www.drkhuroo.org IMAGE OF THE WEEK SEASONAL COUGH IN A 6 YEAR BOY!

QUESTION: A mother brought her 6 year son for consultation. She was worried because the boy has been suffering from intractable cough every year during rainy season. A wet preparation of the sputum is shown. What is your diagnosis and how to treat this entity? ANSWER BY VIEWERS: Dr Bashir Ahmad bashir786@rediffmail.com, answer was Ascariasis pneumonitis (larvae of Ascariasis), treatment: deworming. ANSWER: The child was suffering from recurrent Ascaris Lofflers pneumonia. The sputum examination showed filariform larva of Ascaris lumbricoides. Ascaris larvae are 200 to 300 m long and 13 to 15 m thick. The pulmonary disease occurs during larval migration of the parasite. CASE RECORD: This 6 years old boy presented with high fever (38.5 to 390C), cough, breathlessness and hemoptysis for past one week. Clinical examination revealed tachycardia (pulse 160/min), tachypnoea (respiratory rate 40/min), cyanosis (SpO2 60%), audible wheezing, bilateral wheezes and rales. CBC showed marked leucocytosis (WBC 27X109/L [normal 4.0-10.5 x109/L]) with marked eosinophilia (eosinophils 27% [normal 1.0-6.0%], and very high absolute eosinophils count 7290/cmm [normal <500 cumm]. Liver function and kidney function tests were within normal limits. ABG revealed acute respiratory acidosis (pH 7.3, PaCO2 20 mmHg, HCO3 28 mmol/L). X-ray chest showed bilateral airbronchogram patchy opacities. Sputum examination showed multiple filariform larvae (Fig).

Fig. Wet preparation of sputum showing a filariform larva of Ascaris lumbricoides.

Sputum culture did not reveal any pathogenic organisms. He was admitted to pediatric intensive care, treated with broad cover antibiotics, bronchodilators, nasal oxygen and intravenous hydration. He recovered over next 48 hours; clinical, and biochemical parameters improved and was discharged from the intensive care unit on 4th day. Mother was enquired about his previous episodes of respiratory complaints which the child had been having for last 3 years. These episodes were similar in character but less severe in degree and had recovered after short course of antibiotics and bronchodilators. Larval migration of Ascaris lumbricoides: Ascaris eggs are passed in the feces. The fertilized eggs require 10 to 15 days in the soil for embryonation before they are infective. The larvae undergo two molts, and the third stage is the infective form. Hatching of the eggs does not take place in the soil but occurs in the upper intestines. The eggs in the soil remain viable and capable of infection for a period up to 10 years. They are resistant to usual methods of chemical water purification. Boiling, however, kills the Ascaris egg within minutes. Infection follows ingestion of embryonated eggs in a number of ways. Among children, soil, fingers, and toys are common vehicles of transmission. They acquire infection commonly while playing on infected soil. Geophagia in children can result in massive infections. Eggs can contaminate food and drinking water. Infection is common in those regions where human feces are used as a fertilizer for growing vegetables. In such regions, ingestion of raw salad is a major risk factor for Ascaris infection. Ascaris eggs can survive in pickles for long periods and cause infections in endemic regions. In dry, windy climates, Ascaris eggs can become airborne and be ingested. After ingestion, the shell of the embryonated egg is dissolved by gastric juice, and the embryo emerges in the duodenum as the rhabdoid larva 200 to 300 m long and 13 to 15 m thick. The larvae migrate to caecum and penetrate the surface epithelium of the mucosa. The larvae enter the veins of the portal system and are carried to the liver. In the liver, larvae move freely in the sinusoids. Some may subsequently pass via hepatic veins to the heart and lungs. Some larvae may enter the lymphatic system of bowel and are carried via the thoracic duct to the lungs. The larvae break through the capillary wall and enter the alveolar space and the bronchial tree. During this passage, larvae molt twice and grow considerably in length and width. They ascend the tracheobronchial tree and larynx to the hypopharynx, where they are swallowed. On reaching the small intestines, the larvae attain sexual maturity in 2 to 3 months. In the upper gastrointestinal tract, they molt again before becoming mature worms. The time from the larval infection to maturation is usually 4 months. Pathology of the larval migration including pulmonary disease: The intestinal mucosa reveals minute hemorrhage at places of larval penetration. This results in focal areas of inflammation with infiltration of eosinophils and macrophages. In the hepatic sinusoids, mobile larvae do not elicit an inflammatory response. Dead larvae in the liver, however, stimulate a granulomatous reaction. Larval migration may involve other organs than liver

