He developed jaundice a few days ago and they just got the results of his liver panel back and rushed him to the ER. His enzymes are over 3000 (should be 40 or below), and his bilirubin and ferritin are extremely elevated.

They're checking for acute hepatitis, but it seems that if the ferritin is very high, that would happen over months and be more related to a chronic condition that finally developed into acute symptoms.

I know congestive heart failure is related to lyme, but wasn't sure about liver disease. If so, I'm going to advise them to call Dr. Crist right away and see if he can check for lyme. The ER doctors would probably never even consider it.

Thanks -

Do you know what his symptoms were? Could all of those symptoms be explained by this liver problem?

Please email me. Just click on the letter icon next to the date.

Liver problems have been observed with tick-borne diseases other than Bb, particularly erlichiosis. Most of the studies were veterinary, in dogs. Hope this helps. Good luck.

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Hepatic pathology in human monocytic ehrlichiosis. Ehrlichia chaffeensis infection.

Sehdev AE, Dumler JS.

Dept of Pathology, Johns Hopkins Medical Institutions, Meyer B1-193, 600 N Wolfe St, Baltimore, MD 21287, USA.

Ehrlichia chaffeensis causes human monocytic ehrlichiosis (HME) that usually includes fever, myalgias, and pancytopenia and, in 80% to 90% of patients, elevations in serum transaminase levels. Thus, the pathology of liver injury was studied in liver tissues from 7 patients with laboratory-confirmed HME. H&E and immunohistochemical stains for E chaffeensis and leukocyte markers were examined. Scattered lobular lymphohistiocytic foci and diffuse lymphohistiocytic infiltration and Kupffer cell hyperplasia with increased phagocytosis frequently were present. Various degrees of liver cell injury and death were observed. Cholestasis was evident in 6 cases, sometimes with bile duct epithelial injury. Rare to abundant E chaffeensis-infected mononuclear cells infiltrating lobules or portal regions or in Kupffer cells were observed in 5 patients. The inflammation was out of proportion to the infection in 6 cases. In the absence of infected hepatocytes or biliary epithelial cells, these findings suggest that host inflammatory or immune responses contribute to the liver injury seen in HME.

PMID: 12817434 [PubMed - indexed for MEDLINE]

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Recenti Prog Med. 2001 Sep;92(9):540. Related Articles, Links

[Hepatosplenic cat-scratch disease in the immunocompetent adult]

[Article in Italian]

Zaccala G, Rizzo G, Boldorini R, Garavelli PL, Campanini M.

Strutture Complesse di Medicina Interna II, Azienda Ospedaliera Maggiore della Carita, Novara.

Atypical manifestations of cat-scratch disease have been described in children and immunosuppressed adults. We report the first case of hepatosplenic cat-scratch disease in an immunocompetent subject, demonstration of diversity of this infection. A 33-year-old man presented with prolonged fever, lymphadenopathy and multiple hypodense lesions of liver and spleen in ultrasonographic imaging. The hepatic biopsy showed non-specific inflammatory reactions including granulomata and stellate necrosis. Anti-Bartonella antibodies have been found. The therapy with clarithromycin and doxycycline for many weeks was effective for hepatic lesions. A month ago a history of a cat contact with the presence of a skin lesion has been reported.

Publication Types:

* Case Reports

PMID: 11552311 [PubMed - indexed for MEDLINE]

(edited to fix duplicate entry)

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Przegl Epidemiol. 1997;51(4):441-4. Related Articles, Links

[Difficulties in diagnosis of lyme borreliosis]

[Article in Polish]

Klucinski P, Maslankiewicz A, Ograbek M.

II Katedra i Zaklad Mikrobiologii Slaskiej Akademii Medycznej w Katowicach.

A case of borreliosis in female aged 28 years is presented. Diagnosis was made late. The course of the disease was characterized by long-lasting high fever, enlargement of liver and spleen, pancreatitis, pneumonia of the left lung and anemia. During the antibiotic therapy (rocephin) neutropenia was observed. In every case of long-lasting fever of unknown origin, borreliosis should be taken into consideration.

Publication Types:

* Case Reports

PMID: 9562793 [PubMed - indexed for MEDLINE]

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Clin Infect Dis. 2002 May 1;34(9):1206-12. Epub 2002 Apr 02. Related Articles, Links

Comment in:

* Clin Infect Dis. 2003 Nov 15;37(10):1397-8.

Click here to read
Gastrointestinal and hepatic manifestations of tickborne diseases in the United States.

Zaidi SA, Singer C.

Division of Infectious Diseases, Long Island Jewish Medical Center, Long Island Campus for the Albert Einstein College of Medicine, New Hyde Park, NY, 11040, USA.

Signs and symptoms related to the gastrointestinal tract and liver may provide important clues for the diagnosis of various tickborne diseases prevalent in different geographic areas of the United States. We review clinical and laboratory features that may be helpful in detecting a tickborne infection. Physicians evaluating patients who live in or travel to areas where tickborne diseases are endemic and who present with an acute febrile illness and gastrointestinal manifestations should maintain a high index of suspicion for one of these disease entities, particularly if the patient has received a tick bite. If detected early, many of these potentially serious illnesses can be easily and effectively treated, thereby avoiding serious morbidity and even death.

