Elephantiasis and Tropical Pulmonary Eosinophilia

 

                              Elephantiasis and Tropical Pulmonary Eosinophilia.

                                                  PKGhatak, MD

Round worm infestation of people living along the coast of the Bay of Bengal causes Filariasis. The common nematodes are Wuchereria bancrofti, Brugia malayi, and Brugia timori. Elephantiasis is the result of Lymphatic channels obstruction by the adult nematodes producing gross deformation of the legs of the victims, resembling elephants' legs. Tropical Pulmonary Eosinophilia is produced by the type I hypersensitive reaction to microfilaria antigen, which is released intermittently from the trapped microfilaria in the lung parenchyma.

Life story of the filaria worm:

All the nematodes have a similar life cycle. It consists of 5 stages, part of them in humans and the rest in mosquitoes. A wider variety of mosquitoes - Culex, Anopheles, and Aedes are vectors of human filariasis. The female mosquitoes are infected at the time of feeding on the blood of the infected patients. In the gut and thoracic muscles of the mosquitoes, the microfilaria molt twice and the 3^rd stage larvae are infective microfilariae which move to the salivary apparatus of the mosquitoes and wait for the opportunity to infect humans and carry on to complete two more molting and take up permanent residence in the lymphatic channels, lymph nodes, and spleen of victims as adults worms. The male and female worms unite and a female gives birth to thousands of larvae every day. These microfilaria come out at night and circulate in the systemic blood, hoping to be ingested by a mosquito and to continue the life cycle.

Elephantiasis:

120 million people in a wide area of the world, spanning from India, South Asian countries, Western Pacific islands, Tropical Africa, Brazil, Haiti, Dominican Republic and Guyana are at risk of filariasis.

The adult filaria worms preferentially reside in lymph nodes of the groin and neck. The female worms remain fertile for 5 years out of 9 years of their lives. Lymphatic obstruction produces repeated Staphylococcus and fungal infections and scarring. The lymph flow disruption causes the thickening of the skin, and the skin turns hard and lumpy, and the legs become enormous. In W. Bancrofti infection, the skin of the perineum thickens and causes disfigurement and deformities of the genitalia. The lymph edema that develops from Brugia infection spares the perineum and external genitalia.

Obstruction of the thoracic duct produces bilateral pleural effusion, the fluid is turbid due to the presence of high fat content, specially after a fatty meal. Abdominal pain and Chylous ascites result from abdominal lymphatic obstruction.

Complications: Ulceration and abscess formation, sinus formation from chronic ulcers develop in patients who are not properly cared for. Depression and loss of employment are generally common.

Tropical Pulmonary Eosinophilia (TPE):

Tropical Pulmonary Eosinophilia is much more common in India and in the adjoining countries than Elephantiasis.

TPE is a hypersensitivity eosinophilic inflammation of the respiratory organs. Nocturnal cough, wheezing, fever, loss of weight, blood stained sputum and eosinophilia, at one time thought to be Psudopulmonary eosinophilic tuberculosis. Dr. Weingarten was the first to use the term Tropical Pulmonary Eosinophilia in 1943. The eosinophil count is generally over 3,000/ml. Serum IgE over 1000 mg/dl.

Chest x-ray shows interstitial infiltrates to reticular interstitial pulmonary fibrosis.

Pathology of TPE.

An eosinophils release basic and acidic proteins, peroxide and neurotoxic chemicals in the tissues around the larvae. This weakens the microfilaria and restricts their activities. Complement activation increases opsonization and destruction of microfilaria. The Thymic Lymphocytes type II activation produces IL-4 and IL-5, filaria specific IgM, IgG and IgE and eosinophils. IL-4 potentiates inflammation and Interferon-gamma suppresses inflammation.

