Monday, December 29, 2008
Wednesday, December 17, 2008
TICKS
Ticks are found worldwide. They are blood-sucking, opportunistic parasites that can attach to the skin of a variety of vertebrate hosts. They have no segmentation and are dorsoventrally flat with four pairs of legs .
Although all stages of the tick life cycle can suck blood, it is normally the adult tick that poses a problem for humans. Human tick-associated diseases are most common in the summer months when the likelihood of contact increases during outdoor activities, usually in wooded areas. Being bitten by a tick is often painless and the presence of the tick may not be detected for some time. Often the tick poses no problem for the human host other than an erythromatous papule and it drops off after engorging on blood. Sometimes, the site of attachment may itch and become painful. Secondary infections of the wound site may occur, often as a result of the mouthparts remaining attached after the tick is removed.
Ticks can attach anywhere on the body but are frequently found at the hairline, around the ears, groin, armpits etc.
Whilst the bites of most ticks are inconsequential, they can carry a number of human disease agents including viruses, bacteria and protozoa. There are two families of ticks: the hard ticks (Ixodidae) and the soft ticks (Argasidae) .The Ixodidae attach to their host over a prolonged period of time (several days) while the Argasidae feed rapidly and then drop off. Consequently, they are frequently undetected.
Although most tick-associated problems arise from disease-causing organisms carried by the ticks, in one case – tick paralysis – the problem arises directly from toxins in the tick’s saliva.
Important disease-carrying ticks in the United States are:
Hard ticks:
Dog tick (Dermacentor variabilis) which is found east of the Rocky Mountains and in some areas of the Pacific coast states
Rocky Mountain Wood Tick (Dermacentor andersoni) . As its name suggests, it is found in the Rocky Mountains and also in southwest Canada
Deer Tick (Black-legged tick) (Ixodes scapularis) . This occurs in the north east and north central United States.
Western black legged tick (Ixodes pacificus) which is found in the Pacific coast states of the United States.
Brown dog tick (Rhipicephalus sanuguineus). Also known as the red dog tick . This is found world-wide (all over the US and also southeast Canada) and can complete its entire life cycle indoors. It primarily infests dogs but can feed on other mammals including man.
Lone star tick (Amblyomma americanum) , found in south eastern and south central United States.
Soft ticks:
Various species of Ornithodoros are found in the western United States. The family Argasidae is divided into four genera: Argas, Ornithodoros, Antricola, and Otobius .
DISEASES FOR WHICH HARD TICKS ARE CARRIERS
BACTERIAL DISEASES
ROCKY MOUNTAIN SPOTTED FEVER
There are several hundred reported cases of Rocky Mountain Spotted Fever each year in the United States (ranging, during the past half century, from a low of about 200 to more than 1200 in the early 1980’s). The numbers are again rising (figure 4). Most at risk are children under 15 years of age. Usually, cases occur in the summer because of higher numbers of ticks and more frequent contact of humans with ticks .
EpidemiologyThe causative agent, Ricketsia rickettsii, is carried by the Brown Dog tick and the Rocky Mountain Wood Tick (the two Dermacentor species in the United States). Contrary to its name, only a small proportion of cases are actually reported from the Rocky Mountain states. The highest number of cases in the United States occurs in the south-east and south central regions with the greatest incidence in Oklahoma and North Carolina.
Elsewhere in central and south America, Rhipicephalus sanguineus and Amblyomma cajennense carry Ricketsia rickettsii. The disease is known as fiebre manchada in Mexico; São Paulo fever or fiebre maculosa in Brazil; tick typhus or Tobia fever in Colombia.
SymptomsR. rickettsii is a small bacterium that grows inside cells, particularly endothelial cells that form the walls of small blood vessels . The disease is characterized by nausea, appetite-loss, fever, myalgia and headache. These are followed, 3 to 5 days after the tick bite, by the characteristic rash , which results from leakage of the blood vessels as a result of infected and dying endothelial cells.
Initially, the rash is formed of small, flat, pink, non-itchy macules (spots) on the wrists, forearms, and ankles . Subsequently, the macules become raised on the skin and there is pain (in the abdomen and joints) and diarrhea. The characteristic red rash, which occurs in up to 60% of patients, is found at the extremities (the palms and soles of feet). A minority of patients never progress to this stage. Laboratory tests show thrombocytopenia, hyponatremia and/or elevated levels of liver enzymes. Severe cases require hospitalization and can result in paralysis of the extremities and may even be life-threatening. Very severe sequelae include gangrene that may result in amputation, deafness, and incontinence.
TreatmentTreatment is by antibiotics (doxycycline). Since, if untreated, Rocky Mountain Spotted Fever can be fatal, treatment should be started as soon as this disease is suspected and before any diagnosis is confirmed by laboratory tests.
Laboratory detectionSerologic assays including indirect immunofluorescence microscopy.
PreventionClothes that cover body and anti-tick sprays (often containing DEET) are most often used. It is best to keep away from heavily tick-infested areas. If ticks are discovered on the body, they should be removed immediately using fingers or tweezers.
TULAREMIA
This is also carried by the two Dermacentor species. Tularemia is caused by the bacterium Francisella tularensis, which is carried by rodents, rabbits and hares; as a result tularemia is otherwise known as rabbit fever. One of the several ways that humans can be infected is by being bitten by a tick that has acquired the bacterium after biting one of these animals; however, it can also be inhaled during the handling of infected rodents. There have been no reports to person-to-person transmission. Francisella tularensis is very infectious. Tularemia occurs all across the continental United States but is relatively rare, with about 200 cases being reported each year .
SymptomsThe symptoms of tularemia, which can be fatal if untreated, vary according to the route by which the infection was acquired; often the patient experiences swollen lymph glands, skin ulcers , inflammation of the eyes and throat, diarrhea. This may be followed by atypical pneumonia, pleuritis, and hilar lymphadenopathy. Inhaled tularemia results in rapid fever, chills, headache, myalgia, joint pain, dry cough, and progressive weakness. The pneumonia can result in respiratory distress and failure with blood in the sputum.
Diagnosis is initially from the symptoms but confirmatory laboratory tests using Gram or other stains or immunofluorescence microscopy are used to visualize the infecting bacteria.
TreatmentOral antibitotc treatment using streptomycin, gentamycin, tetracyclines (e.g. doxycycline) or fluoroquinolones, (e.g. ciprofloxacin) is the major form of therapy. Streptomycin or gentamicin can be used intravenously. There is a vaccine that is made from avirulent F. tularensis biovar palaearctica (type B). In addition, antibiotics can be used as post-exposure prophylaxis before the onset of symptoms if infection by F. tularensis is suspected.
