Hookworms and Strongyloides PDF

Hookworms Strongyloides stercoralis By Dr/ Mona Faheem  Hookworms ❖ Species : The two most common types of hookworms that infect humans are: 1. Ancylostoma duodenale known as the old-world hookworm. 2. Necator americanus known as the New-World hookworm or the American kill...

Hookworms Strongyloides stercoralis By Dr/ Mona Faheem  Hookworms ❖ Species : The two most common types of hookworms that infect humans are: 1. Ancylostoma duodenale known as the old-world hookworm. 2. Necator americanus known as the New-World hookworm or the American killer.  Ancylostoma duodenale (Old World hookworm) Geographical distribution: Cosmopolitan, widely distributed in tropical and subtropical countries. Habitat: Small intestine and particularly jejunum. D.H: Man. (the only natural host). Intermediate host: No intermediate host. Diagnostic stage: immature eggs. Infective stage: Third stage filariform larva.  Morphology: ❖ Adult worms Small cylindrical worms with a cup-shaped toothed buccal capsule that carries a pair of glands that secrete anticoagulant peptides into the worm’s buccal cavity, esophagus, and the attachment site Eggs (diagnostic stage): ❑ Size: 60 x 40 μm ❑ Shape: Oval. ❑ Shell: Thin. There is a clear space between the segmented ovum and the eggshell. ❑ Color: translucent. ❑ Content: Freshly laid eggs contain a developing embryo in the early stages of cleavage (4-8 cells). The 3rd stage filariform larva (infective stage). 500- 700 µm long. Sheathed. Sharply pointed tail. Ratio between the length of esophagus to intestine: about 1:2 Life cycle Life cycle 1. Adult worms live in the small intestine of man. They attach themselves to the intestinal mucosa using their buccal capsule. 2. After fertilization, the female worm lays eggs passed out in infected persons’ feces. 3. In the soil, under favorable environmental conditions (moisture, warmth, and shade), the embryo develops inside the deposited eggs and rhabditiform larvae release, and feed on bacteria and other organic matter. 4. After 5 to 10 days, they moult twice to become the third-stage infective filariform larvae. 5. Man can be infected by: (mode of infection) a. Active skin penetration of 3rd stage filariform larvae to his exposed skin (especially hands, feet, arms, and legs). b. Oral route, where the filariform larva, contaminating vegetables or fruits, penetrates the buccal mucosa to reach the venous circulation. 6. Following skin penetration, the larvae enter subcutaneous venules and lymphatics, and migrate to the right side of the heart and to the lungs. 7. Inside the lungs, where the third moult occurs, ascend along the bronchial tree to the trachea, traverse the epiglottis to the esophagus, and are swallowed to reach the intestine. 8. The larvae which reach the small intestine undergo the final moult to form adults which mature and mate. 9. In heavy infections, part of the filariform larvae can reach the left side of the heart and be distributed with general circulation to many human viscera (visceral larva migrans). Disease: Ancylostomiasis. - Some people can develop an Ancylostoma infection without any symptoms. 1. The invasion stage: The filariform larvae penetration of skin results in hypersensitivity reaction which manifests as local irritation, intense itchiness, and vesicular erythematous rash lesions. These are followed by linear serpiginous, and elevated ridges due to the larvae tunneling phenomenon and vesicular rash lesions that are called ground itch or creeping eruption. 2. The pulmonary stage a. Larval migration through lung tissue causes a pulmonary hypersensitive response called verminous pneumonia (eosinophilic pneumonia or Loeffler’s syndrome) which presents clinically in the form of cough, bronchitis, and hemoptysis. b. Visceral larva migrans: can occur in heavy infections. 3. The intestinal stage: The adult worms cause mechanical injury to the mucosa by their buccal capsule and teeth during their blood meal. a. A light infection causes abdominal pain, loss of appetite, and geophagy (pica, urge to eat soil). b. Heavy infections occur most often in children and include dyspepsia, nausea, epigastric distress, acute enteritis with uncontrollable diarrhea, and foul stools. c. Chronic infection results in: Hypoproteinemia: which leads to: - Malnutrition with physical and cognitive impairment due to protein deficiency. Iron deficiency anemia due to blood loss Diagnosis: History and clinical picture.. Laboratory: A. Direct methods: 1. Stool examination: to detect eggs. 2. Stool culture: to detect 3rd stage filariform larva. 3. Baermann's technique for examination of larvae in soil or stool B. Indirect methods: -DNA-based tools for diagnosis of infection could serve as a molecular approach for accurate diagnosis of hookworm in the feces Treatment: A. Antihelminthic treatment. 1. Albendazole. 2. Mebendazole: B. Symptomatic treatment. 1. Iron supplement 2. High protein diet and vitamins.  