Diagnosis of filariasis:

Old standard diagnostic test of direct visualization of microfilaria in the nocturnal blood samples is difficult to identify and often negative, specially in Elephantiasis. Various methods of concentration of blood for easier detection of microfilaria are practically replaced by the PCR test to detect filarial antigen and indirect ELISA antibodies are more in use at present.

Aspiration of lymph nodes and detection of microfilaria in the fluid occasionally provide positive results. Also, in some cases, microfilaria are detected in ascites and pleural fluids.

Treatment of Elephantiasis:

Adult worms are difficult to remove, even by surgery. Ulcerated skin and gross deformed skin segments are removed by surgery.

Treatment of TPE:

In India, where more TPE is seen than Elephantiasis, it is customary to use steroids initially for a few days, then Diethylcarbamazine is used for 21 days. The results are excellent. Recurrence of TPE is due to reinfection rather than failure of treatment.

Albendazole and Ivermectin are also used, but on a limited scale and on a case-by-case basis.

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Onchocerciasis

 

                                                                       Onchocerciasis

                                                                       PKGhatak, MD.

Onchocerciasis is known as River Blindness. 31 nations in Africa, Yemen and several countries in South and Central America where Onchocerciasis is endemic.

A black fly of the Simulium group is the vector, the worm is Onchocerca volvulus and humans are victims and harbor this Nematode worm. In 1915, Dr. Rodolfo Robles found the worm and linked it to eye diseases.

The life cycle of Onchocerca is almost identical to that of Loia loia worm. The areas of exception are the vector is black fly, the habitat of black fly is the fast running rivers and the nematode is Onchocerca volvulus.

The important difference in the pathogenicity of human illness is that the microfilaria are allergenic to humans, while the adult worms are not. The microfilaria wanders around the body underneath the skin in the subcutaneous tissue and produces several different types of skin lesions. The eye diseases produced by Onchocerca are conjunctivitis, corneal scar, uveitis, glaucoma, macular edema and optic atrophy and blindness. Chronic sclerosing keratitis is the main cause of blindness. Onchocerca is the second most common cause of  blindness. 17 million people are at risk and 800, 000 have already lost their eyesight.

Onchocerca microfilaria is in symbiotic relation with the bacteria Walachia group. The dying microfilaria releases bacterial antigen that produces sensitization and allergic reaction, and when Ivermectin produces mass killing of microfilaria, the overabundance of antigen produces anaphylactic shock and deaths.

WHO has elimination programs for this illness. WHO distributes Ivermectin tablets to the participating nations. And has already eliminated it from several countries in South America, Colombia being the first. Ivermectin kills the microfilaria but not the adult worm, as a result, Ivermectin had to be repeated every 6 to 12 months intervals.

Serological tests and PCR tests are available for diagnosis but visualization of microfilaria in the blood is the mainstay locally.

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Loiasis

 

                                                               Loiasis

                                                        PKGhatak, MD.

Loiasis is a human parasitic disease produced by a nematode - Loa loa. It belongs to the Filaria group of round worms. Loiasis is endemic to 11 counties of Central and West Africa. In the rainy season, the disease activity is maximum, which coincides with the breeding season of the Chrysops fly. The fly is a deer fly, locally known as Mango fly or Mangrove fly.

20 million people are at risk of Loiasis and annual incidence is 3 to 10 million. The illness was thought to be benign, now, that is questioned by the finding that the mortality reaches 14 % in local areas where parasitemia is unusually high – over 30,000 microfilaria /ml of blood. Another worm disease, Onchocerciasis, is also endemic in several countries in the very area; and the treatment of Onchocerca by Ivermectin leads to the development of encephalitis and deaths of unsuspected patients having both these two diseases simultaneously.

The first case of Loiasis was reported from San Domingo in 1770, by a French surgeon Mongin who saw the Loa loa worm in the eye of a woman but was unsuccessful in removing it.

The Chrysops fly is unusually aggressive and determined. It lacerates the skin of its victim with its sharp saw like proboscis and then licks the blood from the wound. The bites are quite painful and attempts to drive the fly away, lead to more bites by the same determined fly, who must have a bloody meal for her egg development.