Q FEVER
Various farm animals (cattle sheep goats etc) are the primary carriers of the bacterium Coxiella burnetii which causes Q fever. Spread to humans is usually via inhalation of dust containing dried urine, feces etc of infected animals. However, less commonly, the bacterium can be transmitted via the bite of Dermacentor ticks. Ingestion of contaminated milk can also lead to infection. C. burnetii infects macrophages and survives in the phagolysosome, where the bacteria multiply. The bacteria are released by lysis of the cells and phagolysosomes.SymptomsAcute Q feverMany patients, about half, show no signs of infection but in others after an incubation period of 1 - 2 weeks, there is a sudden onset of fever, headache, general malaise, myalgia, sore throat, chills, sweats, non-productive cough, nausea, vomiting, diarrhea, abdominal pain, and chest pain. The patient may also appear confused. Many patients go on to the symptoms of pneumonia and hepatitis but most recover in a month or two without treatment although acute Q fever has a mortality rate of 1-2%.
Chronic Q feverIf the patient fails to resolve the infection, chronic Q fever results. This can occur a few months after primary infection but can also occur many years later. Endocarditis of the aortic heart valves is the major problem that arises. This usually occurs in people with heart valve disease but also at risk are transplant, cancer and kidney disease patients. The chronic form of Q fever has a fatality rate of about 60 - 70%.
DiagnosisSerology to determine the presence of antibodies against Coxiella burnetii is used.
TreatmentAntibiotics such as doxycyline are used to treat acute Q fever. For chronic Q fever, two protocols have been investigated: doxycycline along with quinolones for at least 4 years and doxycycline with hydroxychloroquine for 1.5 to 3 years.
There is a vaccine used in Australia for persons who may come in contact with C. burnettii but it is not commercially available in the United States.
EHRLICHOSIS
HUMAN EHRLICHOSIS
Human ehrlichosis is carried by Dermacentor variabilis and by Amblyomma americanum and is caused by a number of bacteria of the Ehrlichia family, in the United States principally by Ehrlichia chaffeensis. These bacteria are small gram-negative organisms that infect leukocytes . As with many tick-borne diseases, incidence follows vector distribution with higher incidence during the summer months when tick populations and contact with them are higher. The number of cases has been increasing .
SymptomsAfter an incubation of period of a week to 10 days, the patient presents with myalgia, headache and general malaise. There can also be nausea, vomiting, diarrhea, cough, joint pains and the patient may be confused. Sometimes, there is a rash but this is normally only in pediatric cases. If left untreated, more severe manifestations of the infection can occur, including prolonged fever, renal failure, disseminated intravascular coagulopathy, meningoencephalitis, adult respiratory distress syndrome, seizures, or coma. Mortality rate at this stage is 2 - 3%. More at risk are immune-suppressed patients.
DiagnosisMicroscopy using blood smears or serology to detect anti-Ehrlichia antibodies can be used.
TreatmentAntibiotics such as doxycycline are the recommended treatment.
HUMAN GRANULOCYTIC EHRLICHIOSIS
Human granulocytic ehrlichiosis is caused by a species of Ehrlichia similar to species found in animals (Ehrlichia equi and Ehrlichia phagocytophila) and is transmitted by blacklegged ticks (Ixodes scapularis) and western blacklegged ticks (Ixodes pacificus).
LYME DISEASE
Lyme disease is caused by the spirochete bacterium, Borrelia burgdorferi , which typically infects small mammals in the northeast and north central United States. It is transmitted to humans by Ixodid black legged ticks (deer ticks). There are over 20,000 cases per year in the United States making it the most common tick-borne disease in North America. The disease was first described from the town of Old Lyme in Connecticut but is found on both the east and west coasts and in the Mississippi valley . In Europe, a similar disease is caused by Borrelia garinii or Borrelia afzelii.
Symptoms
Fever, headache and malaise and a characteristic rash named erythemia migrans , which can occur in a few days but sometimes only after a few weeks, are typical of Lyme Disease. The rash (which is usually not painful) often has a bull’s eye appearance since as it grows (up to 30 cm across) the central region clears. If left untreated, the infection spreads and can result in Bell’s Palsy (partial paralysis of muscles in one or both sides of the face), meningitis, heart palpitations and severe joint pain. These symptoms usually resolve in a few weeks but after several months about 60% of patients will get severe joint swelling and arthritis. A small minority may also get neurologic symptoms (tingling of the extremities, shooting pains, numbness)
TreatmentEarly administration with antibiotics (doxycycline, amoxicillin, or cefuroxime axetil) is recommended. Some patients continue with neurological and muscle pain problems even after antibiotic treatment. It is not known what causes these but they may be autoimmune in nature.
DiagnosisVarious laboratory tests include Elisa, western blot
SOUTHERN TICK-ASSOCIATED RASH ILLNESS
This rash is similar to that seen in Lyme disease. The causative organism is not known but it is not Borrelia burgdorferi, the Lyme disease agent. The lone star tick, Amblyomma americanum, is the transmission vector.
SymptomsMalaise, fever, myalgia, arthralgia and a “bulls eye” rash at the site of the tick bite. There are no chronic neurological symptoms as are seen with Lyme disease
TreatmentThe usual oral antibiotics are used and the symptoms quickly resolve.
PROTOZOA
BABESIOSIS
Babesiosis is carried by species of Ixodes including the deer tick (Ixodes scapularis) in the north and mid-west of the United States and in other countries, including Europe. Babesia microti is the usual causative organism and is a hemoprotozoan (i.e. it circulates in the bloodstream). Normally, the two hosts of Babesia microti are ticks and peromyscus mice (Peromyscus leucopus). The tick infects the mice with sporozoites, which reproduce asexually in erythrocytes. These escape to the blood stream where they may form male and female gametes that are taken up by the tick during a blood meal. In the tick, the gametes fuse and go through a sporogonic cycle to form more sporozoites. Humans can also acquire sporozoites when bitten by an infected tick and are usually dead-end hosts but babesiosis has been transmitted to other humans via blood transfusions .
In most cases, infection is asymptomatic but after a week to a month, symptoms can appear. These include fever, chills, sweating, myalgias and fatigue. In severe cases, hepatosplenomegaly and hemolytic anemia can occur. Normally, the patient recovers, although severe cases occur in immuno-compromised patients and the elderly.
Disease cause by another protozoan, Babesia divergens, can cause more severe and sometimes fatal cases of babesiosis.
DiagnosisDiagnosis is by serology, immunofluorescence microscopy and by direct observation of the parasite in blood smears in which “Maltese Cross”-like inclusions in erythrocytes are seen . These consist of four budding merozoites attached together.
