the organism gains access to the kidney, it migrates to the interstitium, renal tubules, and tubular lumen, causing interstitial nephritis and tubular necrosis. When renal failure develops, it is usually due to tubular damage, but hypovolemia from dehydration and from altered capillary permeability can also contribute to renal failure. Liver involvement is seen as centrilobular necrosis with proliferation of Kupffer cells. Jaundice may occur as a result of hepatocellular dysfunction. Leptospires may also invade skeletal muscle, causing edema, vacuolization of myofibrils, and focal necrosis.

Muscular microcirculation is impaired and capillary permeability is increased, with resultant fluid leakage and circulatory hypovolemia. In severe disease, a disseminated vasculitic syndrome may result from damage to the capillary endothelium. Leptospires may invade the aqueous humor of the eye, where they may persist for many months, occasionally leading to chronic or recurrent uveitis. Incubation period is usually around 7 days but can range from 2-30 days. The infection causes systemic illness that often leads to renal and hepatic dysfunction.

Despite the possibility of severe complications, the disease is most often self-limited and nonfatal. Over time, a systemic immune response may eliminate the organism from the body but may also lead to a symptomatic inflammatory reaction that can produce secondary end-organ injury. The disease was first recognized as an occupational disease of sewer workers in 1883. In 1886, Weil described the clinical manifestations in four men who had severe jaundice, fever, and hemorrhage with renal involvement.

Inada et al.identified the causative agent in Japan in 1916. Occupational exposure probably accounts for 30-50% of human cases. The main occupational groups at risk include farm workers, veterinarians, pet shop owners, field agricultural workers, abattoir workers, plumbers, meat handlers and slaughterhouse workers, coal miners, workers in the fishing industry, military troops, milkers, and sewer workers. Although leptospirosis continues to be predominantly an occupational disease since 1970, it has also increasingly been recognized as a disease of recreation.

Recreational activities that present some risk include traveling to tropical areas, canoeing, hiking, kayaking, fishing, windsurfing, swimming, waterskiing, wading, riding trail-bikes through puddles, white-water rafting, and other outdoor sports played in contaminated water. Camping by and traveling to endemic areas also add some risk. Leptospirosis may be spread epidemically in large populations in conditions of widespread flooding. In Brazil, the highest incidence of leptospirosis occurs during the summer months when heavy rains and floods occur in urban areas.

Flooding on a smaller scale may also lead to individuals contracting the disease. Leptospirosis cases were found among those involved in the clean-up process. Urban dwellers are also at increased risk because these residents may be sporadically exposed to rat urine as inner cities deteriorate. The incidence is increasing in urban children. However, human disease remains mainly related to occupation. The natural course of leptospirosis falls into 2 distinct phases: septicemic and immune. During a brief period of 1-3 days between the 2 phases, the patient shows some improvement.

The first stage is called the septicemic or leptospiremic stage because the organism may be isolated from blood cultures, cerebrospinal fluid (CSF) and most tissues. During this stage, which lasts about 4-7 days, the patient develops a nonspecific flulike illness of varying severity. It is characterized by fever, chills, weakness, and myalgias, primarily affecting the calves, back, and abdomen. Other symptoms include sore throat, cough, chest pain, hemoptysis, rash, frontal headache, photophobia, mental confusion, and other symptoms of meningitis.

Because of the abrupt nature of the onset, the patient can often tell exactly when the symptoms started. During the 1-3 day period of improvement that follows the first stage, the temperature curve falls and the patient may become febrile and relatively asymptomatic. The fever then recurs, indicating the onset of the second stage when clinical or subclinical meningitis appears. The second stage is called the immune or leptospiruric stage because circulating antibodies may be detected or the organism may be isolated from urine; it may not be recoverable from blood or CSF.

This stage occurs as a consequence of the body’s immunologic response to infection and lasts 0-30 days or more. Disease referable to specific organs including the meninges, liver, eyes, and kidney is seen. Nonspecific symptoms, such as fever and myalgia, may be less severe than in the first stage and last a few days to a few weeks. Many patients (77%) experience headache that is intense and poorly controlled by analgesics; this often heralds the onset of meningitis. Aseptic meningitis is the most important clinical syndrome observed in the immune anicteric stage.