Prevention and control: 1. Treatment of patients and carriers 2. Sanitation and proper use of sanitary latrines. 3. Wear shoes, and gloves and avoid walking barefoot. 4. Avoid using fertilizer made from human feces. 5. Hygiene measures such as hand washing and avoiding defecation on the ground Strongyloides stercoralis (Dwarf threadworm)  Geographical distribution: Mainly in Tropical & subtropical regions especially in areas of low sanitation and poor hygienic measures. Habitat: The parasitic female lives in the human small intestine (duodenum and jejunum) while the free-living female and male worms freely multiply in the environment. Definitive host: Man &dogs Diagnostic stage: Rhabditiform larva. Infective stage: 3rd stage filariform larva.  Morphology ❖ Adult worms: Cylindrical thread-like worm. The size of parasitic females is larger than the free-living ones. The size of both free-living and parasitic males is similar. Eggs (rarely found in stool):- : Size: 50–70 x 30 μm. Shape: oval. Shell: thin. Color: translucent. Contents: mature (larva). ❖ Rhabditiform larva (L1) [diagnostic stage]: Size: 200-250 μm long. Shape: short buccal cavity, a double bulb esophagus. ❖ Third stage filariform larva (L3) [infective stage]: Size: 500-600 μm long. Shape: long cylindrical esophagus and a notched tail. Life cycle Life cycle Strongyloides stercoralis is a unique parasite as it can develop by a direct parasitic life cycle or an indirect free-living life cycle by alternating generations. 1. Females are embedded by its anterior ends into submucosa of small intestine. 2. Eggs are produced and hatch inside the small intestine. 3. Larvae pass with stool to the soil and moult to form the 3rd stage infective filariform larva. The behavior of the larvae is determined according to the environmental conditions. Indirect development: in favorable environmental conditions, the soil L3 completes its life cycle without a host. They moult twice to develop into adults. Direct development: In unfavorable environmental conditions the larvae starve and try to find a host to live. 5- Humans can be infected by: (Mode of infection) a. Penetration of skin by 3rd stage infective filariform larva. (L3 )during walking barefoot. b. Penetration of the mucous membrane of the mouth by eating food contaminated with L3. c. Autoinfection: Some L1 larvae don’t pass with feces but develop into L3, penetrating the intestinal wall (internal autoinfection) or perianal skin (external autoinfection). D- Hyper-infection: can occur in patients receiving corticosteroids which increase the moulting rate of L1 larvae in the gut. 6. L3 find their way to the circulation and are carried by the blood to lungs → pass into alveoli→ moult →ascends to trachea → pharynx → esophagus → small intestine. 7. In the small intestine, the filariform larvae do their final moult to form male and female adults which mate and lay eggs. Clinical picture 1. The cutaneous phase: 2. - Ground itch: At the entry site of infective larva→ itching, maculopapular or urticarial rashes usually on the feet. - Larva currens: linear, pathognomonic serpiginous urticarial rash in the perianal region (Cutaneous larva migrans). 2. The pulmonary phase: - Due to larval migration in the lungs. - bronchopneumonia with cough, dyspnea, and wheezes. - Larva is found in sputum The intestinal phase: - Female worms become embedded in the mucosa or submucosa leading to epigastric pain, diarrhea with blood & mucus, nausea and weight loss, and malabsorption of fat, proteins, and vitamin B12. - N.B: Strongyloides stercoralis is considered an opportunistic parasite that affects severely immunocompromised patients. Diagnosis History and clinical picture. Laboratory: 1. Stool examination: for detection of rhabditiform or filariform larvae in stool. 2. Culture of stool samples: nutrient agar is the most effective in larvae isolation (method of choice). 3. Baermann funnel technique, Charcoal culture method. 4. Sputum should be examined for larvae with wet mounts. 5. Serological diagnosis can be used to follow up of the efficacy of treatment. 6. Diagnosis of strongyloidiasis in stool using coproantigen has excellent specificity. 7. Duodenal aspiration (Entero-test) is a very accurate technique in hyperinfection because the larvae passed in feces may decrease. 8. Molecular diagnosis: PCR is 100% specific and of high sensitivity. 9. Eosinophilia 10 – 40%  Treatment: 1. Ivermectin 2. Albendazole 3. Mebendazole N.B. Treatment should be repeated after a week to avoid relapse of the intestinal phase, especially in immunocompromised patients. Prevention and Control ❑ Personal prophylaxis: wearing shoes to protect skin from contact with contaminated soil (farmers). ❑ Avoid defecation in soil. Sanitary disposal of human feces. ❑ Avoid use of human feces as fertilizers or disinfection before use. ❑ Mass treatment of patients. ❑ High-risk groups, such as immunosuppressed, farmers, immigrants from endemic areas, and mentally handicapped should be examined periodically and treated.