TreatmentUsual antibiotics used are clindamycin plus quinine or atovaquone plus azithromycin.
VIRUSES
CRIMEAN-CONGO HEMORRHAGIC FEVER
This is caused by a Nairovirus, a member of the Bunyaviridae. It is found in Eastern Europe and throughout the Mediterranean areas of southern Europe, the Middle East, Africa, northwestern China, central and south Asia. Ixorid ticks (genus Hyalomma) spread the virus, which is also carried by numerous species of domestic and wild animals. Person to person transmission through infected blood and other body fluids has been documented.
SymptomsInitially, the patient presents with headache, high fever, back pain, joint pain, stomach pain, and vomiting. There may be flushing, red eyes and throat and small red spots called petechiae on the palate. Hemorrhage ensues after a few days and lasts for a few weeks. this is indicated by severe bruising, nosebleeds, and failure to stop bleedings after a cut or injection. Slow recovery often ensues but mortality can be as high as 50%.
TreatmentSince this is a viral disease, treatment is largely supportive with particular attention to electrolyte balance. Ribavirin has been used. An inactivated vaccine has been used in Eastern Europe.
COLORADO TICK FEVER
This is sometimes confused with a mild case of Rocky Mountain Spotted Fever but Colorado Tick Fever is caused by a coltivirus, a member of the reoviruses. They are endemic to north western North America and are found in Ixodid ticks. The virus distribution closely matches that of its vector, Dermacentor andersoni.
Person-to-person transmission can occur by blood. Prolonged viremia observed in humans and rodents is due to the intraerythrocytic location of virions, which protects them from immune clearance.
SymptomsInfection results in abrupt fever, chills, headache, retro-orbital pain, photophobia, myalgia, abdominal pain, and malaise. Sometimes fever can be diphasic or triphasic, usually lasting for 5 to 10 days. Severe forms of the disease that involve infection of the central nervous system or hemorrhagic fever, pericarditis, myocarditis, and orchitis have been rarely observed, mainly in children. Severity is sufficient to result in hospitalization of approximately 20% of patients. There has been evidence of transmission from mother to child.
FAR EASTERN TICK-BORNE ENCEPHALITIS (Also known as Russian spring-summer encephalitis or Taiga encephalitis)This is caused by a flavivirus which is spread by ixodid ticks (Ixodes persulcatus, I. ricinus and I. cookie). Small animals are the reservoir and the virus is endemic to the former Soviet Union and parts of eastern and central Europe.
SymptomsAbout two weeks after infection, there is a mild influenza-like disease that normally resolves in a few days but which can be followed by meningitis and meningoencephalitis in about one third of cases. In some cases, there may be partial paralysis and mortality may be as high as 25%.
TreatmentSupportive care is normal. There is a vaccine of killed virus that is available in Europe.
POWASSAN ENCEPHALITIS
This is a rare disease caused by a flavivirus carried by Ixodid ticks. There has been less than one case per year reported in the United States but mortality is high. It is widespread in North America and is found in small animal populations including woodchucks.
SymptomsAfter a relatively long incubation period of up to one month, the patient may present with a sore throat, dizziness, headache and confusion. This can proceed to general malaise, vomiting, respiratory distress, fever and convulsions, which then lead to paralysis and possibly coma. Because the virus attacks brain tissue, survivors can have severe neurological problems.
TreatmentSupportive care is indicated.
TICK-BORNE ENCEPHALITIS (Also known as biphasic meningoencephalitis, central European tick-borne encephalitis, Czechoslovak tick-borne encephalitis, diphasic milk fever or viral meningoencephalitis)
This disease results from infection by tick-borne encephalitis virus, which is a member of the Flaviviridae.
SymptomsTick-borne encephalitis starts as mild influenza-like symptoms with fever accompanied by leuko- and thrombocytopenia. This resolves within a few days. However, about one third of patients develop meningitis and meningoencephalitis. This can, in a few cases, be followed by paralysis. The European form of the disease has a mortality rate of under 5%. Most patients recover but about a third may have long-lasting neurological problems.
TreatmentSupportive is indicated. There is an experimental killed vaccine in Europe. In Sweden TBE vaccination is recommended for residents of and regular visitors to TBE endemic areas.
KYASANUR FOREST DISEASE
This disease is similar to Russian spring-summer encephalitis and is also caused by flaviviruses. It is found only in the Kyasanur forest of Northern India. The disease occurs during the dry season as its tick vector (Haemaphyalis spinigera) begins to feed on humans. Local carriers are shrews and monkeys.
LOUPING ILL VIRUS
This is found in the British Isles and is caused by a flavivirus that is carried by pheasants and sheep, among other animals. It can infect many hosts via the tick vector, Ixodes ricinus. It causes mild encephalitis that gives the infected animal an unusual gait (hence its name). However, it can kill livestock and humans not given proper supportive care.
DISEASE CAUSED DIRECTLY BY HARD TICKS
TICK PARALYSIS
In addition to being carriers of disease-causing microorganisms, some ticks (Amblyomma americanum and the two Dermacentor species) can cause tick paralysis. This is a rare disease caused by toxin in the saliva of the tick and results in an acute, ascending, flaccid paralysis caused by reduced acetyl choline or motor neuron action potentials. The paralysis, which is not associated with pain, starts a few days after the bite and comes on gradually over a period of days. The paralysis resolves surprisingly rapidly, usually within a day of the removal of the tick but if the tick is not removed the mortality rate, as a result of respiratory paralysis, can be as high as 10%. Tick paralysis can be confused with other acute neurologic disorders or diseases (e.g., Guillain-Barré syndrome or botulism).
DISEASE FOR WHICH SOFT TICKS ARE CARRIERS
BACTERIA
TICK-BORNE RELAPSING FEVER
Tick-borne relapsing fever is a rare disease (about 25 cases per year in the United States) and is caused by several spirochete bacterial species of the Borelia family. The transmission agents are soft ticks of the genus Ornithodoros. Soft ticks (family Argasidae) differ in many ways from the so-called hard ticks (family Ixodidae), but the most important is that they take brief meals from their host and then drop off. The bite is usually painless. Thus, they are far less likely to be found than the hard ticks that stay attached while feeding for hours. In the wild, these ticks are found in nesting materials when not feeding on their animal host. All stages of the life cycle can take blood meals.
The individual Borrelia species that cause tick-borne relapsing fever are usually associated with specific Ornithodoros tick vectors. B. hermsii is transmitted to humans by Ornithodoros hermsi, B. parkerii is transmitted by Ornithodoros parkeri and B. turicatae is transmitted by Ornithodoros turicata. Each tick is associated with a preferred environment and hosts. Ornithodoros hermsi is found at higher altitudes (1500 – 8000 feet) where it is associated usually with ground squirrels, tree squirrels and chipmunks. Ornithodoros parkeri occurs at lower elevations and inhabit caves and the burrows of ground squirrels, prairie dogs and burrowing owls. Ornithodoros turicata occurs in caves and ground squirrel, prairie dog or burrowing owls burrows in the plains regions of the Southwest United States.