Meningeal symptoms develop in 50% of patients. Cranial nerve palsies, peripheral facial palsy, encephalitis, and changes in consciousness are less common. Mild delirium may also be seen. Symptoms may be nonspecific, and a viral etiology may be suspected. Meningitis usually lasts a few days but occasionally lasts 1-2 weeks. Death is extremely rare in the anicteric cases. Leptospires may be isolated from the blood for 24-48 hours after jaundice appears. Abdominal pain with diarrhea or constipation (30%), hepatosplenomegaly, nausea, vomiting, and anorexia are also seen.

Acalculous cholecystitis may be seen rarely but is clinically significant. Uveitis (2-10%) can develop early or late in the disease and has been reported to occur as late as one year after initial illness. Iridocyclitis and chorioretinitis are other late complications that may persist for years. These symptoms first manifest 3 weeks to 1 month after exposure. Subconjunctival hemorrhage is the most common ocular complication of leptospirosis, occurring in as many as 92% of patients. Leptospires may be present in the aqueous humor.

Renal symptoms (eg, azotemia, pyuria, hematuria, proteinuria, and oliguria are seen in 50% of patients with leptospirosis. Leptospires may be present in the kidney. Pulmonary manifestations occur in 20-70% of patients, usually have a benign course, and may occur in both the icteric and anicteric forms of the disease. However, pulmonary involvement is the main cause of death due to leptospirosis in some countries, usually as a result of pulmonary hemorrhage or acute respiratory distress syndrome. Indeed, the severe pulmonary form of leptospirosis (SPFL) is considered to be one of the major causes of death in patients with severe leptospirosis.

Adenopathy, rashes, and muscular pain are also seen. Weil syndrome is the severe form of leptospirosis and primarily manifests as profound jaundice, renal dysfunction, hepatic necrosis, pulmonary dysfunction, and hemorrhagic diathesis. Approximately 90% of patients manifest a mild anicteric form of the disease, and approximately 5-10% have the severe form with jaundice, otherwise known as Weil disease.

Leptospirosis infection has protean manifestations. As a result, it is frequently misdiagnosed. Approximately 15-40% of exposed patients who do not become ill have serologic evidence of past infection. This statistic includes 15% of abattoir workers, packinghouse workers, and veterinarians. Diagnosis can be made from culturing the Leptospira bacteria from: bodily fluids (during the 1st to the 7th days); cerebrospinal fluid (during days 4-10); and urine (after the 10th day).

diagnosis can also be made from some laboratory exams such as: Microscopic Agglutination Test (MAT), which detects rising antibody titers in a given serologic test; Macroscopic Slide Agglutination Test, which allows presumptive diagnosis because it uses killed antigen, so it is good for screening but is not specific; or Enzyme-Linked Immunnosorbent Assay (ELISA), which uses a broadly reactive antigen, and since it detects IgM, it may be useful for diagnosis within 3-5 days.

Leptospirosis is generally underdiagnosed and underreported because many cases are asymptomatic or mildly symptomatic, self-limited, and nonfatal. For prevention, there is no widely accepted vaccine for human use in the United States, but there are some serovar-specific vaccines used in some European and Asian countries. Taking specific antibiotics prior to exposure to high-risk areas has shown 95% efficacy against the disease.

People who are continually and regularly exposed to these high-risk areas (usually because of occupation) must wear protective clothing, boots, and gloves to minimize exposure to the bacteria. Also, one must avoid ingestion of potentially contaminated soil or water, and swimming and wading in ponds, streams, and lakes with open cuts and sores. The community must also maintain proper rodent control in areas where both humans and their pets may be exposed to the bacteria. Lastly, one must always exercise proper hygiene, including proper handwashing procedures, especially in case of contamination.

Treatment can be done orally, for mild symptoms, or intravenously, if the case is already serious. Oral treatments include antibiotics, particularly doxycyline, ampicillin, azithromycin, ceftriaxone, streptomycin, or amoxicillin. For the more severe cases, intravenous penicillin G is used, and alternatives include amoxicillin, or erythromycin. Hospitalization is usually required and may range from a few weeks to several months, depending on the response of the patient to the medicines given.

Possible complications may occur such as Jarisch-Herxheimer reaction when penicillin is given, meningitis, and severe bleeding.

References: http://www. cdc. gov/leptospirosis/infection/index. html http://en. wikipedia. org/wiki/Leptospirosis http://emedicine. medscape. com/article/788751-overview#a0101 http://aeneary. myweb. uga. edu/lepto. htm http://www. medicinenet. com/leptospirosis/article. htm http://www. emedicine. medscape. com http://www. cdc. gov http://www. who. int http://www. nlm. nih. gov/medlineplus/ency/article/001376. htm.

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