6 Helminth2 - PPT
6 Helminth2 - PPT
6 Helminth2 - PPT
HELMINTH:
Pathogenesis and Defenses
Introduction
Helminth is a general term for a parasitic worm. The helminths include the Platyhelminthes or
flatworms (flukes and tapeworms) and the Nematoda or roundworms.
All helminths are relatively large (> 1 mm long); some are very large (> 1 m long). All have welldeveloped organ systems and most are active feeders. The body is either flattened and covered with
plasma membrane (flatworms) or cylindrical and covered with cuticle (roundworms). Some helminths are
hermaphrodites; others have separate sexes.
Helminths are worldwide in distribution; infection is most common and most serious in poor
countries. The distribution of these diseases is determined by climate, hygiene, diet, and exposure to
vectors.
The mode of transmission varies with the type of worm; it may involve ingestion of eggs or larvae,
penetration by larvae, bite of vectors, or ingestion of stages in the meat of intermediate hosts. Worms are
often long-lived.
Many infections are asymptomatic; pathologic manifestations depend on the size, activity, and
metabolism of the worms. Immune and inflammatory responses also cause pathology.
Nonspecific defense mechanisms limit susceptibility. Antibody- and cell-mediated responses are
important, as is inflammation. Parasites survive defenses through many evasion strategies.
Helminths - worms - are some of the world's commonest parasites. They belong to two major
groups of animals, the flatworms or Platyhelminthes (flukes and tapeworms) and the roundworms or
Nematoda. All are relatively large and some are very large, exceeding one meter in length.
Their bodies have well-developed organ systems, especially reproductive organs, and most
helminths are active feeders. The bodies of flatworms are flattened and covered by a plasma membrane,
whereas roundworms are cylindrical and covered by a tough cuticle. Flatworms are usually
hermaphroditic whereas roundworms have separate sexes; both have an immense reproductive capacity.
The most serious helminth infections are acquired in poor tropical and subtropical areas, but
some also occur in the developed world; other, less serious, infections are worldwide in distribution.
Exposure to infection is influenced by climate, hygiene, food preferences, and contact with vectors. Many
potential infections are eliminated by host defenses; others become established and may persist for
prolonged periods, even years. Although infections are often asymptomatic, severe pathology can occur.
Because worms are large and often migrate through the body, they can damage the host's tissues directly
by their activity or metabolism. Damage also occurs indirectly as a result of host defense mechanisms.
Almost all organ systems can be affected.
Host defense can act through nonspecific mechanisms of resistance and through specific immune
responses. Antibody-mediated, cellular, and inflammatory mechanisms all contribute to resistance.
However, many worms successfully avoid host defenses in a variety of ways, and can survive in the face
of otherwise effective host responses.
Transmission of Infection
Helminths are transmitted to humans in many different ways fig 1
Fig 3. Figure 87-3. Pathogenesis: indirect damage caused by immunopathologic responses (for
example, in Schistosomiasis)
Hypersensitivity-based, granulomatous responses to eggs trapped in the liver cause a physical
obstruction to blood flow, which leads to liver pathology. Hypersensitivity-based inflammatory changes
probably also contribute to the lymphatic blockage associated with filarial infections (Brugia, Wuchereria).
Immune-mediated inflammatory changes occur in the skin, lungs, liver, intestine, CNS, and eyes as
worms migrate through these structures. Systemic changes such as eosinophilia, edema, and joint pain
reflect local allergic responses to parasites. The pathologic consequences of immune-mediated
inflammation are seen clearly in intestinal infections (especially Strongyloides and Trichinella infections).
Structural changes, such as villous atrophy, develop. The permeability of the mucosa changes, fluid
accumulates in the gut lumen, and intestinal transit time is reduced. Prolonged changes of this type may
lead to a protein-losing enteropathy. The inflammatory changes that accompany the passage of
schistosome eggs through the intestinal wall also cause severe intestinal pathology. Heavy infections with
the whipworm Trichuris in the large bowel can lead to inflammatory changes, resulting in blood loss and
rectal prolapse.
The severity of these indirect changes is a result of the chronic nature of the infection. The fact that many
worms are extremely long-lived means that many inflammatory changes become irreversible, producing
functional changes in tissues. Three examples are the hyperplasia of bile ducts in long-term liver fluke
infections, the extensive fibrosis associated with chronic schistosomiasis, and the skin atrophy associated
with onchocerciasis. Severe pathology may also result when worms stray into abnormal body sites.
Defenses Against Infection
1. Nonspecific Resistance
Infective stages attempting to enter via the mouth or through the skin are opposed by the same nonspecific defenses that protect humans from invasion of other pathogens. Following oral ingestion,
parasites must survive passage through the acid stomach to reach the small bowel. The natural parasites
of humans are adapted to do this, but opportunistic parasites may be killed. Similarly, natural parasites