SymptomsInitially, the patient experiences arthralgia, myalgia, headache, chills and fever. This is followed by nausea, cough, photophobia, and dizziness. The patient may be confused. There is often a rash. The incubation period before the onset of the first symptoms is about a week (though it can be shorter or longer). After the onset of disease, symptoms last a few days and then resolve. After a week or two, the symptoms reoccur and in the absence of treatment, recurrence continues for several more episodes. As the fever resolves, the patient may go through a crisis in which first there is a high fever accompanied by confusion and delirium. This “chill phase” lasts up to half an hour. Then there is the “flush phase” in which the temperature drops accompanied by profuse sweating and sometimes a drop in blood pressure.
DiagnosisMicroscope smears of blood, bone marrow or cerebrospinal fluid stained with Giemsa or acridine orange. Serologic testing is also available.
TreatmentAntibiotics are used and symptoms resolve a few days. There can, however, be long-term sequelae including heart and kidney problems, peripheral nerve involvement, ophthalmia, and abortion. Without treatment mortality may be up to 10% of patients.
Whilst the bites of most ticks are inconsequential, they can carry a number of human disease agents including viruses, bacteria and protozoa. There are two families of ticks: the hard ticks (Ixodidae) and the soft ticks (Argasidae) .The Ixodidae attach to their host over a prolonged period of time (several days) while the Argasidae feed rapidly and then drop off. Consequently, they are frequently undetected.
Although most tick-associated problems arise from disease-causing organisms carried by the ticks, in one case – tick paralysis – the problem arises directly from toxins in the tick’s saliva.
Important disease-carrying ticks in the United States are:
Hard ticks:
Dog tick (Dermacentor variabilis) which is found east of the Rocky Mountains and in some areas of the Pacific coast states
Rocky Mountain Wood Tick (Dermacentor andersoni) . As its name suggests, it is found in the Rocky Mountains and also in southwest Canada
Deer Tick (Black-legged tick) (Ixodes scapularis) . This occurs in the north east and north central United States.
Western black legged tick (Ixodes pacificus) which is found in the Pacific coast states of the United States.
Brown dog tick (Rhipicephalus sanuguineus). Also known as the red dog tick . This is found world-wide (all over the US and also southeast Canada) and can complete its entire life cycle indoors. It primarily infests dogs but can feed on other mammals including man.
Lone star tick (Amblyomma americanum) , found in south eastern and south central United States.
Soft ticks:
Various species of Ornithodoros are found in the western United States. The family Argasidae is divided into four genera: Argas, Ornithodoros, Antricola, and Otobius .
DISEASES FOR WHICH HARD TICKS ARE CARRIERS
BACTERIAL DISEASES
ROCKY MOUNTAIN SPOTTED FEVER
There are several hundred reported cases of Rocky Mountain Spotted Fever each year in the United States (ranging, during the past half century, from a low of about 200 to more than 1200 in the early 1980’s). The numbers are again rising (figure 4). Most at risk are children under 15 years of age. Usually, cases occur in the summer because of higher numbers of ticks and more frequent contact of humans with ticks .
EpidemiologyThe causative agent, Ricketsia rickettsii, is carried by the Brown Dog tick and the Rocky Mountain Wood Tick (the two Dermacentor species in the United States). Contrary to its name, only a small proportion of cases are actually reported from the Rocky Mountain states. The highest number of cases in the United States occurs in the south-east and south central regions with the greatest incidence in Oklahoma and North Carolina.
Elsewhere in central and south America, Rhipicephalus sanguineus and Amblyomma cajennense carry Ricketsia rickettsii. The disease is known as fiebre manchada in Mexico; São Paulo fever or fiebre maculosa in Brazil; tick typhus or Tobia fever in Colombia.
SymptomsR. rickettsii is a small bacterium that grows inside cells, particularly endothelial cells that form the walls of small blood vessels . The disease is characterized by nausea, appetite-loss, fever, myalgia and headache. These are followed, 3 to 5 days after the tick bite, by the characteristic rash , which results from leakage of the blood vessels as a result of infected and dying endothelial cells.
Initially, the rash is formed of small, flat, pink, non-itchy macules (spots) on the wrists, forearms, and ankles . Subsequently, the macules become raised on the skin and there is pain (in the abdomen and joints) and diarrhea. The characteristic red rash, which occurs in up to 60% of patients, is found at the extremities (the palms and soles of feet). A minority of patients never progress to this stage. Laboratory tests show thrombocytopenia, hyponatremia and/or elevated levels of liver enzymes. Severe cases require hospitalization and can result in paralysis of the extremities and may even be life-threatening. Very severe sequelae include gangrene that may result in amputation, deafness, and incontinence.
TreatmentTreatment is by antibiotics (doxycycline). Since, if untreated, Rocky Mountain Spotted Fever can be fatal, treatment should be started as soon as this disease is suspected and before any diagnosis is confirmed by laboratory tests.
Laboratory detectionSerologic assays including indirect immunofluorescence microscopy.
PreventionClothes that cover body and anti-tick sprays (often containing DEET) are most often used. It is best to keep away from heavily tick-infested areas. If ticks are discovered on the body, they should be removed immediately using fingers or tweezers.
TULAREMIA
This is also carried by the two Dermacentor species. Tularemia is caused by the bacterium Francisella tularensis, which is carried by rodents, rabbits and hares; as a result tularemia is otherwise known as rabbit fever. One of the several ways that humans can be infected is by being bitten by a tick that has acquired the bacterium after biting one of these animals; however, it can also be inhaled during the handling of infected rodents. There have been no reports to person-to-person transmission. Francisella tularensis is very infectious. Tularemia occurs all across the continental United States but is relatively rare, with about 200 cases being reported each year .
SymptomsThe symptoms of tularemia, which can be fatal if untreated, vary according to the route by which the infection was acquired; often the patient experiences swollen lymph glands, skin ulcers , inflammation of the eyes and throat, diarrhea. This may be followed by atypical pneumonia, pleuritis, and hilar lymphadenopathy. Inhaled tularemia results in rapid fever, chills, headache, myalgia, joint pain, dry cough, and progressive weakness. The pneumonia can result in respiratory distress and failure with blood in the sputum.
Diagnosis is initially from the symptoms but confirmatory laboratory tests using Gram or other stains or immunofluorescence microscopy are used to visualize the infecting bacteria.