The life cycle of Loa loa:

In the gut of the fly, blood containing microfilaria undergoes development to a 3^rd stage of infective microfilaria and in 10 days the microfilaria moves to the proboscis of the fly and is ready to begin its life in humans.

The skin wound and the draining lymph nodes swell and become tender. In 6 months to a year, the worm becomes an adult. The adult worm moves around in the subcutaneous tissue and the sexually mature worms unite and the female worm gives birth to about 20,000 microfilaria every day. The microfilaria move into the pulmonary circulation, and from the lungs, they enter the systemic circulation every day during 10 AM and 3 PM. There they wait for the fly bite and begin their lives inside the fly. Then the cycle repeats. An adult worm can live up to 15 years.

Symptoms produced by the parasite:

Both the adult worm and microfilaria are allergenic to humans.

Most victims, however, are asymptomatic. Generalized itching, urticaria, recurrent muscle and joint pain and tender lumps on the skin over the underlying worm develop. These lumps are common around the knees, ankles and other joints and are called Calabar swellings. The migrating adult worm in the subconjunctiva of the eye and eyelids is a characteristic feature of Loiasis and is an African Eye Worm Disease. Adult worm in the eyes occasionally enters the vitreous humor of the eye, and secondary infection may lead to blindness. The risk of encephalitis when Invective is given is not to be underestimated.

Diagnosis requires visualization of Microfilaria in the blood, collected during daytime, and blood smears are stained with Giemsa stain. Serological tests and PCR antigen recognition tests are neither locally available nor standardized.

Treatment: Three medications, namely, Diethylcarbamazine, Albendazole, Ivermectin, are used in the elimination of both the adult worms and microfilaria. The selection of a particular drug based on the microfilaria load, the patient's symptoms, and allergic history.

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Myiasis

 

                                                                         Myiasis

                                                                  PKGhatak,MD.

Several species of flies seek living animals, including humans, for laying eggs, so that the newly hatched maggots will have an instant source of food to feed on and grow rapidly. Maggot infestation of humans was first described by Frederick William Hope of Jamaica in 1840 when he described a man with maggots eating away his flesh.

The term Myiasis is reversed to invasion by maggots of otherwise normal individuals. Maggots deliberately applied for cleaning and debridement of chronic wounds are not included under this term.

An outline of the life of maggots: Two species of flies - Blowfly and Housefly, seek out humans to lay eggs on any exposed part of the body, from the scalp to the sole of the feet. Each female fly lays about 100 to 300 eggs. Depending on the outside temperature and the type of fly, these eggs hatch in 8 to 12 hours and immediately burrow under the skin and begin feeding and growing. In about 50 to 60 hours, they are fully grown and all the maggots are similar in size and maturity. They stop feeding and fall off the body and pupate. They later emerge as adult flies.

These three species of fly are responsible for most Myiasis – the Botfly, the Tumbu fly and the Screwworm fly.

Myiasis is described under several categories based on the location of the maggots and the symptoms they produce. These categories are Cutaneous, Creeping, Wound, Body cavities, and Accidental Myiasis.

Types of Myiasis.

Cutaneous Myiasis: The back of the head and skin of the back are the favorite places for this fly to lay eggs. Growing maggots produce bumps on the skin. These lesions are painful and itchy. On close examination, a hole is visible on the top of a bump, through which the maggot gets its air to breathe. These holes are used to pull maggots out with a pair of forceps.

Creeping Myiasis: Humans are an accidental host for this parasitic maggot. Maggots can not develop in humans, so the maggots move around underneath the skin and give the victims a creepy sensation. Surgical removal of maggots is necessary.

