Excerpt:

The tick bite transmitted Lyme disease is one of the most common
antropozoonosis, about 10 000 new infections are reported in
Hungary each year.
The progress and clinical presentation can vary, and carditis can
occur in later stages. A serologically verified Lyme disease
caused third degree atrioventricular block in young male
presenting with presyncope. Based on the tick-bites mentioned a
few weeks prior to hospital admission, Lyme carditis was
considered with the administration of antibiotics and monitor
observation.
Typical skin lesions were not recognized and laboratory findings
showed no pathology. An electrophysiological study recorded a
predominant supra-His atrioventricular block. Total regression of
conduction could be detected later and the serological tests
established an underlying Lyme disease. Currently no definite
treatment recommendation is available for the potentially
reversible Lyme carditis. The tick bite seemed to be the key on
our way to diagnosis; however, serological tests proved the
disease to be older than one year. A detailed medical history and
serological tests are essential in identifying the cause and
pacemaker implantation can be avoided. Orv. Hetil., 2010, 39,
1585-1590.

Over the past nine years, we have treated over three hundred children for Lyme Disease in the hospital because they had significant neurologic manifestations of Lyme Disease or, in the minority of cases, an arthritis necessitating hospitalization for intravenous antibiotics.

It is impossible to know how many children have Lyme Disease in our area. One pediatrician with a very large practice sees at least three ECM rashes a day and places the children on either Amoxicillin or penicillin for twenty-one days. Obviously, the majority of the children who are seen early on who manifest the rash do not go on to have chronic problems, but a small percentage do.

In some of our communities with populations of 20,000-25,000 people, as many as sixty percent of the ticks are carrying the Borrelia spirochete so the chance for an infection is very high.

Since 1982, I have seen a large number of children who have had neurologic symptoms due to Lyme Disease. Many of these children are not diagnosed initially because their complaints are vague and thought to be all functional. I have treated a patient who has been sick for five years. Others were sick three and four years before being diagnosed. Recently, we have become more concerned about children with, what are considered, vague symptoms and are becoming more aggressive in diagnosing and treating.

I have seen children develop neurologic symptoms within a few weeks after a tick bite. Others will not develop the symptoms for one year or more.

Less than fifty percent of the children even remember being bitten by a tick and even a smaller percentage than that remember any ECM rash.

The parents recall the children having a flu-like illness that preceded their developing these rather persistent symptoms and usually that flu-like illness will occur six weeks or more after the tick bite or the exposure to the ticks. Many parents claim that after this “flu-like illness,” the child never was well again. The majority, over ninety percent, of the children that we have treated complain of headache. The headache, in a few cases, has been very acute accompanied by papilledema but in the majority of cases the headache comes on gradually, becomes quite persistent and does not respond to over-the-counter analgesics.

In addition to the headache, the children complain of photophobia, dizziness, a stiff neck, backache, somnolence and, those that are in school, have problems with memory and difficulty concentrating. Some patients have developed progressive weakness.

The parents complain that preschoolers develop mood swings and become very irritable and they see a personality change.

Among the children that are school-age and those who are in adolescence, chest pain is a very frequent complaint. At least seventy percent have complained of chest pain. About fifty percent have complained of abdominal pain. More than half the children have arthralgia usually involving the knee and sometimes the wrist.

Other complaints include palpitations, tingling, numbness, rashes that come and go, usually malar rashes, and sore throats that are excruciatingly painful.

It is easy to see how this long list can be very non-specific and many of these children are thought to have functional problems.

Children present with central or peripheral nervous system manifestations frequently. The central nervous system manifestations include an encephalopathy. These children have difficulty with memory, concentration and learning new material in school. They have an excessive amount of fatigue and have a wake-sleep disturbance, either becoming hypersomniac or insomniac.

Rarely, we have seen children present with an encephalitic picture.

There have been reports of individuals having stroke from Lyme. We have one child who presented with the sudden onset of a hemiplegia and aphasia.

Patients may have involvement of the optic nerve with an optic neuritis or a papillitis, resultant vision loss.

Peripheral neuropathy with distal parasthesias, subtle weakness, diminished deep tendon reflexes have also been seen.

The laboratory work-up is rather unrevealing. CBC’s are almost always normal. Sed Rates of greater than 30 have occurred in only ten percent of the patients and we have had only two patients who have Sed Rates of 100 or more. EEG’s have been abnormal in one-third of the patients showing bilateral sharp waves and some slowing. The CAT Scans have been normal but a number of MRI’s have been abnormal showing evidence of increased signal in the white matter.

