Human Babesiosis
Differential diagnosis
Malaria
Babesiosis or
piroplasmosis is a malaria-like parasitic disease caused by infection with a
eukaryotic parasite in the order Piroplasmida, typically a Babesia or
Theileria, in the phylum Apicomplexa. Human babesiosis transmission via tick
bite is most common in the Northeastern and Midwestern United States and parts
of Europe, and sporadic throughout the rest of the world. It occurs in warm
weather.[3] People can get infected with Babesia parasites by the bite of an
infected tick, by getting a blood transfusion from an infected donor of blood
products, or by congenital transmission (an infected mother to her baby).
Ticks transmit the human strain of babesiosis, so it often presents with
other tick-borne illnesses such as Lyme disease. After trypanosomes, Babesia is
thought to be the second-most common blood parasite of mammals. They can have
major adverse effects on the health of domestic animals in areas without severe
winters. In cattle the disease is known as Texas cattle fever or redwater.
Signs and symptoms
Half of all children and a
quarter of previously healthy adults with Babesia infection are asymptomatic.
When people do develop symptoms, the most common are fever and hemolytic
anemia, symptoms that are similar to those of malaria.[5] People with symptoms
usually become ill 1 to 4 weeks after the bite, or 1 to 9 weeks after
transfusion of contaminated blood products. A person infected with babesiosis
gradually develops malaise and fatigue, followed by a fever. Hemolytic anemia,
in which red blood cells are destroyed and removed from the blood, also
develops. Chills, sweats, and thrombocytopenia are also common symptoms.
Symptoms may last from several days to several months.
Less common symptoms and
physical exam findings of mild-to-moderate babesiosis:
Headache
Muscle pain
Anorexia
Nonproductive cough (mucus
is not coughed.
Arthralgias
(noninflammatory joint pain, unlike arthritis, which is inflammatory)
Nausea
Vomiting
Sore throat
Abdominal pain
Pink eye/Conjunctivitis
Photophobia (abnormal
intolerance to visual perception of light)
Weight loss
Emotional lability
Depression
Hyperesthesia (more
sensitive to stimuli)
Enlarged spleen
Pharyngeal erythema
Enlarged liver
Jaundice (yellowing of the
skin and of the sclera)
Retinopathy with splinter hemorrhages
Retinal infarcts
Neutropenia
In more severe cases,
symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F), shaking
chills, and severe anemia (hemolytic anemia). Organ failure may follow, including
adult respiratory distress syndrome. Sepsis in people who have had a
splenectomy can occur rapidly, consistent with overwhelming post-splenectomy
infection. Severe cases are also more likely to occur in the very young, very
old, and persons with immunodeficiency, such as HIV/AIDS patients.
A reported increase in
human babesiosis diagnoses in the 2000s is thought to be caused by more
widespread testing and higher numbers of people with immunodeficiencies coming
in contact with ticks, the disease vector. Little is known about the occurrence
of Babesia species in malaria-endemic areas, where Babesia can easily be
misdiagnosed as Plasmodium. Human patients with repeat babesiosis infection may
exhibit premunity.
Cause
Babesia species are in the
phylum Apicomplexa, which also has the protozoan parasites that cause malaria,
toxoplasmosis, and cryptosporidiosis. Four clades of Babesia species infect
humans. The main species in each clade are:]
B. microti (<3 µm)
B. duncani
B. divergens (cattle
parasite seen mostly in Europe) and B. venatorum (roe deer parasite, formerly
called EU1), most closely related to the large Babesia clade
Large Babesia (>3 µm)
mostly infects ungulates, but also includes K01 strain (an isolated case
observed in South Korea, see isolated cases)
Pathophysiology
Babesia lifecycle
Babesia parasites
reproduce in red blood cells, where they can be seen as cross-shaped inclusions
(four merozoites asexually budding, but attached together forming a structure
looking like a "Maltese cross")[and cause hemolytic anemia, quite
similar to malaria.
Unlike the Plasmodium
parasites that cause malaria, Babesia species lack an exoerythrocytic phase, so
the liver is usually not affected.
In nonhuman animals,
Babesia canis rossi, Babesia bigemina, and Babesia bovis cause particularly
severe forms of the disease, including a severe haemolytic anaemia, with
positive erythrocyte-in-saline-agglutination test indicating an immune-mediated
component to the haemolysis. Common sequelae include haemoglobinuria
"red-water", disseminated intravascular coagulation, and
"cerebral babesiosis" caused by sludging of erythrocytes in cerebral
capillaries.
In bovine species, the
organism causes hemolytic anemia, so an infected animal shows pale mucous
membranes initially. As the levels of bilirubin (a byproduct of red blood cell
lysis) continue to increase, the visible mucous membranes become yellow in
color (icterus) due to the failure of the liver to metabolize the excess
bilirubin. Hemoglobinuria is seen due to excretion of red-blood-cell lysis
byproducts via the kidneys. Fever of 40.5 °C (105 °F) develops due to release
of inflammatory byproducts.
Diagnosis
Only specialized
laboratories can adequately diagnose Babesia infection in humans, so Babesia
infections are considered highly under-reported. It develops in patients who
live in or travel to an endemic area or receive a contaminated blood
transfusion within the preceding 9 weeks, so this aspect of the medical history
is vital. Babesiosis may be suspected when a person with such an exposure
history develops persistent fevers and hemolytic anemia. The definitive
diagnostic test is the identification of parasites on a Giemsa-stained
thin-film blood smear.
