Ascariasis is a human infection caused by a roundworm

Ascaris lumbricoides and characterized by early pulmonary and later intestinal symptoms. Being the only reservoir humans are infected by eating food (e. g. vegetables) contaminated with mature ova. These hatch in the duodenum and the larvae migrate through the wall of the small intestine and are carried by the lymphatics and bloodstream to the lungs. Here they pass into alveoli, ascend the respiratory tract and are swallowed. They mature in the jejunum, where they remain as adult worms. Disease may be caused by both the larval migration through the lung and the presence of the adult worm in the intestine.

Infection with the adult worm is usually diagnosed by finding eggs in the stool. Occasionally, adult worms are passed in the stool or vomited. Larvae are occasionally found in the sputum during the pulmonary phase.

A tangled mass of worms may cause intestinal obstruction (mostly in children or young adults) with typical colicky pains, «acute abdomen» syndrome, vomiting with intestinal contents and specific X-ray findings; a heavy infestation will compete for nourishment and contribute to malabsorption.

The complications of ascariasis may require surgery. The surgical approach in intestinal obstruction requires that the tangled mass of the worms should be descended to the large intestine during laparotomy with subsequent medical therapy; enterotomy and removal of the helminth may occasionally be indicated.

Ascaris limbricoides-associated appendicitis lacks specific signs. The adult worms may inadvertently be found in a patient operated on for acute appendicitis, in which obstruction of the appendix can be evident.

Other complications include blockage of the bile or pancreatic duct, which may only rarely be found. The maturation of the worms in the intestine can lead to penetration through Vater's ampulla into the common bile duct and the biliary tree. This, in turn, results in obstructive jaundice, suppurative cholangitis, acute cholecystitis, hepatic abscess.

The clinical picture of biliary ascariasis includes the signs of obstructive jaundice, suppurative cholangitis, hepatic abscess with acute onset and rapid progression of sepsis characterized by severe toxaemia.

ERCP, ultrasound scanning, CT may help establish the definitive diagnosis.

The surgical methods include cholecystor choledochectomy, parasite extraction with external bile duct drainage.

Pancreatic involvement (inflammation) in ascariasis occurs if the worms gain entrance to the main pancreatic duct, which results in chronic indurative or acute (e. g. haemorrhagic) pancreatitis. The only option is surgery - pancreaticotomy with removal of the worms and postoperative specific antiparasitic drug therapy.

Ascaris lumbricoides-associated GI tract (oesophagus, stomach, intestine) perforation results from ulcerative and necrotic changes of the mucosal membranes, which, in turn, may produce the clinical signs of peritonitis.

Postsurgical complications of ascariasis are due to active migration of the worms following the operation. They may also be vomited with occasional subsequent mechanical asphyxia caused by their penetration into respiratory tract.

Surgeries that involve incision of hollow organs may be complicated by discharging of the worms into the free abdominal cavity through sutures with subsequent suppurative peritonitis.

Severity of the postsurgical complications of ascariasis requires that each elective surgery should be preceded by identification of the ova in faeces. Once the diagnosis of ascaris has been confirmed, preoperative drug therapy is mandatory.

AMOEBIASIS

Amoebiasis is an infection usually caused by Entamoeba histolytica and mainly characterized by ulcers in the colon and possible haematogenous spread of the parasite to visceral organs (the liver, lung, brain, etc.) with development of abscesses. The parasite formerly termed E. histolytica is now known to consist of two separate species, non-pathogenic E. dispar and pathogenic E. histolytica, which are distinguished by molecular techniques, isoenzyme studies, or monoclonal antibody typing after culture of trophozoites.

The disease is common throughout the tropics, particularly in Central Asia, the Caucasus, occasionally in other regions.

The motile trophozoite, the parasitic form, dwells in the bowel lumen where it feeds on bacteria or tissue. With diarrhoea, the fragile trophozoites pass unchanged in the liquid stool and rapidly die. If diarrhoea is not present, the organisms usually encyst before leaving the gut. The cyst, the infective form of the orgamism, resists environmental changes and may be spread either directly, i.e. from person to person, or indirectly, i.e. via food (e.g. lettuce) and water.

The main reservoir of the infection is human who discharges amoebic cystic with faeces.

In the colon, the parasite penetrates the submucosal layer, which results in inflammation, necrosis of tissues and ulcers. Via the intestinal vessels, amoebae spread to the internal organs where they cause abscesses. The intestinal wall may perforate to lead to suppurative peritonitis. Clinical signs of intestinal amoebiasis are similar to those of bacterial dysentery and includes fever, weakness, fatiguability or malaise, bloody and mucous diarrhoea, sometimes resembling of «raspberry jelly» in appearance. Identification amoebae in faeces and specific serologic reactions confirm the diagnosis.