TreatmentOral antibitotc treatment using streptomycin, gentamycin, tetracyclines (e.g. doxycycline) or fluoroquinolones, (e.g. ciprofloxacin) is the major form of therapy. Streptomycin or gentamicin can be used intravenously. There is a vaccine that is made from avirulent F. tularensis biovar palaearctica (type B). In addition, antibiotics can be used as post-exposure prophylaxis before the onset of symptoms if infection by F. tularensis is suspected.
Q FEVER
Various farm animals (cattle sheep goats etc) are the primary carriers of the bacterium Coxiella burnetii which causes Q fever. Spread to humans is usually via inhalation of dust containing dried urine, feces etc of infected animals. However, less commonly, the bacterium can be transmitted via the bite of Dermacentor ticks. Ingestion of contaminated milk can also lead to infection. C. burnetii infects macrophages and survives in the phagolysosome, where the bacteria multiply. The bacteria are released by lysis of the cells and phagolysosomes.SymptomsAcute Q feverMany patients, about half, show no signs of infection but in others after an incubation period of 1 - 2 weeks, there is a sudden onset of fever, headache, general malaise, myalgia, sore throat, chills, sweats, non-productive cough, nausea, vomiting, diarrhea, abdominal pain, and chest pain. The patient may also appear confused. Many patients go on to the symptoms of pneumonia and hepatitis but most recover in a month or two without treatment although acute Q fever has a mortality rate of 1-2%.
Chronic Q feverIf the patient fails to resolve the infection, chronic Q fever results. This can occur a few months after primary infection but can also occur many years later. Endocarditis of the aortic heart valves is the major problem that arises. This usually occurs in people with heart valve disease but also at risk are transplant, cancer and kidney disease patients. The chronic form of Q fever has a fatality rate of about 60 - 70%.
DiagnosisSerology to determine the presence of antibodies against Coxiella burnetii is used.
TreatmentAntibiotics such as doxycyline are used to treat acute Q fever. For chronic Q fever, two protocols have been investigated: doxycycline along with quinolones for at least 4 years and doxycycline with hydroxychloroquine for 1.5 to 3 years.
There is a vaccine used in Australia for persons who may come in contact with C. burnettii but it is not commercially available in the United States.
EHRLICHOSIS
HUMAN EHRLICHOSIS
Human ehrlichosis is carried by Dermacentor variabilis and by Amblyomma americanum and is caused by a number of bacteria of the Ehrlichia family, in the United States principally by Ehrlichia chaffeensis. These bacteria are small gram-negative organisms that infect leukocytes . As with many tick-borne diseases, incidence follows vector distribution with higher incidence during the summer months when tick populations and contact with them are higher. The number of cases has been increasing .
SymptomsAfter an incubation of period of a week to 10 days, the patient presents with myalgia, headache and general malaise. There can also be nausea, vomiting, diarrhea, cough, joint pains and the patient may be confused. Sometimes, there is a rash but this is normally only in pediatric cases. If left untreated, more severe manifestations of the infection can occur, including prolonged fever, renal failure, disseminated intravascular coagulopathy, meningoencephalitis, adult respiratory distress syndrome, seizures, or coma. Mortality rate at this stage is 2 - 3%. More at risk are immune-suppressed patients.
DiagnosisMicroscopy using blood smears or serology to detect anti-Ehrlichia antibodies can be used.
TreatmentAntibiotics such as doxycycline are the recommended treatment.
HUMAN GRANULOCYTIC EHRLICHIOSIS
Human granulocytic ehrlichiosis is caused by a species of Ehrlichia similar to species found in animals (Ehrlichia equi and Ehrlichia phagocytophila) and is transmitted by blacklegged ticks (Ixodes scapularis) and western blacklegged ticks (Ixodes pacificus).
LYME DISEASE
Lyme disease is caused by the spirochete bacterium, Borrelia burgdorferi , which typically infects small mammals in the northeast and north central United States. It is transmitted to humans by Ixodid black legged ticks (deer ticks). There are over 20,000 cases per year in the United States making it the most common tick-borne disease in North America. The disease was first described from the town of Old Lyme in Connecticut but is found on both the east and west coasts and in the Mississippi valley . In Europe, a similar disease is caused by Borrelia garinii or Borrelia afzelii.
Symptoms
Fever, headache and malaise and a characteristic rash named erythemia migrans , which can occur in a few days but sometimes only after a few weeks, are typical of Lyme Disease. The rash (which is usually not painful) often has a bull’s eye appearance since as it grows (up to 30 cm across) the central region clears. If left untreated, the infection spreads and can result in Bell’s Palsy (partial paralysis of muscles in one or both sides of the face), meningitis, heart palpitations and severe joint pain. These symptoms usually resolve in a few weeks but after several months about 60% of patients will get severe joint swelling and arthritis. A small minority may also get neurologic symptoms (tingling of the extremities, shooting pains, numbness)
TreatmentEarly administration with antibiotics (doxycycline, amoxicillin, or cefuroxime axetil) is recommended. Some patients continue with neurological and muscle pain problems even after antibiotic treatment. It is not known what causes these but they may be autoimmune in nature.
DiagnosisVarious laboratory tests include Elisa, western blot
SOUTHERN TICK-ASSOCIATED RASH ILLNESS
This rash is similar to that seen in Lyme disease. The causative organism is not known but it is not Borrelia burgdorferi, the Lyme disease agent. The lone star tick, Amblyomma americanum, is the transmission vector.
SymptomsMalaise, fever, myalgia, arthralgia and a “bulls eye” rash at the site of the tick bite. There are no chronic neurological symptoms as are seen with Lyme disease
TreatmentThe usual oral antibiotics are used and the symptoms quickly resolve.
PROTOZOA
BABESIOSIS
Babesiosis is carried by species of Ixodes including the deer tick (Ixodes scapularis) in the north and mid-west of the United States and in other countries, including Europe. Babesia microti is the usual causative organism and is a hemoprotozoan (i.e. it circulates in the bloodstream). Normally, the two hosts of Babesia microti are ticks and peromyscus mice (Peromyscus leucopus). The tick infects the mice with sporozoites, which reproduce asexually in erythrocytes. These escape to the blood stream where they may form male and female gametes that are taken up by the tick during a blood meal. In the tick, the gametes fuse and go through a sporogonic cycle to form more sporozoites. Humans can also acquire sporozoites when bitten by an infected tick and are usually dead-end hosts but babesiosis has been transmitted to other humans via blood transfusions .
In most cases, infection is asymptomatic but after a week to a month, symptoms can appear. These include fever, chills, sweating, myalgias and fatigue. In severe cases, hepatosplenomegaly and hemolytic anemia can occur. Normally, the patient recovers, although severe cases occur in immuno-compromised patients and the elderly.
