Helminthic Diseases

The term "Helminths" means "worms" in parasitology. It refers to parasitic worms, which comprise two large phyla: Phylum Platyhelminths (flatworms) and Phylum Nemathelminths or Nematoda (true roundworms), and two smaller ones: Phylum Nematomorpha (hair snakes) and Phylum Acanthocephala (thorny-headed worms), in addition to one class group from phylum Annelida, the class Hirudinea (Leeches).

1.0Helminthic Diseases Introduction

• Helminths exhibit distinct adaptations for parasitic life and survival compared to protozoa. 
• Many parasitic helminths lack or have a simplified digestive tract due to their nutrient-rich environments within hosts. 
• For example, trematodes and cestodes have microvilli-like teguments for nutrient absorption. 
• While vital systems are simplified, their reproductive systems are highly efficient. Internal autoinfection is rare, and worm populations within a host depend on external infective stages. 
• Helminth life cycles vary: some, like pinworms, have simple direct cycles, while others involve soil (e.g., Ascaris, hookworms) or intermediate hosts (e.g., snails, crabs, fish). Some species use paratenic hosts for transmission. 
• Tissue-migrating helminths often cause eosinophilia and symptoms like hepatomegaly, pneumonitis, asthma, cysts, or neurological disturbances.

2.0Groups of Helminths 

I- Phylum: Platyhelminths 

This phylum includes three classes: 

1 Class: Turbellaria. 

2 Class: Trematoda. 

3 Class: Cestoda.

• Trematoda class has THREE recognized subclasses: 
• Monogenea, Digenea and Aspidogasterea. Only Digenea (Digenetic Trematodes) produce infections in man. 
• To simplify the study, Digenetic Trematodes are also classified into groups according to the location of the adult fluke (worm) in the host's body: 

1. Liver (or hepatic) flukes, ex: Fasciola hepatica Clonorchis sienensis 

2. Intestinal flukes, ex: Fasciolopsis buski Heterophyes heterophyes 

3. Blood flukes, ex: Schistosomes 

4. Lung flukes, ex: Paragonimus westermani

1. Class: Trematoda

Ex: Blood flukes or Schistosomes

• The blood flukes are referred to as a family called Schistosomatidae. 
• The worm's name, Schistosoma, is because of the split body on the ventral side of the male, which the female holds during insemination and egg laying. 
• Human infection with blood flukes is often referred to as Schistosomiasis or Bilharziasis in honor of Theodor Bilharz, who, in 1852, discovered the parasite Schistosoma haematobium at the postmortem of a man who died in Cairo, Egypt. 
• He said that these worms cause haematuria in the farmers, and they lay eggs with terminal spine discharges with urine. 
• The genus Schistosoma has three species parasitized on man: 

1. Schistosoma mansoni, which causes intestinal Schistosomiasis. 

2. Schistosoma haematobium causes the vesicle Schistosomiasis or urinary Bilharziasis. 

3. Schistosoma japonicum, which causes the oriental intestinal Schistosomiasis. 

The worms of the family Schistosomatidae are characterized by: 

1. They need one intermediate host to complete their life cycle. 

2. They inhabit the circulatory system in their host's body, where their bodies adapt to this environment. 

3. They are dioecious (two sexes). 

4. The eggs are non-operculated and fully embryonated when discharged from their host's body. 

5. The cercaria is characterized by its forked tail. They can penetrate the skin of the final host (the human).

• The adult schistosome has an oral sucker around its mouth and a ventral sucker just behind the gut's bifurcation. 
• Males are shorter and thicker than females, with tubercled outer surfaces varying by species, while females have smooth bodies. 
• A ventral groove, called the gynecologic canal, allows the male to hold the threadlike female. The male uses its suckers to attach to blood vessel walls, enabling the female to deposit eggs in smaller venules.  
• The eggs are large, thin-shelled, non-operculated, covered with tubercles, and have species-specific spines, making their morphology a key diagnostic feature. 
• Schistosomes can live up to 30 years in human hosts, though their average lifespan is typically under 5 years.

3.0Life Cycle of Helminthic

• Adult schistosomes reside in the mesenteric veins that drain the intestine (S. mansoni and S. japonicum) or the vesicular veins serving the urinary bladder (S. haematobium). 
• The female usually migrates to the smaller venules before depositing eggs. The eggs of the Schistosomes are laid in the smaller venules, obstructing the normal blood flow. 
• Obstruction of the venules, pressure exerted by the worm, increase in egg size, and hypermotility of the parasitized organ cause the blood vessel to rupture and discharge the eggs into surrounding tissues. 
• The enclosed miracidium in the egg is poorly developed at the oviposition but is well formed before it reaches the lumen of the infected organ. Maturation of the miracidium inside the egg while in the tissues takes place within about (1) week (S. mansoni and S. haematobium) or (12) days (S. japonicum), after which the egg sheds into the lumen of the organ and evacuated in the feces (intestinal type) or urine (vesicle type). 
• When the eggs reach fresh water, hatching occurs, and the miracidia become free swimming. The miracidium penetrates an appropriate snail (the intermediate host) and develops into a sporocyst, then produces a secondary (daughter) sporocyst, which gives rise to the cercarial generation. 
• At that time, fork-tailed cercariae are produced over several weeks (inside the snail tissues); when mature, the cercariae emerge from the snail by secretions from a pair of escape glands located in the cephalic region of the cercaria and swim about in the water.