Perforation and gangrene of the colon lead to suppurative peritonitis. The diagnosis is based on clinical signs of peritonitis characterized by endotoxic shock, but peritoneal irritation is usually slight. Abrupt deterioration of the patient's condition or onset of the signs suggestive of peritonitis should serve as an indication for laparoscopy. Once the diagnosis has been made urgent surgery is necessary to perform. Intestinal gangrene requires bowel resection, while in pronounced necrosis around the perforating ulcers the resection should be followed by with colostoma if suturing is inopera.

Amoebiasis-associated colitis may occasionally be complicated by amoebic granuloma (i.e. perifocal infiltrate in the intestinal wall around the ulcer) as a result of absence of specific treatment. Morphologically, the granuloma is productive inflammation with necrotic foci in the intestinal wall. The caecum and ascending colon are most commonly affected.

Abdominal palpation reveals tender mass of rubbery consistency in the right lower quadrant.

The diagnosis is based on history of chronic amoebiasis, clinical data and the results of colonos-copy. Identification of amoebae in faeces is a direct confirmation of the diagnosis. The suppuration of the infiltrate may cause bowel perforation and faecal peritonitis. Large amoebic granulomas may result in intestinal obstruction. In non-complicated amoebic granuloma, drug therapy is indicated. Failures of medical therapy may require elective surgery, while in suppuration and intestinal obstruction urgent surgery is needed.

Amoebic appendicitis results from specific ulcers in the appendicular mucosa with suppuration and lacks specific clinical signs.

In extensive ulcers intestinal bleeding is possible. The source of bleeding localized in the distal part of the large bowel produces profuse haemorrhage with scarlet blood, while that in the upper part of the GI tract results in discharge of tarry blood. Conservative measures to replenish the circulating blood volume are used to control bleeding (see Chapter V) which should be coupled with antiprotozoal therapy.

Surgery (resection of intestine) may be necessary in profuse intestinal bleeding, colonoscopy helping identify the source of bleeding.

Liver abscess is the most common surgical complication of amoebiasis and occurs in 2-10% of cases. The specificity of the liver abscess consists in the absence of the suppurative membrane, it contains necrotised tissues with odourless coffee-like liquid pus, while suppuration produces offensive green or whitish pus.

In 80-90% of cases abscesses are found in the right lobe of the liver.

Amoebic abscess is a severe complication with toxaemia, hepatic failure, exacerbation of intestinal amoebiasis. The patients complain of the pain in right hypochondriac region radiating to the right scapula and right shoulder.

In superficial abscesses, swelling of the skin, tenderness at intercostal spaces and the liver with hepatomegaly may be found.

In chronic liver abscess the signs of severe debilitating disease predominate: dry flabby grey skin, icteric sclerae, signs of malnutrition, sometimes pedal or shin oedema. The liver is enlarged (but less tender than in acute condition), of dense consistency, sometimes bosselated. Liver abscess may perforate the abdominal or thoracic cavities, retroperitoneal space, bile ducts and even the abdominal wall.

To make the diagnosis of liver amoebiasis abscess special methods of examination are used: X-ray, scintigraphy, ultrasound and CT scanning. USor CT-guided laparocentesis may help confirm the diagnosis as does identification of amoebae in pus.

The treatment of liver abscess includes combination of amoebicides, antibacterial and detoxication therapy. Small, even multiple abscesses, may be treated by USor CT-guided laparocentesis coupled with aspiration and administration of amoebicidic and antibacterial drugs.

In unsuccessful conservative treatment or abdominal perforation, the incision and drainage of the abscess are indicated.

Lung abscess. The spread of amoebae to the lungs leads to pneumonia or lung abscess. The clinical signs or X-ray findings of amoebic pneumonia and abscess are similar to those of non-specific pulmonary conditions.

Abscess requires antibacterial therapy and, if in vain, is tapped and pus aspirated with following administration of antiseptics into the cavity.

Brain abscess (mostly multiple) is a rare complication. Apart from clinical methods, special methods of investigation (cerebral CT, US) are used to make the diagnosis of brain amoebiasis. Antiamoebic and antibacterial drugs are indicated; however, in formed abscesses surgery (removal of the abscess together with its capsule) may be necessary.

All surgical complications invariably require antiamoebic therapy (emetine, metronidazole, chloroquine ).

The prevention of the amoebic complications includes personal precautions against contracting amoebiasis in tropics and subtropics, i.e. not eating fresh uncooked vegetables nor drinking unboiled water and aggressive treatment of patients with intestinal amoebiasis.