Body cavity Myiasis: The fly deliberately targets the ear canals, nose, mouth, and eyes. Growing maggots produce secondary infection and usually lead to serious respiratory, gastrointestinal and neurological complications. From the roof of the nose or eye sockets, the maggots penetrate the base of the brain. Meningitis, encephalitis and brain abscesses are usual complications. Surgical removal of maggots is often required.

Wound Myiasis: Open wounds are within easy reach of flies. Maggots eat away dead and dying tissue and, in general, do not invade normal living tissues.

Accidental Myiasis: Farmers in Africa and South American countries, at times, have to drink water from the nearby streams, which are usually contaminated with fly eggs. These eggs hatch in the stomach of the victims. Growing maggots produce nausea, vomiting and diarrhea. Maggots die due to low oxygen in the G-I tract or are removed by administration of medication and purgation.

In the USA, Myiasis is not seen in the local population.

South American countries and tropical Africa are endemic to Myiasis.

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Rickettsiapox

 

                                                           Rickettsiapox

                                                        PKGhatak, MD

Rickettsiapox is a milder form of systemic disease, the predominant lesion is the skin infection produced by Rickettsia akari. This bacterium is a parasite of the house mouse mite. In an overcrowded squalid apartment building infested with mice harboring R. akari as a parasite.

A cluster of cases in New York City in 1946 led to the discovery of the mite and bacterium by an amateur entomologist, Charles Pomerantz. Earlier, investigators considered rickettsiapox as modified chicken pox.

The mite bite produces a red papule, which turns into a vesicle and heals, leaving a black eschar. A week later, the patient develops a sudden onset of chills, fever, headaches, diffuse body aches and pain and photophobia. After 2 to 4 days, the entire body is covered with red maculopapular eruptions, soon they turn into vesicles. The skin lesions heal in 10 days and the scabs are shed.

Skin biopsy when treated with conjugated antirickettsia globulin can detect rickettsia antigen. PCR tests are also developed. The 4-fold rise in antibody titer is a standard initial diagnostic test. Antibiotic Doxycycline is given for 7 days.

The disease is milder in comparison with other forms of rickettsiosis and is usually self-limited.

Rickettsiapox is endemic in the Balkan States, Korea, Ukraine, South Africa, and major US cities. The average incidence of rickettsial is about 30 /year in the USA.

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Epidemic Typhus

 

                                             Rickettsia prowazekii.

                                                PKGhatak, MD

Rickettsia genera have many pathogenic species and out of them, Rickettsia prowazekii is the deadliest for humans. During WWI, a score of soldiers fought and died in the trenches and another score died in the field hospitals because the soldiers were infested by a parasite, body lice loaded with R. prowazekii.

The US army developed a vaccine, using inactivated R. prowazekii, that saved many soldiers on the US side, but the vaccine was abandoned because of toxicity. No new or effective vaccine has been produced since then.

The disease is known as Epidemic Typhus. Typhus means hazy – the term aptly describes the mental conditions of the soldiers. There are two other forms of the same illness present, and fortunately, both of them produce milder symptoms and fewer fatalities. The initial infection is followed by several months or years of normal health, then R. prowazekii, which had remained dormant in the lymphatic tissue, reemerges and produces illness. The disease is called Brill Zinsser Disease. In the southern states of the USA, flying squirrels are harbors of R. prowazekii and humans are accidental victims.

Body lice are infected by sucking patients blood. R. prowazekii multiplies in the gut of the louse and then bursts open. The bacteria remain alive in the dead lice and in the feces of lice. As patients itch, the bite sites get smeared with the bacteria. Dried feces along with the bacteria can float in the air and infect people as they inhale the contaminated air. This characteristic of R. prowazekii leads to certain countries to use these bacteria as a terrorist weapon. Consequently, the US government prohibited the culture of R. prowazekii in laboratories. Only in government facilities, under strict conditions, culture is permitted.