and lungs. Migration to kidney, heart, and brain has been observed. Convulsions may occur during invasion of the brain. Larvae in these organs are rapidly killed and granulomas are formed. Pulmonary disease caused by Ascaris is due to larvae during their pulmonary migration and maturation. In the pulmonary capillaries and alveoli, larvae are surrounded by eosinophils and neutrophils. The larvae in the bronchial tree are surrounded by mucus, edema, and inflammatory cells. It presents a self-limiting pneumonia lasting for 2 to 3 weeks and occurs 4 to 16 days after ingestion of the embryonated eggs. The disease is caused by larvae in the terminal air spaces and bronchioles, which provoke infiltration with polymorph nuclear leukocytes, eosinophils, desquamation of epithelium, and exudation of serous fluids leading to plugging of air spaces and consequent consolidation. The consolidation may be limited to lobules; however, in some cases, it may extend to a single lobe or even multiple lobes. The dead larvae in the lungs stimulate a granulomatous reaction similar to that in the liver. Invasion of the blood stream by the larvae results in peripheral eosinophilia. Clinical syndrome of pulmonary Ascariasis: Ascaris pneumonia is common in children and presents as sudden onset of fever (39.5 to 40oC), frequent spasms of cough and wheezing, dyspnea, and Substernal distress. In heavy infection, cough is productive with hemoptysis. Patients may be in status asthmatics and require admission to an intensive care unit. An urticarial rash or angioneurotic edema may precede or accompany pulmonary manifestations. Abdominal symptoms, such as right quadrant pain and vomiting, may occur. Physical examination often simulates an atypical pneumonia. X-ray examination of the chest usually shows diffuse mottling and prominence of peribronchial regions. There is generally a high eosinophilia. The filariform larvae of A. lumbricoides can usually be seen on sputum or gastric aspirate examination. Occasionally, there is some biochemical evidence of hepatocellular damage, suggesting larval liver disease. Epidemiology of Ascaris pneumonia: The disease is common in endemic zones, associated with Ascaris infection and reinfection. The disease is more severe with reinfections. Children are more susceptible to Ascaris pneumonia. Seasonal attacks occur after the onset of spring rains, restarting transmission of Ascaris. In Kashmir, Ascariasis is highly endemic and over 70% children and about 30% adults are infected. Thus pulmonary Ascariasis must be a common disease in this community. In fact majority of the children get infected and reinfected during each high susceptible season especially after rainy season. However, there is lack of reports of this disease from this community. This points to the fact that most of these respiratory episodes in children are managed as allergic bronchitis, asthma or viral or bacterial pneumonias. Parasitic etiology of such episodes needs to be explored by high degree of suspicion, blood counts and sputum examination for larvae. Management of this entity is supportive and none of the antihelmintic drug therapy has anti-larval effect.

REFERENCES. 1. Khuroo MS. Ascariasis. Gastroenterol Clin North Am. 1996; 25(3):553-77. 2. Valentine CC, Hoffner RJ, Henderson SO. Three common presentations of ascariasis infection in an urban Emergency Department. J Emerg Med. 2001; 20(2):135-9. 3. Ramsey W. Ascaris pneumonitis: case presentation. Iowa Med. 1989; 79(10):484-6. 4. Tomashefski JF, Butler T, Islam M. Histopathology and etiology of childhood pneumonia: an autopsy study of 93 patients in Bangladesh. Pathology. 1989;21(2):71-8. 5. Berk SL, Verghese A. Parasitic pneumonia. Semin Resp Infect. 1988; 3(2):172-8. SOURCE: The case report was drawn from case records of Dr. Khuroos Medical Clinic and review was prepared by Mehnaaz Sultan Khuroo MD, host website www.drkhuroo.org, E-mail: mkhuroo@yahoo.com