Disease cause by another protozoan, Babesia divergens, can cause more severe and sometimes fatal cases of babesiosis.
DiagnosisDiagnosis is by serology, immunofluorescence microscopy and by direct observation of the parasite in blood smears in which “Maltese Cross”-like inclusions in erythrocytes are seen . These consist of four budding merozoites attached together.
TreatmentUsual antibiotics used are clindamycin plus quinine or atovaquone plus azithromycin.
VIRUSES
CRIMEAN-CONGO HEMORRHAGIC FEVER
This is caused by a Nairovirus, a member of the Bunyaviridae. It is found in Eastern Europe and throughout the Mediterranean areas of southern Europe, the Middle East, Africa, northwestern China, central and south Asia. Ixorid ticks (genus Hyalomma) spread the virus, which is also carried by numerous species of domestic and wild animals. Person to person transmission through infected blood and other body fluids has been documented.
SymptomsInitially, the patient presents with headache, high fever, back pain, joint pain, stomach pain, and vomiting. There may be flushing, red eyes and throat and small red spots called petechiae on the palate. Hemorrhage ensues after a few days and lasts for a few weeks. this is indicated by severe bruising, nosebleeds, and failure to stop bleedings after a cut or injection. Slow recovery often ensues but mortality can be as high as 50%.
TreatmentSince this is a viral disease, treatment is largely supportive with particular attention to electrolyte balance. Ribavirin has been used. An inactivated vaccine has been used in Eastern Europe.
COLORADO TICK FEVER
This is sometimes confused with a mild case of Rocky Mountain Spotted Fever but Colorado Tick Fever is caused by a coltivirus, a member of the reoviruses. They are endemic to north western North America and are found in Ixodid ticks. The virus distribution closely matches that of its vector, Dermacentor andersoni.
Person-to-person transmission can occur by blood. Prolonged viremia observed in humans and rodents is due to the intraerythrocytic location of virions, which protects them from immune clearance.
SymptomsInfection results in abrupt fever, chills, headache, retro-orbital pain, photophobia, myalgia, abdominal pain, and malaise. Sometimes fever can be diphasic or triphasic, usually lasting for 5 to 10 days. Severe forms of the disease that involve infection of the central nervous system or hemorrhagic fever, pericarditis, myocarditis, and orchitis have been rarely observed, mainly in children. Severity is sufficient to result in hospitalization of approximately 20% of patients. There has been evidence of transmission from mother to child.
FAR EASTERN TICK-BORNE ENCEPHALITIS (Also known as Russian spring-summer encephalitis or Taiga encephalitis)This is caused by a flavivirus which is spread by ixodid ticks (Ixodes persulcatus, I. ricinus and I. cookie). Small animals are the reservoir and the virus is endemic to the former Soviet Union and parts of eastern and central Europe.
SymptomsAbout two weeks after infection, there is a mild influenza-like disease that normally resolves in a few days but which can be followed by meningitis and meningoencephalitis in about one third of cases. In some cases, there may be partial paralysis and mortality may be as high as 25%.
TreatmentSupportive care is normal. There is a vaccine of killed virus that is available in Europe.
POWASSAN ENCEPHALITIS
This is a rare disease caused by a flavivirus carried by Ixodid ticks. There has been less than one case per year reported in the United States but mortality is high. It is widespread in North America and is found in small animal populations including woodchucks.
SymptomsAfter a relatively long incubation period of up to one month, the patient may present with a sore throat, dizziness, headache and confusion. This can proceed to general malaise, vomiting, respiratory distress, fever and convulsions, which then lead to paralysis and possibly coma. Because the virus attacks brain tissue, survivors can have severe neurological problems.
TreatmentSupportive care is indicated.
TICK-BORNE ENCEPHALITIS (Also known as biphasic meningoencephalitis, central European tick-borne encephalitis, Czechoslovak tick-borne encephalitis, diphasic milk fever or viral meningoencephalitis)
This disease results from infection by tick-borne encephalitis virus, which is a member of the Flaviviridae.
SymptomsTick-borne encephalitis starts as mild influenza-like symptoms with fever accompanied by leuko- and thrombocytopenia. This resolves within a few days. However, about one third of patients develop meningitis and meningoencephalitis. This can, in a few cases, be followed by paralysis. The European form of the disease has a mortality rate of under 5%. Most patients recover but about a third may have long-lasting neurological problems.
TreatmentSupportive is indicated. There is an experimental killed vaccine in Europe. In Sweden TBE vaccination is recommended for residents of and regular visitors to TBE endemic areas.
KYASANUR FOREST DISEASE
This disease is similar to Russian spring-summer encephalitis and is also caused by flaviviruses. It is found only in the Kyasanur forest of Northern India. The disease occurs during the dry season as its tick vector (Haemaphyalis spinigera) begins to feed on humans. Local carriers are shrews and monkeys.
LOUPING ILL VIRUS
This is found in the British Isles and is caused by a flavivirus that is carried by pheasants and sheep, among other animals. It can infect many hosts via the tick vector, Ixodes ricinus. It causes mild encephalitis that gives the infected animal an unusual gait (hence its name). However, it can kill livestock and humans not given proper supportive care.
DISEASE CAUSED DIRECTLY BY HARD TICKS
TICK PARALYSIS
In addition to being carriers of disease-causing microorganisms, some ticks (Amblyomma americanum and the two Dermacentor species) can cause tick paralysis. This is a rare disease caused by toxin in the saliva of the tick and results in an acute, ascending, flaccid paralysis caused by reduced acetyl choline or motor neuron action potentials. The paralysis, which is not associated with pain, starts a few days after the bite and comes on gradually over a period of days. The paralysis resolves surprisingly rapidly, usually within a day of the removal of the tick but if the tick is not removed the mortality rate, as a result of respiratory paralysis, can be as high as 10%. Tick paralysis can be confused with other acute neurologic disorders or diseases (e.g., Guillain-Barré syndrome or botulism).
DISEASE FOR WHICH SOFT TICKS ARE CARRIERS
BACTERIA
TICK-BORNE RELAPSING FEVER
Tick-borne relapsing fever is a rare disease (about 25 cases per year in the United States) and is caused by several spirochete bacterial species of the Borelia family. The transmission agents are soft ticks of the genus Ornithodoros. Soft ticks (family Argasidae) differ in many ways from the so-called hard ticks (family Ixodidae), but the most important is that they take brief meals from their host and then drop off. The bite is usually painless. Thus, they are far less likely to be found than the hard ticks that stay attached while feeding for hours. In the wild, these ticks are found in nesting materials when not feeding on their animal host. All stages of the life cycle can take blood meals.
