Tropical pulmonary eosinophilia - IgG antibodies to heartworms. IgG antibodies for differential diagnosis with Schistosoma spp., Strongyloides stercoralis, Ascaris lumbricoides, Toxocara spp. and Basiodiobolus ranarum.

 

Information 11/03/15.

 

Tropical pulmonary eosinophilia (TPE: Pulmonary Eosinophilia Tropical) is a disease caused by a hypersensitivity reaction larvae (microfilaria) lymph filaria, Wuchereria bancrofti specifically against and Brugia malayi. This disease prevails in India, Southeast Asia, Africa, South America and other tropical and subtropical countries. However, pulmonary eosinophilia, is a process that appears, to a greater or lesser extent in all helminth infections biological cycle in which the larvae penetrate the pulmonary circulation areas or routes before reaching its final organizational location. This cycle curre with Strongyloides stercoralis, Ascaris lumbricoides, Toxocara spp., Ancylostoma duodenale, Necator americanus, or Schistosoma spp. (see below ).

 

Wuchereria bancrofti has sexual dimorphism. Adult males are long and thin, with a curved tail 40 to 50 mm in length and 1 mm diameter. In contrast, the female is 60 to 100 mm and up to three times wider than the male. Adult parasites Brugia malayi are filiform, 13-25 mm long and 70 to 80 microns wide, while the female has a size of 43 to 55 mm long and 130-170 microns wide. The microfilariae of Brugia malayi measured .mu.m 177-230 long and 5 to 6 microns wide and have sheaths. Unlike Wuchereria bancrofti, Brugia malayi microfilaria of cephalic space has a length, a column of compact nuclei and nuclei and subterminal terminal in separated by a short constriction tail.

 

The life cycle of these parasites involves an intermediate host which acts as a biological vector, where microfilariae mature to adults evolve later. The usual biological vectors are mosquitoes of the Culex, Anopheles, Aedes and Mansonia species that acquire and transmit the larvae (microfilaria) through bites during feeding. In the definitive host microfilariae mature into adults, as in people. The bite of the mosquito vector causes inoculation of the larvae reach the lymphatic route to localize in lymphatic system. From the lymph system, where adult females are located, they will release microfilariae (first instar larvae of the parasite) to the peripheral circulation. The microfilarisas can be trapped, largely in the pulmonary circulation. In the circulation remains waiting to be ingested by mosquito during feeding. In the mosquito, the microfilariae develop in 1 to 2 weeks infective larvae (third stage). During the following insect stings, the larvae infect a vertebrate host, thus completing the cycle.

Pulmonary tropical eosinophilia occurs primarily in young adult males who have resided in areas endemic for Wuchereria bancrofti and Brugia malayi. Clinical manifestations vary among individuals and depend on the level of exposure to infective mosquito bite, the number of adults living in the nodes of the infected host, duration of infection, as well as genetic and immunological factors. The disease can vary from acute eosinophilic alveolitis to histiocytic infiltration. Affected individuals occur most frequently asthmatic symptoms, paroxysmal cough and wheezing (especially at night), chronic interstitial lung disease, relapsing fever, peripheral eosinophilia intense (> 3,000 eosinophils / ul) and can be seen sometimes microfilariae degeneration in lung tissue. Other symptoms may include weight loss, weakness, fatigue and malaise. The delay in treatment initiation can lead to progressive and irreversible interstitial fibrosis lung disorder. Eosinophilic alveolitis can be suppressed with treatment for 3 weeks with diethylcarbamazine, so the answer to this treatment has been considered as a diagnostic test. However, in some patients continuous moderate eosinophilic alveolitis.

 

The pathogenesis of this process has been controversial. For years it has admitted that the entrapment of microfilariae larvae in the lung parenchyma were the cause of a local immune reaction causing all the pathogenesis of signs and clinical manifestations of pulmonary tropical eosinophilia. Currently it is known that there is an antigenic similarity between the gamma glutaryl transpeptidase-larval stage L3 of Brugia malayi, and gamma glutaryl transpeptidase-present in the surface of the human lung epithelium. For this antigenic similarity, the induced immune response microfilariae can generate a hypersensitivity reaction within the lungs, responsible for the signs and clinical manifestations of the process.