The incubation period is 10 to 14 days. The skin bite sites and the local lymph nodes may become tender. Sudden fever, conjunctivitis, headaches and mental confusion are usual initial symptoms. Deafness due to the 8th cranial nerve lesion, macular skin rashes which spread centrifugally from the axilla but spare the palms and soles and later become confluent and hemorrhagic, and enlarged spleen are characteristic features.

The pathology of the Epidemic typhus is vasculitis. This results in multiorgan infection. Renal failure, pneumonia, myocarditis, gangrene of extremities, encephalitis, and death.

In epidemics, the diagnosis is based on clinical grounds and treatment is started immediately without waiting for any laboratory test results. The choice of antibiotic is Doxycycline, but Chloramphenicol or Riphampine can be used as a substitute in special circumstances.

In Brill Zinsser disease, the presence of serum IgG antibodies is common. In Endemic typhus, IgM antibodies appear in the blood in 5 to 12 days. The PCR test is rarely used, because as of now, 7 different genotypes are in circulation.

The mortality is 10%. Morbidity is significant, with most having an amputation or organ impairment.

Recent endemics:

Isolated Epidemic Typhus occurs in Siberia, but Russia experienced a local outbreak of Epidemic Typhus. Peru and Burundi also had Epidemic Typhus recently. The endemic areas of Epidemic Typhus are Central and Northeast Africa, Central and South America

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Rocky Mountain Spotted Fever

                                     Rocky Mountain Spotted Fever

                              P K Ghatak, MD

Rocky Mountain spotted fever is a catchy name but unfortunately, this disease is neither that common in the Rocky Mountain area, nor the only spotty fever. This illness is caused by an unusual bacterium, Rickettsia rickettsii, and transmitted to humans by a dog tick.

Skin rashes of various types are common findings in diseases transmitted by tick bite, flea bite, and bites from lice and mites.

The Rickettsia family of organisms has many characteristics similar to viruses and other features like bacteria. Rickettsia lives as a parasite in the arthropods without harming them. Humans and other animals are susceptible to illness and if the treatment is delayed, deaths generally follow. In 1896, a US Army major Dr. Marshall Wood described Rocky Mountain Spotted Fever (RMSF). In 1899, the first description of a RMSF was published in a medical journal. The case came from the Snake River valley of Idaho. In 1906, Dr. Howard Ricketts identified the pathogen in the blood of a patient; also recovered the same organism from a guinea pig, after inoculating it with the eggs of infected ticks.

At risk people:

The majority of RMSF occur in the US States east of the Mississippi River, most frequently from the Carolinas and Virginia. Arkansas, Oklahoma, and Tennessee. In Arizona, the brown dog tick is the vector. In recent years, the incidence of RMSF is on the rise in Arizona.

The annual incidence of RMSF in the USA is 2.2 per million people.

Clinical feature:

The incubation period is 2 to 14 days. The initial symptoms are like any other viral illness. The skin rash generally appears on the 2nd day onwards and by 5 days the majority will develop red petechia which gave the disease its name. The petechiae start on the wrist, they appear successively on the forearms, ankles, legs and toes. These rashes are tiny, flat pink colored macules and nonpruritic. Rashes also appear on palms and soles. The rashes change color to brawn and towards the end of the illness turn to black eschars and finally fall off the body.  

                                        Skin rashes on the ankle.

If the patient remains untreated just for a few days, the bacteria spread rapidly through the entire body. The patient becomes deadly sick and develops multisystem failure.

Pathology:

Rickettsia rickettsii invade directly the endothelial cells of blood vessels. The organism rapidly multiplies and spreads. Just in a day or two, all the major organs of the body are inflamed.

Diagnosis:

Blood cultures are difficult to grow in the laboratory. Cultures medium must contain nucleated living cells.

Rise of antibody titer 4 times over the base value, is too late for the patients to wait for treatment. The treatment must begin with the suspicion of RMSF. Skin biopsy is very valuable. Identifying the Rickettsia with immuno-histologic staining is relied upon, but a skin biopsy must be obtained before starting antibiotics. Antibody level does not rise till the 2^nd week of the illness, so it is not helpful in clinical situations, the PCR test is the other diagnostic test.