The individual Borrelia species that cause tick-borne relapsing fever are usually associated with specific Ornithodoros tick vectors. B. hermsii is transmitted to humans by Ornithodoros hermsi, B. parkerii is transmitted by Ornithodoros parkeri and B. turicatae is transmitted by Ornithodoros turicata. Each tick is associated with a preferred environment and hosts. Ornithodoros hermsi is found at higher altitudes (1500 – 8000 feet) where it is associated usually with ground squirrels, tree squirrels and chipmunks. Ornithodoros parkeri occurs at lower elevations and inhabit caves and the burrows of ground squirrels, prairie dogs and burrowing owls. Ornithodoros turicata occurs in caves and ground squirrel, prairie dog or burrowing owls burrows in the plains regions of the Southwest United States.
SymptomsInitially, the patient experiences arthralgia, myalgia, headache, chills and fever. This is followed by nausea, cough, photophobia, and dizziness. The patient may be confused. There is often a rash. The incubation period before the onset of the first symptoms is about a week (though it can be shorter or longer). After the onset of disease, symptoms last a few days and then resolve. After a week or two, the symptoms reoccur and in the absence of treatment, recurrence continues for several more episodes. As the fever resolves, the patient may go through a crisis in which first there is a high fever accompanied by confusion and delirium. This “chill phase” lasts up to half an hour. Then there is the “flush phase” in which the temperature drops accompanied by profuse sweating and sometimes a drop in blood pressure.
DiagnosisMicroscope smears of blood, bone marrow or cerebrospinal fluid stained with Giemsa or acridine orange. Serologic testing is also available.
TreatmentAntibiotics are used and symptoms resolve a few days. There can, however, be long-term sequelae including heart and kidney problems, peripheral nerve involvement, ophthalmia, and abortion. Without treatment mortality may be up to 10% of patients.
Tuesday, October 21, 2008
CHIKUNGUNYA VIRUS IN INDIA
CHIKUNGUNYA VIRUS IN INDIA
Chikungunya is a relatively rare form of viral fever caused by an alpha virus (RNA Virus) that is spread by the bite of an infected Aedes aegypti mosquito. The virus is classified under arboviruses which are transmitted by arthropod vectors.
The name is derived from the Makonde word meaning “ that which bends up” in reference to the stooped posture developed as a result of the arthritic symptoms of the disease. The disease was first described in 1952 following an outbreak on the Makonde plateau along the border between Tanganyika and Mozambique.
Chikungunya virus was first isolated from Indian subcontinent in 1963 from Calcutta, since then there have been several reports of Chikungunya virus infection in different parts of India. The last outbreak of Chikungunya virus infection occurred in India in 1971. subsequently the virus had ‘disappreared’ from the subcontinent. However, recent reports of large scale outbreak of fever caused by Chikungunya virus infection in several parts of South India have confirmed the reemergence of this virus.
The symptoms of this infection include abrupt onset of fever, chills, headache and severe joint pain with or without swelling (usually the smaller joints), low back pain and rash. The symptoms are most often clinically indistinguishable from those observed in dengue fever. Therefore it is very important to clinically distinguish Dengue from Chikungunya virus infection. Unlike Dengue Hemorrhagic manifestations are relatively rare and as a rule shock is not observed in Chikungunya virus infection. Most often Chikungunya is a self limiting febrile illness. However, neurological complications such as meningoencephalitis and mother to child transmission has been observed.
The precise reasons for the reemergence of Chikungunya in the Indian subcontinent in not known. Although it is well recognized that reemergence of viral infection are due to a variety of social, environmental, behavioral and biological changes. The challenge faced during this large outbreak in the country has been the lack of rapid diagnostic facilities. Although, the National Institute of Virology at Pune, has been a great help in determining the etiology of the outbreak, relying on one institute in the country to render diagnostic help for case management would be a foolish task. It would be therefore desirable to ensure that several virology laboratories in the country are enrolled and networked to deliver rapid diagnosis in large outbreak such as this as well other emerging viral infections like Chandipura and Avian Influenza.
PRINCE.C.P
Lecturer in Microbiology
Chikungunya is a relatively rare form of viral fever caused by an alpha virus (RNA Virus) that is spread by the bite of an infected Aedes aegypti mosquito. The virus is classified under arboviruses which are transmitted by arthropod vectors.
The name is derived from the Makonde word meaning “ that which bends up” in reference to the stooped posture developed as a result of the arthritic symptoms of the disease. The disease was first described in 1952 following an outbreak on the Makonde plateau along the border between Tanganyika and Mozambique.
Chikungunya virus was first isolated from Indian subcontinent in 1963 from Calcutta, since then there have been several reports of Chikungunya virus infection in different parts of India. The last outbreak of Chikungunya virus infection occurred in India in 1971. subsequently the virus had ‘disappreared’ from the subcontinent. However, recent reports of large scale outbreak of fever caused by Chikungunya virus infection in several parts of South India have confirmed the reemergence of this virus.
The symptoms of this infection include abrupt onset of fever, chills, headache and severe joint pain with or without swelling (usually the smaller joints), low back pain and rash. The symptoms are most often clinically indistinguishable from those observed in dengue fever. Therefore it is very important to clinically distinguish Dengue from Chikungunya virus infection. Unlike Dengue Hemorrhagic manifestations are relatively rare and as a rule shock is not observed in Chikungunya virus infection. Most often Chikungunya is a self limiting febrile illness. However, neurological complications such as meningoencephalitis and mother to child transmission has been observed.
The precise reasons for the reemergence of Chikungunya in the Indian subcontinent in not known. Although it is well recognized that reemergence of viral infection are due to a variety of social, environmental, behavioral and biological changes. The challenge faced during this large outbreak in the country has been the lack of rapid diagnostic facilities. Although, the National Institute of Virology at Pune, has been a great help in determining the etiology of the outbreak, relying on one institute in the country to render diagnostic help for case management would be a foolish task. It would be therefore desirable to ensure that several virology laboratories in the country are enrolled and networked to deliver rapid diagnosis in large outbreak such as this as well other emerging viral infections like Chandipura and Avian Influenza.
PRINCE.C.P
Lecturer in Microbiology
Tuesday, October 14, 2008
GLOBAL WARMING
WHAT IS GLOBAL WARMING?
Carbon dioxide and other gases warm the surface of the planet naturally by trapping solar heat in the atmosphere. This is a good thing because it keeps our planet habitable. However, by burning fossil fuels such as coal, gas and oil and clearing forests we have dramatically increased the amount of carbon dioxide in the Earth’s atmosphere and temperatures are rising.