Publication Types:

* Review
* Review, Tutorial

PMID: 11941547 [PubMed - indexed for MEDLINE]

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Lab Anim Sci. 1996 Oct;46(5):507-15. Related Articles, Links

Comparative pathogenesis of human WA1 and Babesia microti isolates in a Syrian hamster model.

Wozniak EJ, Lowenstine LJ, Hemmer R, Robinson T, Conrad PA.

Department of Pathology, Immunology, and Microbiology, School of Veterinary Medicine, University of California, Davis 95616, USA.

The pathogenesis of a newly recognized, molecularly and antigenically distinct human babesial isolate (WA1) and Babesia microti, the common cause of human babesiosis in the United States, were compared in a Syrian hamster model. A group of 33 adult female hamsters were inoculated intraperitoneally with either WA1-infected, B. microti-infected, or uninfected hamster erythrocytes. All WA1-infected animals became parasitemic by postinoculation (PI) day 3 or 4 and were severely lethargic and dyspneic by PI days 6 to 10. Death often occurred spontaneously by PI day 10, with parasitemia of 12 to 90%. Hamsters inoculated with B. microti became parasitemic by PI day 7 and developed peak parasitemia (42 to 60%) by PI day 14 that subsequently decreased to low or undetectable values. Although the B. microti-infected hamsters developed severe anemia, they generally remained asymptomatic. Postmortem examination of WA1-infected hamsters revealed intravascular aggregates of large mononuclear inflammatory cells that occasionally occluded small to medium veins, pulmonary leukoclastic phlebitis, thrombosis, and multifocal coagulative necrosis in the heart, spleen, lung, and liver. No vascular lesions or areas of coagulative necrosis were detected in any B. microti-infected or control hamsters. The results of this study suggest that marked leukocytosis followed by acute necrotizing phlebitis resulting in disseminated intravascular coagulation, thromboembolism, and infarction may be central to the pathogenesis of WA1 infections.

PMID: 8905583 [PubMed - indexed for MEDLINE]

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Severe babesiosis in Long Island: review of 34 cases and their complications.

Hatcher JC, Greenberg PD, Antique J, Jimenez-Lucho VE.

Division of Infectious Diseases, Department of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-8153, USA.

Thirty-four consecutive patients were hospitalized with diagnosis of severe Babesia infection over the course of 13 years. The average time from onset of symptoms to diagnosis was 15 days. When compared with uninfected febrile control patients, affected patients complained significantly more often of malaise, arthralgias and myalgias, and shortness of breath (P<.05), and they more often had thrombocytopenia and abnormal liver function (P<.05). Forty-one percent of patients with Babesia developed complications such as acute respiratory failure, disseminated intravascular coagulation, congestive heart failure, and renal failure. Analysis of data revealed that complicated babesiosis was more commonly associated with the presence of severe anemia (hemoglobin level <10 g/dL; P=.01) and higher parasitemia levels (>10%; P=.08). Patients were treated with a combination of drugs that included clindamycin, quinine, atovaquone, or azithromycin. Despite treatment, parasitemia persisted for an average of 8.5 days (range, 3--21 days). Exchange transfusion was performed for 7 patients, and it effectively reduced the high levels of parasitemia. Three patients died. Improved outcomes may result with prompt recognition and treatment of babesiosis.

PMID: 11283800 [PubMed - indexed for MEDLINE]

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Pathology of acute fatal babesiosis in hamsters experimentally infected with the WA-1 strain of Babesia.

Dao AH, Eberhard ML.

Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

A strain of Babesia (strain WA-1), recently isolated from a human in Washington State, was found to be unusually virulent for hamsters; it caused acute infection and death in a large proportion of animals 5 to 7 days after inoculation. To assess the basic pathologic lesions associated with this infection, 30 male Syrian hamsters (Mesocricetus auratus) were inoculated intraperitoneally with the WA-1 strain. Twelve animals (40%) died within 5 to 6 days. The other 18 animals, all infected and clinically ill, were killed on the sixth or seventh day for biochemical study. All 12 animals that died from the infection showed high parasitemia, heavy intravascular hemolysis, and pronounced vascular stasis with red-cell sequestration in the spleen, liver, lungs, kidneys, and brain. Serologic study revealed severe anemia (mean hematocrit, 29) with hemolyzed serum and marked elevation of the serum transaminases. The mechanism of death was thought to be diffuse anoxic tissue damage secondary to vascular stasis, which led to multiorgan failure.

After checking everything and after torturing us for some weeks with diagnosis of liver cancer and an autoimmune self-destroying liver, they finally settled for hepatitis of unknown origin.

Over the next years his bloodwork improved dramatically. Now he is on abx for Lyme and the results of his last liver check were absolutely perfect.

Today we are convinced that this was Lyme hepatitis which is not so uncommon.