Treatment:

Doxycycline is the preferred antibiotic. The treatment must be continued till the patient is febrile. In pregnancy, chloramphenicol or Rifampin can be used as an alternative.

A report says

RMSF has become increasingly more common in certain areas of Arizona. Between 2003 and 2018, approximately 430 cases were reported, with an associated case-fatality rate of approximately 5%. The mortality rate in untreated cases of RMSF is 20-25%. Mortality rates can be as low as 5% with proper antibiotic therapy and as high as 70% in untreated elderly individuals. Death in 5 days can be expected in fulminant cases. The classic clinical triad of fever, headache, and rash may be present in less than 5% of patients in the first 3 days of illness but increases to 60-70% by the second week after tick exposure. The absence or delayed appearance of a rash increases the difficulty of diagnosis”.

 edited: Dec .2025

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Lyme Disease

                                                         Lyme Disease 

                                   P.K.Ghatak, M.D.

Lyme disease was unknown in the USA, but in 1970 an outbreak of a tick borne disease in Lyme, Connecticut established its name and proved to be the most common vector borne disease in the USA. About 30,000 cases of Lyme disease are reported each year. The bacterium belongs to the Spirochete family, and Lyme disease is due to Borrelia burgdorferi. The other important member of this family is syphilis.

Spirochetes are gram negative, spiral in shape, measuring 3 to 500 micrometers long and 0.03 to 3 micrometers in diameter and are motile due to the presence of variable numbers of flagella arranged along the axis

The vector is a tick – Ixodes scapularis, rarely another tick - Amblyomma americium (Lone star tick) transmit the spirochetes in the southern states.

Population from Maine to Maryland and New Jersey, Pennsylvania, Wisconsin is prone to increase tick bites due to the increasing number of deer in the woods.

The adult tick must feed 48–72 hours during that time, B. Burgdorferi enters the wound from the tick's saliva contamination.

The incubation varies from a few days to several weeks following the tick bite.

Based on the time of presentation and symptoms, the disease is conveniently separated into 3 groups.

1. Initial. Skin rash and slight fever. The skin rash is the hallmark of Lyme disease at this stage. The rash is red to violet in color, target like lesions called Erythema marginatum.

2. Early disseminated disease usually developed in 2 -3 weeks but may be late, as late as 10 weeks. The presenting symptoms are painful swelling of one knee or ankle, musculoskeletal pain, conjunctivitis, heart block, and Bell's palsy.

3. Late or chronic. After months of quiet period, the asymmetrical arthritis of hands and spine, headaches, peripheral neuropathy, muscle weakness, cranial nerve palsy develop and persist for a long time despite treatment.

The skin rashes are due to an inflammatory reaction from the presence of spirochetes in the skin. The spirochete may enter fibroblasts and live in them permanently. In the early state, 50% of patients are seropositive, it becomes 100 % as weeks and months progress. Arthritis develops from cross-reaction of the spirochetal membrane protein with the host's connective tissue and neural tissues. The newly formed complex is antigenic. The antibodies react with the complex, and organ damages take place from released pro-inflammatory cytokines. People having HLA-DR$ and HLA-DR2 are likely to suffer most.

Chronic neurological manifestations are the results from the presence of the remnant DNA of the spirochetes in the nervous system of the victims, which triggers an excess production of Interferon alpha.

CDC recommends the following procedures.

Initial stage: ELISA immunoassay of IgM and IgG.

Confirmatory stage: Western blot testing.

a). Symptomatic for less than 30 days. Perform both IgM and IgG Western blot tests.

b). Symptomatic for more than 30 days, only IgG Western blot test is advised.

c). A newer test -  the C6 peptide test, which was prevalent in Europe, has been approved as an alternative to the Western blot test. C6 peptide test is less expensive and equally sensitive as the Western blot test.

