Acanthamoebiasis and Immunosuppression Case Report

Aj, Martínez

doi:10.1097/00005072-198209000-00007

Cited by 86 publications

(39 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The concerted action of these immune cells results in sequestration of amoebae and is instrumental in slowing the progression of GAE. This outcome is consistent with the observation that granulomas are rarely observed in immunocompromised individuals (34) and in mice with experimentally induced immune suppression following treatment with the cannabinoid delta-9-tetrahydrocannabinol (⌬ 9 -THC) (8).…”

supporting

confidence: 90%

Acanthamoeba culbertsoni Elicits Soluble Factors That Exert Anti-Microglial Cell Activity

et al. 2010

View full text Add to dashboard Cite

Acanthamoeba culbertsoni is an opportunistic pathogen that causes granulomatous amoebic encephalitis (GAE), a chronic and often fatal disease of the central nervous system (CNS). A hallmark of GAE is the formation of granulomas around the amoebae. These cellular aggregates consist of microglia, macrophages, lymphocytes, and neutrophils, which produce a myriad of proinflammatory soluble factors. In the present study, it is demonstrated that A. culbertsoni secretes serine peptidases that degrade chemokines and cytokines produced by a mouse microglial cell line (BV-2 cells). Furthermore, soluble factors present in cocultures of A. culbertsoni and BV-2 cells, as well as in cocultures of A. culbertsoni and primary neonatal rat cerebral cortex microglia, induced apoptosis of these macrophage-like cells. Collectively, the results indicate that A. culbertsoni can apply a multiplicity of cell contact-independent modes to target macrophage-like cells that exert antiamoeba activities in the CNS.Acanthamoeba culbertsoni belongs to a group of free-living amoebae, such as Balamuthia mandrillaris, Naegleria fowleri, and Sappinia pedata, that can cause disease in humans (46,56). Acanthamoeba spp. are found worldwide and have been isolated from a variety of environmental sources, including air, soil, dust, tap water, freshwater, seawater, swimming pools, air conditioning units, and contaminated contact lenses (30). Trophozoites feed on bacteria and algae and represent the infective form (47, 56). However, under unfavorable environmental conditions, such as extreme changes in temperature or pH, trophozoites transform into a double-walled, round cyst (22, 45).Acanthamoeba spp. cause an infection of the eye known as amoebic keratitis (AK), an infection of the skin referred to as cutaneous acanthamoebiasis, and a chronic and slowly progressing disease of the central nervous system (CNS) known as granulomatous amoebic encephalitis (GAE) (22,23,30,56). GAE is most prevalent in humans who are immunocompromised (30,33,40) and has been reported to occur among individuals infected with the human immunodeficiency virus (HIV) (28). It has been proposed that Acanthamoeba trophozoites access the CNS by passage through the olfactory neuroepithelium (32) or by hematogenous spread from a primary nonneuronal site of infection (23,24,33,53).In immune-competent individuals, GAE is characterized by the formation of granulomas. These cellular aggregates consist of microglia, macrophages, polymorphonuclear cells, T lymphocytes, and B lymphocytes (24, 30). The concerted action of these immune cells results in sequestration of amoebae and is instrumental in slowing the progression of GAE. This outcome is consistent with the observation that granulomas are rarely observed in immunocompromised individuals (34) and in mice with experimentally induced immune suppression following treatment with the cannabinoid delta-9-tetrahydrocannabinol (⌬ 9 -THC) (8).Microglia are a resident population of macrophages in the CNS. These cells, along with CNS-invading perip...

show abstract

supporting

confidence: 90%

Acanthamoeba culbertsoni Elicits Soluble Factors That Exert Anti-Microglial Cell Activity

et al. 2010

View full text Add to dashboard Cite

show abstract

“…There was no significant increase in titers (acute phase, 1:16; convalescent phase, 1:32) despite sufficient time between the serial samples for a rise in antibodies to develop. We postulate that the failure to develop a serologic response may have been due to the underlying diagnosis of hypogammaglobulinemia and that treatment with high-dose corticosteroids may have blunted the humoral immune response, as has been previously reported (14). Of note, however, is that detection of stably elevated titers of antibodies to Mycoplasma pneumoniae and Ehrlichia chaffeensis suggests that this patient was able to mount an immunologic response to other infectious agents in the past.…”

Section: Case Reportsupporting

confidence: 52%

“…In the home, they can be recovered from humidifiers, aquariums, biofilms in sink drains and water faucets, and soil in potted plants. Amebae have been isolated from the nasal mucosae of various groups of healthy individuals, including military recruits, students, and children, suggesting that while colonization and subclincal infections are relatively common, invasive disease is, fortunately, a rarity (3,12,14).…”

Section: Case Reportmentioning

confidence: 99%

Inability To Make a Premortem Diagnosis of Acanthamoeba Species Infection in a Patient with Fatal Granulomatous Amebic Encephalitis