The decision to do a spinal tap on a patient with Lyme Disease is based on the physical findings. Obviously, if a patient has papilledema, they will be tapped after a CAT Scan or MRI shows no mass lesion. But in other cases, the decision to do the tap is based primarily on the need for additional diagnostic information or where there is a question as to whether the diagnosis is something other than Lyme. We have tapped about twenty-five [sic] patients so far. The majority have had normal spinal fluid findings. Usually, they have no elevation of their white cells. Protein and sugars are normal. Cultures are negative. Interestingly, however, at least fifty percent of them show increased pressure with opening pressures greater than 200, sometimes as high as 400. Every patient with papilledema has had a pressure of at least 300 or more except for one girl whose opening pressure was 260 but she had obvious papilledema and also loss of vision in her left eye. Eight of the patients had a pleocytosis with cells ranging from 60 to 700, predominantly lymphocytes. Only two patients showed a positive CSF titer.

The diagnosis of Lyme Disease is a clinical one. The serology, if positive, is helpful. We consider a positive serology as a 1:128 IFA; ELISA that is greater than .79. Urine antigens can also be measured. The tests on urine antigens are still considered investigational.

We will treat patients with negative serologies without hesitation if they truly have a number of the symptoms and are incapacitated by them. We have had children who have been out of school for an entire year because they have been too sick to leave the house.

Other children have had to give up all extracurricular activities, sports, etc. because they are too sick and too weak to participate. Every patient we have treated with the diagnosis of Neurologic Lyme Disease has had persistent complaints. These children have a headache and frequently chest pain. Many of them have seen numerous doctors without any specific diagnosis being made and many of them have had antibiotics for various reasons along the way, sore throats, otitis media, rash and, therefore, never developed an antibody response to their spirochetal infection.

The diagnosis of Neurologic Lyme Disease is a clinical one, not a laboratory one. If the patient’s symptoms are compatible with the diagnosis, the patient is ill, the disease is having a significant effect on the person’s ability to function, then they deserve treatment. I believe it is safer to be aggressive and treat someone under those circumstances than to allow them to continue suffering indefinitely.

Treatment consists of intravenous antibiotics, ceftriaxone, cefotaxime, ampicillin given for as long as is necessary, minimum of four-six weeks initially. Many patients are treated for months if they continue to be clinically ill.

Patients can take Benadryl if they develop pruritis. I encourage them to eat yogurt to try to prevent diarrhea while they are on the antibiotics. Aspirin is the best medication to relieve the pain but, because of the reluctance in the past of physicians to prescribe aspirin in children, many of them are given other NSAIDS.

During treatment and even afterward, they need to rest. They cannot resume full activity as soon as they have been treated. About twenty-five percent of the patients we have treated have had to be re-treated and of these re-treated, the vast majority then do well. Usually, if I treat them initially with ceftriaxone, I will re-treat them with either ceftriaxone or cefotaxime or ampicillin.

Many of the children I have seen with these complaints have been given the benefit of antibiotics by mouth to no avail. Once the patients have these neurologic complaints and, in some cases the positive neurologic findings, they truly deserve a course of aggressive intravenous antibiotic treatment, perhaps more than one time.

Background: Most cases of human babesiosis in North America are caused
by Babesia microti, which is endemic in the northeastern and upper
midwestern United States. Although the disease is usually transmitted by
a tick bite, there has been an increase in the number of
transfusion-transmitted cases reported. We describe a fatal case of
transfusion-transmitted babesiosis in a nonendemic state, Delaware.

Case Report: The patient was a 43-year-old Caucasian woman with history
of transfusion-dependent Diamond-Blackfan syndrome, hepatitis C, and
splenectomy. She was admitted initially for presumptive pneumonia. The
next day, a routine examination of the peripheral blood smears revealed
numerous intraerythrocytic ring forms, consistent with Babesia. The
parasitemia was approximately 5% to 6%. The diagnosis was confirmed by
positive polymerase chain reaction (PCR) for B. microti DNA and high
titer of antibody to B. microti (1:2048). Despite aggressive therapy
including clindamycin and quinine antibiotics, the patient expired 3
days after admission. Subsequently, 13 blood donors were tested for B.
microti. All tested donors were negative by PCR. However, one donor
living in New Jersey had a significant elevated B. microti antibody
titer (1:1024).

Conclusions: We believe that this is the first reported case of
transfusion-transmitted babesiosis in Delaware, a nonendemic state. Our
case illustrates that clinicians should consider babesiosis in the
differential diagnosis of immunocompromised patients who have fever and
recent transfusion history, even in areas where babesiosis is not
endemic. It also demonstrates the need for better preventive strategies
including more sensitive, specific, and rapid blood donor screening
tests to prevent transfusion-transmitted babesiosis.

http://dx.doi.org/10.1111/j.1537-2995.2009.02454.x