So-called "Maltese
cross formations" on the blood film are diagnostic (pathognomonic) of
babesiosis, since they are not seen in malaria, the primary differential
diagnosis.[9] Careful examination of multiple smears may be necessary, since
Babesia may infect less than 1% of circulating red blood cells, thus be easily
overlooked.
Serologic testing for
antibodies against Babesia (both IgG and IgM) can detect low-level infection in
cases with a high clinical suspicion, but negative blood film examinations.
Serology is also useful for differentiating babesiosis from malaria in cases
where people are at risk for both infections. Since detectable antibody
responses require about a week after infection to develop, serologic testing
may be falsely negative early in the disease course.
A polymerase chain
reaction (PCR) test has been developed for the detection of Babesia from the
peripheral blood. PCR may be at least as sensitive and specific as
blood-film examination in diagnosing babesiosis, though it is also
significantly more expensive. Most often, PCR testing is used in
conjunction with blood film examination and possibly serologic testing.
Other laboratory findings
include decreased numbers of red blood cells and platelets on complete blood
count.
In animals, babesiosis is
suspected by observation of clinical signs (hemoglobinuria and anemia) in
animals in endemic areas. Diagnosis is confirmed by observation of merozoites
on thin film blood smear examined at maximum magnification under oil using
Romonovski stains (methylene blue and eosin). This is a routine part of the
veterinary examination of dogs and ruminants in regions where babesiosis is
endemic.
Babesia canis and B.
bigemina are "large Babesia species" that form paired merozoites in
the erythrocytes, commonly described as resembling "two pears hanging
together", rather than the "Maltese cross" of the "small
Babesia species". Their merozoites are around twice the size of small
ones.
Cerebral babesiosis is
suspected in vivo when neurological signs (often severe) are seen in cattle
that are positive for B. bovis on blood smear, but this has yet to be proven
scientifically. Outspoken red discoloration of the grey matter post mortem further
strengthens suspicion of cerebral babesiosis. Diagnosis is confirmed post
mortem by observation of Babesia-infected erythrocytes sludged in the cerebral
cortical capillaries in a brain smear.
Treatment
Treatment of asymptomatic
carriers should be considered if parasites are still detected after 3 months.
In mild-to-moderate babesiosis, the treatment of choice is a combination of
atovaquone and azithromycin. This regimen is preferred to clindamycin and quinine
because it has fewer side effects. The standard course is 7 to 10 days, but
this is extended to at least 6 weeks in people with relapsing disease. Even
mild cases are recommended to be treated to decrease the chance of
inadvertently transmitting the infection by donating blood. In severe
babesiosis, the combination of clindamycin and quinine is preferred. In
life-threatening cases, exchange transfusion is performed.In this procedure,
the infected red blood cells are removed and replaced with uninfected ones.
Imizol is a drug used for treatment of babesiosis in dogs. Extracts of
the poisonous, bulbous plant Boophone disticha are used in the folk medicine of
South Africa to treat equine babesiosis. B. disticha is a member of the
daffodil family Amaryllidaceae and has also been used in preparations employed
as arrow poisons, hallucinogens, and in embalming. The plant is rich in
alkaloids, some of which display an action similar to that of scopolamine.
Epidemiology
Babesiosis is a
vector-borne illness usually transmitted by Ixodes scapularis ticks. B. microti
uses the same tick vector as Lyme disease and may occur in conjunction with
Lyme. The organism can also be transmitted by blood transfusion. Ticks of
domestic animals, especially Rhipicephalus (Boophilus) microplus and R. (B.)
decoloratus transmit several species of Babesia to livestock, causing
considerable economic losses to farmers in tropical and subtropical regions.
In the United States, the
majority of babesiosis cases are caused by B. microti, and occur in the
Northeast and northern Midwest from May through October. Areas with especially
high rates include eastern Long Island, Fire Island, Nantucket Island, and
Martha's Vineyard. The Centers for Disease Control and Prevention now
requires state health departments to report infections using Form OMB No.
0920-0728. In 2014, Rhode Island had an incidence of 16.3 reported
infections per 100,000 people.
In Europe, B. divergens is
the primary cause of infectious babesiosis and is transmitted by I. ricinus.
Babesiosis has emerged in
Lower Hudson Valley, New York, since 2001.
In Australia, one locally
acquired case of B. microti has been reported, which was fatal. A subsequent
investigation found no additional evidence of human Babesiosis in over 7000
patient samples, lead in the authors to conclude that Babesiosis was rare in
Australia.A similar disease in cattle, commonly known as tick fever, is spread
by Babesia bovis and B. bigemina in the introduced cattle tick Rhipicephalus
microplus. This disease is found in eastern and northern Australia.
Isolated cases
A table of isolated cases
of babesiosis, which may be underestimated given how widely distributed the
tick vectors are in temperate latitudes.
History
The disease is named for
the genus of the causative organism,[32] which was named after the Romanian
bacteriologist Victor Babeș. In 1888, Victor Babeș identified the
microorganisms in red blood cells as the cause of febrile hemoglobinuria in cattle.[5]
In, Theobald Smith and Frederick Kilborne discovered that a tick was the vector
for transmission in Texas cattle. The agent was B. bigemina. This was the first
demonstration that an arthropod could act as a disease vector to transmit an
infectious agent to a vertebrate host.
In 1957, the first human
case was documented in a splenectomized Croatian herdsman.. The agent was B.
divergens. In 1969, the first case was reported in an immunocompetent
individual on Nantucket Island. The agent was B. microti, and the vector was
the tick I. scapularis. cEquine babesiosis (caused by the protozoan
Theileria equi) is also known as piroplasmosis (from the Latin piro, meaning
pear + Greek plasma, a thing forme
Jan Ricks Jennings, Senior
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