• Cercariae are triggered to attach and penetrate mammalian skin by its secretions. Using muscular suckers and glandular mucoid secretions, the cercaria adheres and penetrates the skin, aided by secretions from its penetration glands. 
• During this process, the cercaria undergoes three key changes: shedding its tail, losing its surface coat, and expending its gland contents. At this stage, it is called a schistosomulum.
• Once in the dermis, schistosomula enter the peripheral capillaries or lymphatic system, migrating to the heart and lungs. By the third day post-penetration, they appear in pulmonary capillaries. 
• By day four, they feed on host erythrocytes, rapidly growing and developing in the lung parenchyma. 
• From there, they may crawl against the bloodstream through the heart and hepatic vein into the liver or passively reach the liver via pulmonary veins, arterial channels, and intestinal capillaries.
• Around three weeks post-penetration, the worms reach the hepatic portal veins, mature sexually, and mate by day 40. 
• Mated pairs migrate against the portal bloodstream to venules at their target sites for egg-laying: small intestine venules (S. japonicum), colon venules (S. mansoni), and urinary bladder venules (S. haematobium).

4.0Development of Helminthic Disease

• Incubation (or prepatent) period: It starts from skin penetration to the appearance of eggs in the excreta (10-12) week; it includes slight bleeding, skin irritation in the penetration region appears as a rash, cell infiltration in the lungs, inflammatory reaction, infiltration of the eosinophils and sensitization in the liver. 
• Acute period (or stage): this is when the female is in full activity of egg laying in the venules, accompanied by tissue destruction and bleeding that exits with urine or feces. It is the most important symptom of bilharzia infection. There is also inflammation around the eggs in the tissues. 
• Chronic period (or stage): This stage is characterized by stable or decreased egg output, more tissue fibrosis around the egg area, which forms pseudo tubercles, and tissue proliferation and repair.

5.0Pathology

• The first symptom of schistosomiasis is localized dermatitis, marked by itching and swelling at the site of cercarial penetration, which resolves within four days.
• In advanced cases, hepatosplenomegaly (enlarged liver and spleen) is common. Eggs trapped in the intestines, urinary bladder, liver, and spleen trigger inflammatory reactions, leading to cirrhosis, anemia, and granuloma (pseudotubercle) formation around the eggs.  
• Severe complications arise from increased portal blood pressure as the liver becomes fibrotic and engorged. 
• This can cause fluid buildup in the peritoneal cavity and the development of new blood vessels bypassing infected organs. These fragile vessels are prone to rupture, potentially causing life-threatening bleeding.

6.0Helminthic Infections Symptoms

• S. mansoni: The clinical signs include abdominal pain and diarrhea, the feces mixed with mucus and pus. 
• S. haematobium: The symptoms during the incubation period are parallel those of the two intestinal types of the disease. When the cercaria reaches the heart and lungs, it may cause jaundice and bleeding in the pulmonary capillaries, leading to eosinophilia, especially around the small worms. When they reach the portal system, they continue in the growth and the discharge of the metabolic products, which leads to toxic symptoms and anorexia, headache and general malaise. During egg laying, the blood initially appears in the urine without pain. Still, in the progressive case, a burning sensation appears with urination and between the urination periods. 
• S. japonicum: In the acute stage, diarrhea and eggs appear in the feces, as well as daily fever, epigastric pain, and continued enlargement of the liver; the patient loses appetite and weight, and the blood picture is one of anemia and increased serum globulin levels with continued high eosinophilia.

7.0Helminthic Diagnosis

• The most reliable way to diagnose schistosomiasis is by identifying characteristic eggs in excreta or tissue biopsies, particularly rectal biopsies for all three species. 
• Radiology can also detect calcified eggs in urine for S. haematobium. 
• Immunodiagnostic methods show promise but require confirmation through egg identification, as false positives may occur due to concurrent parasitic infections or exposure to animal schistosome cercariae, which can cause swimmer's itch.  
• During the prepatent period, specific diagnosis is not possible. In the acute stage, eggs can typically be found in feces (S. mansoni, S. japonicum) or urine (S. haematobium). Recovery methods include sedimentation, acid-ether concentration, or thick smears.

8.0Helminthic Treatment

• Treatment can't be expected to undo the chronic inflammatory lesions (fibrosis) that occur in the stages of healing and repair. Schistosoma japonicum, the most pathogenic one, is the least responsive to treatment. 
• Schistosoma haematobium, the least pathogenic, is the most responsive one. Treatment should only be given when eggs are demonstrated. 
• The chemotherapeutic agent recommended for all species of human schistosomes is praziquantel. In the schistosomes, this drug disrupts the integrity of the tegument and exposes the inaccessible antigens, which become targets for host antibodies. Niridazole is also effective in S. japonicum.

9.0Control of Helminthic Diseases

The World Health Organization (WHO) identifies four key strategies for controlling schistosomiasis: population-based chemotherapy through repeated drug treatment for infected individuals, use of molluscicides, implementation of biological controls like predatory snails and fish, and public education.

Swimmer’s Itch:

• Cercarial dermatitis, or swimmer's itch, is an intriguing aspect of schistosome biology. Although not life-threatening, it can negatively impact the economy in tourist regions during outbreaks. 
• The condition occurs when cercariae from blood flukes that typically infect aquatic birds and mammals penetrate human skin. 
• This causes pustules and an itchy rash at the entry points. Since humans are unsuitable hosts, the cercariae do not mature and are destroyed by the immune system. 
• Allergens released from the dying cercariae trigger a localized inflammatory reaction.