Bloch

Schuster

2005

J Clin Microbiol

View full text Add to dashboard Cite

Granulomatous amebic encephalitis (GAE), an infection of immunocompromised hosts, is almost uniformly fatal. A case of GAE in a patient who failed to mount a serologic response to Acanthamoeba polyphaga is presented. Although Acanthamoeba polyphaga that is sensitive to multiple antimicrobials grew from brain tissue, an inability to make a premortem diagnosis precluded therapy. CASE REPORTA 70-year-old female presented for medical attention with lethargy and seizures. Symptoms began 36 days earlier when she was hospitalized with syncope. An evaluation at that time included magnetic resonance imaging (MRI), revealing a focal area of edema in the right temporal lobe consistent with an acute infarction, and she was discharged to a rehabilitation facility with a diagnosis of cerebrovascular accident. She was readmitted with worsening ataxia, lethargy, and generalized seizures. Her past medical history included chronic neutropenia secondary to myelodysplastic syndrome, hypogammaglobulinemia treated with monthly intravenous gamma globulin, asplenia, steroid-dependent discoid lupus (prednisone, 20 mg twice a day), and diabetes mellitus.On exam, the patient was afebrile and hemodynamically stable. An ocular exam did not reveal papilledema. Her neck was supple. She was oriented only to person. A neurological examination was otherwise nonfocal. Laboratory studies included a platelet count of 355 ϫ 10 9 /liter, a hematocrit of 32.8%, and a white blood cell count of 2.8 ϫ 10 9 /liter, which was unchanged from her baseline leukopenia. A lumbar puncture (Table 1) was significant for lymphocytic pleocytosis and hypoglycorrhacia. A repeat MRI revealed intense contrast enhancement of the right posterior temporal lobe, with two new contrast-enhancing areas in the medial temporal lobe. A stereotactic biopsy of the right temporal lobe performed on day 42 was nondiagnostic, with results showing a reactive gliosis with lymphocytic infiltrate in the leptomeninges, but no amebae or granulomas, and negative bacterial, fungal, and mycobacterial cultures.The patient's hospital course was significant for progressive obtundation, requiring intubation for airway protection. The results of repeat lumbar punctures are provided in Table 1. Serial MRI revealed persistent abnormal signal intensity in the temporal lobes, with new areas of uptake in the right basal ganglia, pons, and left occiput. Extensive diagnostic evaluation was unrevealing except for a stable elevation in titers of antibodies to Mycoplasma pneumoniae (1.425 in the acute phase and 1.645 in the convalescent phase) and Ehrlichia chaffeensis (1:128 in the acute phase and 1:128 in the convalescent phase) and evidence of prior Epstein-Barr virus infection (viral capsid antigen immunoglobulin G titer of Ͼ10, viral capsid antigen immunoglobulin M titer of Ͻ10, and EBNA titer of Ͼ10). Despite empirical treatment with acyclovir, decadron, and plasmaphoresis, the patient died 100 days after her initial presentation.Hematoxylin and eosin-stained sections of the patient's brain obtained at ...

show abstract

“…As for the route and time of infection, the patient had been to Southeast Asia more than 20 years before disease onset; therefore, the possibility of an acquired oral infection cannot be ruled out. In Japan, dysenteric amoebiasis is most commonly caused by E. histolytica infection [9] , with a particularly high incidence among homosexuals. However, it is noteworthy that our patient was not homosexual and that colitis developed during chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Fulminant amoebic colitis during chemotherapy for advanced gastric cancer

Hanaoka¹,

Higuchi²,

Tanabe³

et al. 2009

WJG

View full text Add to dashboard Cite

A 52-year-old man had bloody stools during chemotherapy for gastric cancer. A colonoscopy revealed necrotizing ulcer-like changes. A biopsy confirmed the presence of amoebic trophozoites. Subsequently, peritonitis with intestinal perforation developed, and emergency peritoneal lavage and colostomy were performed. After surgery, endotoxin adsorption therapy was performed and metronidazole was given. Symptoms of peritonitis and colonitis resolved. However, the patient's general condition worsened with the progression of gastric cancer. The patient died 50 d after surgery. Fulminant amoebic colitis is very rarely associated with chemotherapy. Amoebic colitis should be considered in the differential diagnosis of patients who have bloody stools during chemotherapy.

show abstract

Acanthamoebiasis and Immunosuppression Case Report

Cited by 86 publications

References 0 publications

Acanthamoeba culbertsoni Elicits Soluble Factors That Exert Anti-Microglial Cell Activity

Acanthamoeba culbertsoni Elicits Soluble Factors That Exert Anti-Microglial Cell Activity

Inability To Make a Premortem Diagnosis of Acanthamoeba Species Infection in a Patient with Fatal Granulomatous Amebic Encephalitis

Fulminant amoebic colitis during chemotherapy for advanced gastric cancer

Contact Info

Product

Resources

About