Initial stage: The preferred antibiotic is Doxycycline by mouth for 10 to 21 days. Children, pregnant and lactating women should have Amoxicillin or Cefuroxime axetil PO for 10 to 21 days.

With cardiac, neurological or musculoskeletal involvement, the treatment should be continued for 28 days.

In late stage: Parenteral Ceftriaxone, or Cefuroxime or Penicillin G in high doses given for 14 to 28 days.

Post-treatment Lyme Disease:

About 20% of patients who completed recommended treatment continue to be moderately symptomatic for 6 months or longer. The common symptoms are fatigue, musculoskeletal pain, hearing loss, headaches, ambulatory and balance problems, paresthesias, depression and sleeping difficulties, and other symptoms.

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St.Louis Encephalitis

               St. Louis Encephalitis

                   P K Ghatak, MD

St. Louis encephalitis virus is an indigenous Americas virus. Songbirds, finches, house sparrows and other species of birds harbor this virus and are immune. Birds are reservoirs of the virus and are the source of human infection. The virus is active over a wide territory from Northern Canada to Argentina. But the St. Louis virus (STLV) infection is limited to the warm months of August to early October in the North-East, and Mississippi River water-shed areas. The annual incidence of SLEV infection varies between 3 and 70 cases per 100, 000 population.

Fever starts abruptly 1 to 3 weeks after the mosquito bite. The majority of patients suffer only a few days of sore throat, aches, and fever. Elderly people with underlying diseases like diabetes, cancer, and heart disease are susceptible to more serious illnesses. More seriously ill patients continue to be sick and have headaches, confusion, neck pain, and transient cranial nerve palsy. In children, convulsions are common. Severely affected patients lose consciousness and develop coma. Fatality rates among elderly men may run as high as 20 % in some years.

In 1933 SLEV was identified in St. Louis, Missouri. In that year, 1,000 cases of encephalitis were recorded. During 2014 -2015, a limited outbreak in Arizona followed by 2016-2017 in California occurred. Argentina, in 2005, had an outbreak in Córdoba.

SLEV is transmitted by several species of Culex mosquitoes

Detecting viral antigen by PCR in the CSF and or serum is diagnostic. ELISA antibody IgM and IgG test is also an accepted diagnostic method.

The gray matter is mostly affected. And the white matter is spared. The lesions are dominant in the basal ganglion and other midbrain ganglia and cerebellum, and lesions are also present in the cerebral cortex and spinal cord. About 30 % of encephalitis cases develop hyponatremia from Inappropriate antidiuretic hormone secretion (SIADH), and its complications – cerebral edema and Central pontine myelinolysis

Children who recovered from encephalitis may suffer from poor intellectual development later in life.

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Babesiosis

                                                           Babesiosis 

                                                     P K Ghatak, MD

Babesiosis is a parasitic infection transmitted to humans by a tick.

In 1888, Viktor Babes in Romania detected the parasite from the blood of the infected cattle. Humans are accidental victims. In the USA, the main organism is Babesia microti, however, B. divergens, B. cressa, B. ventorum, and B. duncan species can occasionally cause illness.

The vector is a tick, Ixodes scapularis. It usually feeds on white footed mouse and other small animals.

At risk of Babesiosis :

The people in the coastal areas of the Northeastern states and the Great Lakes states are mostly at risk of contracting Babesia and in recent years, an increase in Babesiosis cases has been reported.

The parasite:

Babesia microti is a unicellular organism, lives in the RBCs of vertebrates. Humans are accidental victims. At a given time, several forms of the parasites are seen inside the RBCs, each one measures 2 x 1.5 micrometers, usually ring-shaped but other forms are rods, pyriform, motile amoeba like, and a characteristic Maltese form is also present.

The reservoir of parasites:

The usual animal is the white-footed mouse, but other mammals are also act as reservoirs.