The vast majority of scientists agree that global warming is real, it’s already happening and that it is the result of our activities and not a natural occurrence. The evidence is overwhelming and undeniable.
We’re already seeing changes. Glaciers are melting, plants and animals are being forced from their habitat, and the number of severe storms and droughts is increasing.
The number of Category 4 and 5 hurricanes has almost doubled in the last 30 years.
Malaria has spread to higher altitudes in places like the Colombian Andes, 7,000 feet above sea level.
The flow of ice from glaciers in Greenland has more than doubled over the past decade.
At least 279 species of plants and animals are already responding to global warming, moving closer to the poles.
If the warming continues, we can expect catastrophic consequences.
Deaths from global warming will double in just 25 years -- to 300,000 people a year.
Global sea levels could rise by more than 20 feet with the loss of shelf ice in Greenland and Antarctica, devastating coastal areas worldwide.
Heat waves will be more frequent and more intense.
Droughts and wildfires will occur more often.
The Arctic Ocean could be ice free in summer by 2050.
More than a million species worldwide could be driven to extinction by 2050.
There is no doubt we can solve this problem. In fact, we have a moral obligation to do so. Small changes to your daily routine can add up to big differences in helping to stop global warming. The time to come together to solve this problem is now – TAKE ACTION
Carbon dioxide and other gases warm the surface of the planet naturally by trapping solar heat in the atmosphere. This is a good thing because it keeps our planet habitable. However, by burning fossil fuels such as coal, gas and oil and clearing forests we have dramatically increased the amount of carbon dioxide in the Earth’s atmosphere and temperatures are rising.
The vast majority of scientists agree that global warming is real, it’s already happening and that it is the result of our activities and not a natural occurrence. The evidence is overwhelming and undeniable.
We’re already seeing changes. Glaciers are melting, plants and animals are being forced from their habitat, and the number of severe storms and droughts is increasing.
The number of Category 4 and 5 hurricanes has almost doubled in the last 30 years.
Malaria has spread to higher altitudes in places like the Colombian Andes, 7,000 feet above sea level.
The flow of ice from glaciers in Greenland has more than doubled over the past decade.
At least 279 species of plants and animals are already responding to global warming, moving closer to the poles.
If the warming continues, we can expect catastrophic consequences.
Deaths from global warming will double in just 25 years -- to 300,000 people a year.
Global sea levels could rise by more than 20 feet with the loss of shelf ice in Greenland and Antarctica, devastating coastal areas worldwide.
Heat waves will be more frequent and more intense.
Droughts and wildfires will occur more often.
The Arctic Ocean could be ice free in summer by 2050.
More than a million species worldwide could be driven to extinction by 2050.
There is no doubt we can solve this problem. In fact, we have a moral obligation to do so. Small changes to your daily routine can add up to big differences in helping to stop global warming. The time to come together to solve this problem is now – TAKE ACTION
Thursday, October 2, 2008
malayalam kavitha
കക്കൊസില് തൂറാം
പട്ടരുകുട്ടി തൂറാന് പോയികുണ്ടിയിന്മേല് തേള് കുത്തി
പട്ടരുകുട്ടി കരഞ്ഞു പോയി
പാവം പാവം പട്ടരുകുട്ടി .
Wednesday, October 1, 2008
Entamoeba histolytica
Several protozoan species in the genus Entamoeba infect humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba, associated with intestinal and extra intestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.
Life Cycle:
Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ( : noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ( : intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ( : extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).
Geographic Distribution:Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.
Clinical Features:A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions).
Laboratory Diagnosis:Entamoeba histolytica must be differentiated from other intestinal protozoa including: E. coli, E. hartmanni, E. gingivalis, Endolimax nana, and Iodamoeba buetschlii (the nonpathogenic amebas); Dientamoeba fragilis (which is a flagellate not an ameba); and the possibly pathogenic Entamoeba polecki. Differentiation is possible, but not always easy, based on morphologic characteristics of the cysts and trophozoites. The nonpathogenic Entamoeba dispar, however, is morphologically identical to E. histolytica, and differentiation must be based on isoenzymatic or immunologic analysis. Molecular methods are also useful in distinguishing between E. histolytica and E. dispar and can also be used to identify E. polecki. Microscopic identification of cysts and trophozoites in the stool is the common method for diagnosing E. histolytica. This can be accomplished using:
§ Fresh stool: wet mounts and permanently stained preparations (e.g., trichrome).
§ Concentrates from fresh stool: wet mounts, with or without iodine stain, and permanently stained preparations (e.g., trichrome). Concentration procedures, however, are not useful for demonstrating trophozoites.
In addition, E. histolytica trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
Diagnostic findings:
§ Microscopy
§ Immunodiagnosis
§ Molecular methods for discriminating between E. histolytica and E. dispar
§ Morphologic comparison with other intestinal parasites
§ Bench aid for E. histolytica
Treatment:For asymptomatic infections, iodoquinol, paromomycin, or diloxanide furoate (not commercially available in the U.S.) are the drugs of choice. For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess), the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanide furoate
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Life Cycle:
Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ( : noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ( : intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ( : extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).
Geographic Distribution:Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.
Clinical Features:A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions).
Laboratory Diagnosis:Entamoeba histolytica must be differentiated from other intestinal protozoa including: E. coli, E. hartmanni, E. gingivalis, Endolimax nana, and Iodamoeba buetschlii (the nonpathogenic amebas); Dientamoeba fragilis (which is a flagellate not an ameba); and the possibly pathogenic Entamoeba polecki. Differentiation is possible, but not always easy, based on morphologic characteristics of the cysts and trophozoites. The nonpathogenic Entamoeba dispar, however, is morphologically identical to E. histolytica, and differentiation must be based on isoenzymatic or immunologic analysis. Molecular methods are also useful in distinguishing between E. histolytica and E. dispar and can also be used to identify E. polecki. Microscopic identification of cysts and trophozoites in the stool is the common method for diagnosing E. histolytica. This can be accomplished using:
§ Fresh stool: wet mounts and permanently stained preparations (e.g., trichrome).
§ Concentrates from fresh stool: wet mounts, with or without iodine stain, and permanently stained preparations (e.g., trichrome). Concentration procedures, however, are not useful for demonstrating trophozoites.
In addition, E. histolytica trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
Diagnostic findings:
§ Microscopy
§ Immunodiagnosis
§ Molecular methods for discriminating between E. histolytica and E. dispar
§ Morphologic comparison with other intestinal parasites
§ Bench aid for E. histolytica
Treatment:For asymptomatic infections, iodoquinol, paromomycin, or diloxanide furoate (not commercially available in the U.S.) are the drugs of choice. For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess), the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanide furoate
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