FILARIASIS

Filariasis is a group of diseases occurring in tropical and subtropical countries (Africa, South America and South Asia) and caused by Filarioidea.

For surgery, the conditions due to infection with Wuchereria bancrofti and Brugia malayi are of prime significance, the two nematodes affecting the lymphatic system.

Wuchereria bancrofti is found only in humans; Brugia malayi is often spread to man from an animal host. The adult filarioidea are found in the human lymphatic system. Microfilariae released by gravid females are found in the peripheral blood, usually at night. Infection is spread by many species of mosquitoes; vectors of W. bancrofti are Aedes, Culex, and Anopheles; of B. malayi, Anopheles andMansonia. The microfilariae are ingested by the mosquito, undergo development in the insect's thoracic muscles for eight to thirty-five days, and, when mature, migrate to its mouthparts. When the infected mosquito bites a new host (humans, monkeys, dogs, cats), microfilariae penetrate the bite puncture and eventually reach the lymphatics, where they develop to the adult stage. This, in turn, affects the function of the lymphatics and causes allergic lymphangitis or even lymphatic obstruction (e.g. in the thoracic duct).

The persistent lymphatic obstruction results in elephantiasis.

The clinical features of the disease include bouts of fever accompanied by pain, headache, malaise (stage 1). The lymph nodes tend to be hard and tender, the lymphatic vessels are tender and show erythaema along their course. Lymphangitis extends from proximal to distal limb segment. Inflammation of the spermatic cord and axillar lymph nodes precedes lymphangitis. Simultaneously, urticaria-like rash with pruritus is evident at various body areas.

Further attacks follow in several months or years, temporary oedema becomes more persistent and regional lymph nodes enlarge. Progressive enlargement, coarsening, corrugation and fissuring of the skin and subcutaneous tissue with warty superficial excrescences develop gradually, causing irreversible «elephantiasis» with vascular rupture, chyluria and chylous effusions (stage 2).

Complication by pyogenic infection results in abscesses or phlegmons.

Stage 3 of the disease is characterized by elephantiasis of the lower limbs and scrotum, and occasionally of the upper limbs, breast and vulva. The diagnosis is based on the clinical features and identification of microfilariae in blood or lymph fluid.

Treatment. At initial stages, the antiparasitic drug therapy with diethylcarbamazine (0, 1 g q 8 hours for 7-10 days) is indicated, with regular identification of micrifilariae in the blood. If required, the course may be repeated.

Secondary infection serves as an indication for antibacterial therapy.

Abscesses, pleural empyema, peritonitis and elephantiasis all require surgery (debridement of the skin, subcutaneous fat, fasciae). To cover the skin defect, the dermatome flaps from intact removed skin areas or other body areas (skin grafting) are used.

In scrotal elephantiasis, the skin, subcutaneous fat, testicle capsules are removed within the limits of intact tissues.

The surgery should be performed it the parasite is no longer found on serial blood tests. The identification of the filarioidea requires preoperative specific drug therapy.

FASCIOLIASIS

Fascioliasis is a parasitic disease caused by a trematode Fasciola hepatica (a liver fluke) and characterized by involvement of the liver and bile ducts.

The condition is found worldwide, most often in France and Cuba.

Apart from human, other mammalian hosts are sheep, goats and cattle, while intermediate ones are freshwater snails.

F. hepatica is only accidentally transmitted to humans via consumption of wild watercress or other plants grown on the grazing land of infected animals. These excrete eggs in their faeces, from which ciliated miracidia emerge. They enter the intermediate host in which larval development takes place. Eventually, cercaria are released and these encyst on aquatic or surface vegetation. After ingestion by a mammalian host, the parasites encyst, migrate through the intestinal wall and penetrate the liver capsule after traversing the peritoneal cavity. Immature flukes reach the bile duct by passing through hepatic parenchyma and after maturation begin to produce ova. Adult flukes remain within the biliary tract or gallbladder for many years.

The fluke affects the epithelium of the bile ducts to increase the risk of suppurative infection (suppurative cholecystitis, liver abscess, cholangitis) or obstructive jaundice that require surgery. The signs of suppuration of the gallbladder, bile ducts in the patients with established fascioliasis strongly suggests the complications of fascioliasis. The destruction in the liver, bile ducts of whatever origin requires urgent surgery, during which the flukes may be identified.

Irrespective of the site of F. hepatica, the surgery is performed in compliance with the general principles. Specific drug therapy is with hexachlorparaxicol or emetine hydrochloride.

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