The vector:

The deer tick - Ixodes scapularis.

How human infection occurs:

In outdoor work or recreational activities, when people are not properly protected, they can get deer licks on their legs, head and other exposed areas of the body. As the tick feeds on the blood, the wound gets contaminated with the saliva of the tick, containing the parasites.

In unusual circumstances, contaminated blood transfusion can infect recipients. Still rarely, babies are infected in utero via the placenta. The incubation period is 1 to 4 weeks. 

Diagnosis:

The diagnosis of Babesiosis is difficult. Unless the healthcare provider has a high degree of suspicion of this illness, the disease can go undetected for a prolonged time.

Detecting ring form of the parasite is not easy from the artifacts and malaria parasites even with careful examination of Giemsa stained blood smears. A Maltese Cross shaped form of the parasite inside the RBC is diagnostic. The PCR test for parasite antigen in blood is diagnostic.

Treatment:

A combination of Atovaquone and Azithromycin for 7 to 10 days. Severely ill patients with higher parasitemia are treated with Clindamycin IV and Quinine by mouth for 7 to 10 days. Exchange transfusion may be required. Longer period of therapy may be required.

Many patients may develop significant adverse effects; in others, one or both combinations proved to be adequate to eliminate the parasite.

A brief description of the life cycle of Babesia microti:

The parasite has two multiplication cycles -  (a)budding and (b) sexual reproduction, and needs two hosts – a tick and a mammal.

The deer ticks lay eggs on the grasses and vegetation. In the spring, these eggs hatch. The young ticks are promptly infected by Babesia. Inside the adult ticks, the parasites multiply by asexual methods. These young forms are transmitted to small animals or humans by the adult ticks during their bloody meals. In the RBCs of mammals, the parasites multiply and transform to other shapes, and some parasites change themselves into male and female units. And waits for an opportunity to be transferred to ticks at the next feeding time of another tick. Inside the ticks, the sexual units mate and reproduce many young parasites. And the cycle repeats.

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Powassan Encephalitis

                           Powassan virus encephalitis

                     P.K.Ghatak, MD

Powassan is a town in Ontario, Canada. This virus causes febrile illness and in some cases encephalitis, meningitis, and Polio like illness. The POW virus was first isolated in Powassan in 1932 from the brain tissue of an 8-year-old boy. The virus is named POW virus (Powassan). POW virus is an arbovirus and belongs to the family Flaviviridae and genus Flavivirus. It is transmitted by a deer tick (Ixodes) from the small ground animals to humans. In the USA, the two species of deer ticks are responsible for the transmission of POW virus - Ixodes scapularis and Ixodes cookiei. The deer tick, in addition to POW virus, transmits Lyme disease (a spirochete), Anaplasma phagocytotrophum, previously known as Ehrlichiosis (a bacterium) and also Babesiosis ( an intracellular parasite). 

 People living in the Northern Hemisphere, which includes Canada, Russia, and the USA, are at risk of infection while working outdoors, camping, fishing, or other outdoor activities. In the USA, land around the Great Lakes has a large deer population and so the POW virus, and people in the New England States have seen an increase in the incidence of POW infection. 

Incidence in the USA:

On the average, 20 to 40 people are infected with POW virus each year.

The incidence of encephalitis among the infected group is not known. Fatality rate of those who develop neurological complications is 10%. And 50% of those recovered show neurological impairment. Incubation period is 1 to 5 weeks. The bite of the tick is usually short and in 15 minutes, viral entry to the body is complete.

Clinical features:

The initial symptoms are similar to those of the flu. The majority of the patients recover within 10 days. A handful of recovered patients develop the second phase of illness marked by severe headaches, high fever, meningeal irritation, various degrees of confusion, coma, polio like illness. Diagnosis and management are no different from other viral encephalitis mentioned before. Humans are the end host, and human blood does not carry enough load of virus to infect a tick.

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