Parasitic Diseases

Treatment & Control

Max J. Miller, Edgar Love

• Publisher: CRC Press
• Year: 2020
• ISBN:
  9781000141634
• Edition: 1
• Topic: Medicine
• Subtopic: Immunology

Based on papers presented at the XI International Congress for Tropical Medicine and Malaria, this publication provides an authoritative evaluation of treatment and control of helminth parasite infections. A section on leprosy and a brief review of malaria vaccination are included. A comprehensive review of the history of schistosomiasis control programs presents information unavailable elsewhere. This book is of special interest to professionals concerned with health problems of less developed countries and in particular to public health officials, epidemiologists and clinicians dealing with patients in or returning from the tropics.

Section I. Schistosomiasis

Chemotherapy and Its Use in Control

Complementary Methods of Control

Evaluation of Control

Country Profiles of Control Programs

Economics and Mathematical Models

Chapter 1

THE PATHOLOGY OF HUMAN SCHISTOSOMA HAEMATOBIUM INFECTION

J. H. Smith and J. D. Christie

TABLE OF CONTENTS

Introduction

II. General Pathology

III. Progression (Activity) of the Disease

IV. Intensity of Infection

V. Focalization of S. haematobium Egg Deposition

VI. Patterns of Egg Accumulation over the Duration of the Disease

VII. Systematic Review of Lesions Produced by S. haematobium in Man

A. Urethra, Prostate, Seminal Vesicles, and Bladder Outlet Obstruction

B. Other Male and Female Genital Organs

C. Urinary Bladder

D. Urolithiasis

E. Ureters and Schistosomal Obstructive Uropathy

F. Gastrointestinal Tract

G. Other Sites

References

INTRODUCTION

Schistosomiasis comprises a group of chronic diseases caused by schistosomes, a genus of digenetic parasitic worms which cohabitate the venous plexes of the viscera. Schistosoma haematobium dwells principally in the perivesical venous plexus in humans and causes urinary schistosomiasis (bilharziasis), which is endemic in many parts of Africa and the Middle East, and is now considered a major public health problem.^{1, 2, 3, 4, 5, 6}

Schistosomal disease results directly from schistosome eggs and from the granulomatous host response to them.^{7, 8, 9, 10, 11, 12} Eggs are deposited in venules and small veins of the viscera and may be (1) extruded into the lumen of these hollow viscera; (2) trapped in the visceral wall and be destroyed or calcified; or (3) dislodged from the venule and enter the venous blood to microembolize distant organs. The bewildering array of serious clinicopathologic syndromes that has been ascribed to S. haemotobium results from the interaction of four factors. Both the severity of disease and probability of sequelae and complications are closely related to (1) the intensity; (2) the duration of infection; (3) the clinical disease progressing through the active stage into an inactive, but still dangerous stage; and (4) the fact that egg deposition is nonuniform and may randomly focus on a physiologically vital area at any time during the course of oviposition. These four factors — intensity, duration, activity, and focalization — relate to morbidity and mortality in this infection.¹

II. GENERAL PATHOLOGY

S. haematobium adult worm pairs are widely distributed throughout the pelvic and mesenteric venous plexes with oviposition predominating in the pelvic lower urinary tract^2,3 The reason for such localization is unknown. Oviposition in S. haematobium is concentrated in patches.^3,4,6 The perioval granulomata of all schistosome infections have been shown to be T-cell-dependent host responses.^{7, 8, 9, 10} In humans, S. haematobium granulomata are of an intensity which is intermediate between S. mansoni and S. japonicum.¹³ S. haematobium egg shells are not acid fast, while S. mansoni and S. japonicum eggs are acid fast, and this feature can be used to differentiate the species of eggs in histologic sections of tissue from patients residing in areas where both S. masoni and S. haematobium are endemic.¹ S. haematobium deposits groups of eggs in a given site, rather than individual eggs, and thus produces composite, rather than unioval, granulomata.^1,5,13

III. PROGRESSION (ACTIVITY) OF THE DISEASE

The morphology of S. haematobium lesions in the human lower urinary tract is highly variable.^5,13,15 In sites of recent oviposition, perioval granulomatous inflammation results in large, bulky, hyperemic, and polypoid masses projecting from the mucosa into the lumen of the involved organ. However, as oviposition at such a site ceases, entrapped eggs are destroyed or calcified, and inflammation wanes, being supplanted by fibrous tissue to produce the characteristic sandy patches of urinary schistosomiasis. These patches have the appearance and consistency of fine, tan sand when incised by a scalpel.^1,5,13 Working with experimental S. haematobium in chimpanzees, von Lichtenberg originally postulated that since the spectrum of lesions formed a continuum from polyploid patch through fibrous patch to sandy patch, these differing lesions reprsented a progression; individual patches commencing at different times but evolving at similar rate would account for the heterogeneity of lesions encountered in the human disease.⁶ von Lichtenberg’s concept allowed classification of the disease into a series of stages: an early active stage involving only polyploid granulomatous lesions; a chronic inactive stage characterized only by sandy patches; and two intervening stages, chronic active and late residual.^4,13 This system has been applied to unselected autopsy series and has become a powerful tool in understanding the evolut...

Table of contents

• Cover
• Title Page
• Copyright Page
• Preface
• The Editors
• Contributors
• Table of Contents
• Section I. Schistosomiasis
• Section II. Trematodes
• Section III. Onchocerciasis
• Section IV. Cestodes
• Section V. Nematodes
• Section VI. Leprosy
• Section VII. Malaria
• Index