 

Eosinophils are proinflammatory cells packed cytoplasmic granules red-orange containing cationic proteins (core proteins, eosinophil cationic protein, peroxidase eosinophilic neurotoxin eosinophil), cytokines (interleukins and tumor necrosis factor) and lipid mediators (leukotriene C4). Cationic proteins of eosinophil granules are the primary mediators of toxicity associated with eosinophils to kill microbes and human tissues. Eosinophils in the bone marrow after being stimulated interleukins IL-3, IL-5 and GM-CSF (Granulocyte Macrophage Colony Stimulating Factor-). IL-5 is the most specific for the selective differentiation of eosinophils and release from the bone marrow into the peripheral blood circulation. Eosinophilia corresponds to a Th2 - type response in patients with an allergic process or parasitic diseases.

 

Other processes for differential diagnosis:

 

Schistosomiasis: During Schistosoma spp. migratory larval forms (schistosomula) pass through the pulmonary circulation before passing the blood circulation to reach placed in the abdominal venous plexuses and mature adults. In these patients there is a peripheral eosinophilia, and can present the box labeled Katayama fever, with fever and multiple pulmonary nodules. Proper treatment to treat infection with adult worms is ineffective against larval stages, and symptoms required for improved administration of corticosteroids.

 

Infections by several species of nematodes: several species of nematodes perform a life cycle in the host organism before settling on its final status to mature adults. This occurs with Ascaris lumbricoides, than after ingestion of mature eggs and the output of the larva, it will cross the intestinal wall, reach the lung, penetrate into the alveoli, and be swallowed to again reach the intestine and mature adults. The same occurs with hookworms (Ancylostoma duodenale and Necator americanus), which after penetration of its filariform through the skin, will reach the lung to the bloodstream, and penetrate into the alveoli to be swallowed and reach their location in the intestine, where they mature to adults. Cercariae Schistosoma spp. also they penetrate through the skin, reaching pulmonary circulation and pass through the pulmonary capillaries to reach the left heart and be carried with the circulation to the abdominal venous plexus where they mature to adults. The box named cutaneous larva migrans occurs when Toxocara eggs are ingested. (equivalent to Ascaris lumbricoides other animal species such as dog and cats) whose larvae hatch, through the intestinal wall, and circulate through the tissues without knowing reach the way back to the intestine through the passage through the pulmonary alveoli, so they can also reach the lung and give to a pulmonary eosinophilia.

 

Basiobolomicosis (Basidiobolus ranarum): Basidiobolus ranarun is a saprophyte fungus found worldwide, the Order Entomophthorales, Class Zygomycetes, found in decaying vegetation, fruits, food, soil, gastrointestinal tract of reptiles, amphibians, fish, and insectivorous bats , among others. Penetration to produce infections can occur through the skin after biting insects, scratches or minor cuts. This fungus can not survive at 4 therefore should be considered to preserve culture specimens. In infected tissues results in a phenomenon called eosinophilic reaction Splendore-Hoeppli eosinophilic infiltration and necrosis. Other related species that can give similar pictures are Conidiobolus coronatus, Conidiobolus incongrurus and Pythium insidiosum.

 

Recommended tests for diagnosis:

 

The diagnosis is based on epidemiological history of residence in areas of endemic filariasis, clinical and radiological and if the cause most common manifestations, the existence of elevated blood eosinophilia (> 3000-3600 / uL), antibody detection , filariasis, the therapeutic response to treatment for 3 weeks with dietrilcarbamazina that should cause the decrease in eosinophilia in three months.

Tests in IVAMI:

• Detection of antibodies against filarial antigen by ELISA using Acanthocheielonema perstans.

• Detection of antibodies against other helminths infections requiring differential diagnosis in clinical pulmonary eosinophilia accompanied by peripheral (Strongyloides stercoralis, Ascaris lumbricoides, Toxocara spp., Schistosoma spp.).

Recommended sample:

 

• Serum (0.5 to 1 mL).

Preservation and shipment of sample:

 

• Refrigerated (preferred) for less than 2 days.

• Frozen: over 2 days.

 

Delivery term:

 

• Antibodies against filarial: 48 to 72 hours.

• Antibodies to Strongyloides stercoralis, Ascaris lumbricoides, Toxocara canis, Schistosoma spp .: 48 to 72 hours.

Cost of the test:

 

Consult ivami@ivami.com .