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Dengue Fever, Babesiosis, and Leptospirosis

The importance of these three fevers for the radiologist is that patients are likely to be referred for chest and perhaps abdominal imaging. Apart from involvement of the gallbladder in Dengue hemorrhagic fever and the lungs in leptospirosis, none of these diseases have specific imaging findings in spite of their often severe clinical illnesses. All are easily confused clinically with other tropical diseases, and any other cause of fever.

Anyone living in or coming from the tropics may become ill with malaise, fever, chills, headaches, and conjunctival suffusion; the differential diagnosis is then bewildering. Apart from the more serious forms of fever, such as malaria, typhoid, and typhus, there are legions of parasites and organisms which all present in the same nonspecific way; and, of course, the patient may have an upper respiratory infection or "flu".

Dengue Fever

Dengue fever is caused by single-strand RNA viruses of the family Togaviridae, genus Flavivirus. These arthropod or animal (arbor) viruses are mainly spread worldwide by day-biting Aedes aegypti mosquitoes. Severe outbreaks have occurred in the United States (Texas, Louisiana, and Hawaii), Australia (Queensland and New South Wales), Japan, Greece, the Caribbean, Polynesia, Melanesia, and the Philippines: Dengue fever is now endemic in much of Southeast Asia. In the first 6 months of 1995 the WHO reported more than 140,000 cases of Dengue and more than 3,600 patients with Dengue hemorrhagic fever, of whom 38 died, in 12 Latin American and Caribbean countries. The number of afflicted people can be very high (e.g., several million in Japan); the most severe varieties of Dengue fever are seldom seen in visitors or short-term residents.

The clinical presentation varies. Dengue may cause only a mild fever with minimal respiratory or gastrointestinal symptoms, usually diagnosed as flu or upper respiratory infection. In older children and adults there can be a sudden high fever (up to 41°C, 105°F) with headache, back and muscle pain, and a transient rash. Lymphadenopathy, anorexia, constipation, and depression may develop after a few days, followed by a further generalized rash (which spares the palms of the hands and the soles of the feet). There is often persistent bradycardia. In children particularly, Dengue hemorrhagic fever may have an initial mild onset, and become a severe illness with bleeding, rapid respiration, and cyanosis. This may progress to Dengue shock syndrome, in which there is circulatory collapse, the liver enlarges, and hemorrhage increases. After 48 hours, with treatment, convalescence is fairly rapid. Untreated, about half the patients may die.

Imaging in Dengue hemorrhagic fever (or in the milder syndromes) does not reveal any specific pulmonary or other abnormalities, except in severe cases associated with hepatomegaly. Ultrasonography will then show thickening of the wall of the gallbladder and, in some patients, ascites. There is a definite correlation between the severity of the illness and the increasing thickness of the gallbladder wall. In 93% of patients with grade III or IV disease (WHO classification of Dengue syndromes), the gallbladder wall thickness will exceed 3 mm. When there is ascites, the gallbladder wall is significantly thicker than in those patients without intraperitoneal fluid.



Piroplasmosis. Texas tick fever. Texas cattle fever. Red water fever. Biliary fever.


Babesiosis is a protozoan infection with a small intraerythrocytic parasite commonly found in animals. Human infection was thought to be uncommon, but a series of 136 cases seen between 1982 and 1991 in the state of New York, as well as other isolated cases worldwide, suggest that it may often go unrecognized. The first human case was described in 1957, although the disease has been recognized in animals since the nineteenth century. There are at least 70 different species of Babesia responsible for this infection, but in North America the majority of human infections are caused by B. microti and in Europe by B. divergens (which may be the same as B. bovis).

Geographic Distribution

Human infections have been reported from the former Yugoslavia, France, Great Britain, Ireland, the former Soviet Union, Mexico, and the eastern, southern, and western United States. Animal infection is worldwide, and human infection is possible anywhere.


Babesia are transmitted by ixodid (hard-bodied) ticks, the parasites being ingested along with the host's blood. Large numbers of infectious sporozoites are produced during the sexual phase within the tick. They are returned to the vertebrate host in the tick's saliva. The primary reservoirs are dogs, small rodents, horses, donkeys, goats, cattle, sheep, and deer. Human infection is more common in patients who have had splenectomies prior to being bitten by the infected ticks: in the series from New York state, 23% had concurrent Lyme disease. However, infection has also occurred in patients with normal spleens and a normal immune response. The infection can be transmitted by blood transfusion.

Clinical Characteristics

Some patients are entirely asymptomatic or have an illness so mild that it is possible that many cases are not recognized. Clinically the course of the illness is usually relatively benign, with fever and moderate hemolytic anemia due to hemolysis. Other patients will be more severely ill, with sweating, chills, myalgia, arthralgia, and extreme fatigue, as well as the expected fever and hemolytic anemia. One patient with transfusion-induced babesiosis developed fatal adult respiratory disease syndrome (ARDS). Such cases are often mistaken clinically for malaria caused by Plasmodium falciparum or vivax; the Babesia closely resemble these malarial parasites, but contain no pigment. Use of thick and thin blood smears with Giemsa staining is the best way to confirm the diagnosis. The parasitemia and fatigue may persist for weeks or months, in spite of symptomatically satisfactory treatment. Depression is also part of the disease pattern. Death from hemoglobinuric nephrosis (acute tubular necrosis) has been reported. It is likely that babesiosis is a much more severe illness after splenectomy.

lmaging Diagnosis

There are no significant radiological findings in human babesiosis. Chest x-rays have been normal in patients with quite severe fever. One patient who became infected with Babesia after transfusion became seriously ill and developed acute pulmonary edema. The capillary wedge pressure and cardiac index were normal. The chest radiographic findings progressed to ARDS and the patient died. The sequence was similar to the acute noncardiogenic pulmonary edema of malaria. It must be emphasized that this is an unusual event and respiratory complaints or abnormal chest radiographs are rare.

