Just a few points of clarification on E. histolytica infection...
Steve Kayes says:
- However, according to the text by Markel and Voege (1981) p.26
-they say that most cases of E.h. are asymptomatic and the organisms live
-happily in the colon on bacteria.
A lot has happened in the last 15 years. It is now recognized by almost
everyone in the field of amebiasis that most asymptomatic infections
ascribed to E. histolytica are actually due to the cryptic, non-invasive
species E. dispar, previously known as 'nonpathogenic E. histolytica'.
These organisms are morphologically identical to E. histolytica but
biochemically, immunologically and genetically quite distinct. E. dispar
accounts for almost all 'E. histolytica' infections in developed countries
and has never been isolated from a patient with invasive disease.
Thus the oft quoted infection numbers for E. histolytica (500 million
infected worldwide) are probably as much as 10 fold too high, the majority
being due to E. dispar. The estimated 40 million cases of invasive
disease per year are all due to E. histolytica. About 10% of these are
thought to develop extraintestinal lesions (mostly liver abscesses) and
there are estimated to be 50-100,000 deaths per year. Asymptomatic
carriers of E. histolytica sensu stricto appear to be rare.
- Markel and Voege on the same page go on to question the
-significance of proposed etiology of "amebic hepatitis" and conclude by
-saying that it is clear that spread of the infection to the liver may
-occur in cases in which intestinal complaints never develop.
I was surprised to hear of amebic hepatitis still being discussed in
1981 - I thought it had been gone since the 1960s. Looking at a 1972
edition (17th) of Manson's Tropical Diseases it says: (p176) "Rogers
originally described a condition of 'amoebic hepatitis' as a very
early stage of liver abscess." and (p178) "The dominant clinical condition
of 'amoebic hepatitis' (the very early stage of liver abscess, see
above...) is a swinging fever, raised sedimentation rate, characteristic
leucocytosis, and a slightly enlarged and tender liver..." Neither of
two recent clinical reviews on amebiasis even mention amebic hepatitis
(Reed, Clinical Infectious Diseases 14, 385-393 (1992); Ravdin, Clin
Infect Dis 20, 1453-1466 (1995)).
The latter statement of Markel and Voege is true, however. Many liver
abscess patients have no concurrent intestinal infection and often have
no history of dysentery.
C. Graham Clark, Ph.D.
Laboratory of Parasitic Diseases,
National Institutes of Health,
Bethesda, MD 20892-0425, USA
e-mail: gclark at nih.gov