The only other occasional abnormality is nonspecific hepatomegaly, which can be confirmed by ultrasonography (or CT) scanning. There are no characteristic features which permit an imaging diagnosis of babesiosis.



Weil's disease. Spirochetosis. Icterohaemorrhagica. Canicola fever. Rice worker's disease.


Amongst the many causes of fevers, leptospirosis must be considered even by the radiologist who sees a patient with an abnormal chest radiograph. In brief, leptospirosis is the result of infection with one of the spirochetes in the family Leptospiraceae. There are at least seven distinct groups, and over 180 serovars, with most human infections caused by Leptospira interrogans. Leptospirosis occurs worldwide as a zoonosis in wild or domestic animals. Water or soil contaminated with urine from infected animals is a common method of transmission. The spirochetes enter through damaged skin or mucosa.

Clinical Characteristics

Most human infections are mild. The clinical course is usually biphasic, starting with an acute leptospiremic phase which lasts 4 to 8 days, and with fever which may reach 41°C (105°F) but is more commonly 39°-40°C (102°-104°F). To the generalized "flu" symptoms must be added others of more clinical significance. Jaundice, which appears within the first week in severe infections, may have a poor prognosis: up to 30% of patients who are jaundiced will die. Renal failure is the most common fatal complication. A hemorrhagic diathesis is the cause of pulmonary lesions: hemorrhages occur in the lungs, pleura, or pericardium, and in severe infections there may be acute hemorrhagic lobar pneumonia. Chest radiographs, particularly of jaundiced patients, show abnormalities in about 40% of patients. There is no clear correlation with any clinical manifestation other than jaundice.

Meningitis is the most frequent neurological complication, but is infrequent during the initial acute illness. Headaches can be intense, unrelenting, and accompanied by painful myalgia, sometimes with nausea and vomiting. Uveitis may occur, sometimes delayed for several weeks after the onset of the fever.

During the acute phase of infection, there is renal involvement in 70% to 80% of patients, with proteinuria and red and white cells in the urine. These do not give an indication of the extent of the renal involvement, but severe kidney failure can result in oliguria or anuria (usually in the 2nd week of the disease). In its early stages, during the fever and systemic malaise, leptospirosis could be misdiagnosed as a renal infection.

In the 2nd week the illness usually abates, but there may be relapses. The spirochetes may persist in the proximal convoluted tubules of the kidney and be shed in the urine, to infect other hosts. This is the leptospiruric phase. Mild infections result in complete recovery and many infections are self-limited. If treatment is given early, the underlying vascular damage is prevented. Severe cases may need several months of convalescence. As indicated above, untreated jaundiced patients have a mortality of up to 30%. Considering that in some tropical countries over 30% of the rural population may have Leptospira interrogans antibodies, it is not a disease to be ignored.

lmaging Diagnosis

There have been numerous descriptions of the pulmonary abnormalities which may be found on the chest radiographs of patients with leptospirosis. Almost all have emphasized that there is little or no correlation between the extent of the lung involvement and the severity of the disease or the prognosis. The prevalence of abnormal chest radiographs varies from 67% to 23%, although in most series there are significantly more abnormalities (up to two or three times as many) in jaundiced compared with nonjaundiced patients. Only in China is there a high prevalence in nonjaundiced patients.

There is agreement that the radiographic abnormalities result from hemorrhagic pneumonia or, rarely, pulmonary hemorrhage. The most common radiographic abnormalities are increased nonsegmental peripheral pulmonary densities, with poorly defined margins, variable opacity and size, and no loss of volume. There is usually more than one such area, and small lesions often become confluent. In some patients whole lobes, or even more than one lobe, may be involved. Resolution is usually complete in 7 to 10 days, taking longer when there is extensive involvement. In about 10% of patients there may be a relapse 6 to 14 days, and sometimes even 20 days, after the radiographs have cleared.

Other patients will develop linear atelectasis, particularly at the lung bases. Pleural and pericardial effusions occur, but less commonly than the pulmonary changes: these effusions are often hemorrhagic. Cardiomegaly may be related to circulatory stress and anemia rather than directly to the leptospirosis. Although the speed of resolution varies, the majority of chest radiographs return to normal and there are no reports of long-term residual abnormalities.

It is important to emphasize again that radiographic pulmonary abnormalities may be seen without any clinical chest symptomatology and that the radiographic findings cannot be used to determine severity of the infection or the rate of recovery. The radiographic patterns, varying from small soft patchy opacities to confluence and large areas of consolidation, reflect the hemorrhagic infection and in ill, febrile patients make the differential diagnosis difficult, because bacterial or viral pneumonias may present with similar changes. In general, the abnormalities due to pulmonary hemorrhage change and resolve more rapidly than does pneumonia due to pulmonary infections.

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Copyright: Palmer and Reeder