Archive for October, 2008

Heavy Metal Poisoning: Lead

U.S. Agency for Toxic Substances and Disease Registry lists toxic substances according to their prevalence and the severity of their toxicity and lead is in number one position. Recently the development of K-X-ray fluorescence (KXRF) instruments has made it possible to measure bone lead levels (which, in turn, reflect cumulative exposure over many years, as opposed to blood lead levels, which reflect recent exposure). High bone lead levels measured by KXRF are associated with increased risk of hypertension in both men and women. High maternal bone lead levels were found to cause lower birth weight, head circumference, birth length, and lower neurodevelopmental performance in children by age 2.   

Sources of lead poisoning:  Manufacturing of auto batteries, ceramics, fishing weights, lead crystal, demolition of lead-painted houses and bridges; stained glass making, soldering, environmental exposure to paint chips, plumbing, firing ranges (from bullet dust), food or water from lead pipes are the main sources of lead poisoning.  Contaminated herbal remedies, candies and exposure to the combustion of leaded fuels also contribute to the lead poisoning.

Lead can be absorbed through ingestion or inhalation and organic lead (e.g., tetraethyl lead) is absorbed through skin. In blood lead is concentrated in RBCs. Distributed in soft tissue, with ½ life of about 30 days. 15% of lead is sequestered in bone with ½ life of more than 20 years. Lead is excreted mainly in urine, but also appears in other fluids including breast milk.

 Toxicity: Acute poisoning with blood lead levels (BPb) of more than 60–80 µg/100ml can cause impaired neurotransmission and neuronal cell death, which lead to central and peripheral nervous system effects. If blood lead level is more than 80 µg/100ml it can cause acute encephalopathy with convulsions, coma, and death. 

Subclinical exposure of lead in children (BPb 25–60 µg/100ml) is associated with anemia, mental retardation, language deficit, motor function, balance, behavior, hearing, and school performance. Impairment of IQ can occur at even lower levels.

In adults, chronic subclinical exposures (BPb 40 µg/100ml) are associated with an increased risk of anemia, demyelinating peripheral neuropathy (mainly motor), and impairments of reaction time, hypertension, and ECG conduction delays. Chronic renal failure, diminished sperm counts and spontaneous abortions in females is seen.

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Posted by - October 28, 2008 at 1:27 am

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Heavy Metal Poisoning: Cadmium

Cadmium poisoning can be a serious health problem from mining of cadmium. There was serious cadmium poisoning from contamination of food and water by mining effluents in Japan, in 1946 lead to outbreak of “itai-itai” (“ouch-ouch”) disease. The disease was so named because of cadmium-induced bone toxicity that led to painful bone fractures.

Sources of arsenic poisoning: Metal plating, battery, pigment, smelting, and plastics industries and incineration of these products are the main sources of cadmium poisoning. Tobacco smoking and consumption of food that concentrate cadmium like grains and cereals are also important source of cadmium poisoning.

Clinical manifestations: Acute cadmium inhalation causes pneumonitis 4–24 hours after inhalation and acute ingestion causes gastroenteritis. Chronic exposure causes anosmia (loss of smell), yellowing of teeth, emphysema, microcytic hypochromic anemia that do not respond to iron therapy, proteinuria (protein in urine), calciuria (calcium crystals in urine), leading to chronic renal failure, osteomalacia, and fractures.

Symptoms of cadmium poisoning due to inhalation include chest pain, breathlessness, fever, pulmonary edema, nausea and high pulse rate. Symptoms due to ingestion are nausea, vomiting, cramps, and diarrhea.

Diagnosis: If poisoning is due to recent exposure, serum cadmium is about 5µg/dL. Urinary cadmium (10µg/g creatinine) and/or urinary ?2-microglobulin more than 750µg/g creatinine (but urinary ?2-microglobulin also increased in other renal diseases such as pyelonephritis, so it is not reliable).

Treatment: There is no effective and specific treatment for cadmium poisoning. Chelation is not useful and dimercaprol can aggravate renal toxicity. So the main management is further avoidance of exposure to cadmium and supportive therapy. Vitamin D is given for osteomalacia.

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Posted by - October 21, 2008 at 4:01 pm

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Heavy Metal Poisoning: Arsenic

Metals like arsenic pose a significant threat to health through occupational as well as environmental exposures. U.S. Agency for Toxic Substances and Disease Registry ranks arsenic third, according to its prevalence and severity.

Sources of arsenic poisoning: Smelting and microelectronics industries, pesticides, fungicides, herbicides, contamination of deep-water wells, coal, incineration of these products and folk remedies are the main sources of arsenic poisoning. Water pollution is a source of arsenic poisoning.

 Acute arsenic poisoning can cause necrosis of intestinal mucosa with resulting hemorrhagic gastroenteritis, fluid loss, hypotension, delayed cardiomyopathy, acute tubular necrosis and hemolysis. Chronic arsenic poisoning can cause diabetes, vasospasm (spasm of blood vessels), peripheral gangrene due to peripheral vascular insufficiency, peripheral neuropathy, and cancer of skin, liver, lung, bladder and kidney.

Lethal dose: The lethal dose of arsenic is 120–200 mg in adults and 2 mg/kg in children.

Clinical manifestations: Nausea, vomiting, abdominal pain, diarrhea, coma, delirium and seizure can be seen. Typical garlic like odor is characteristic sign in arsenic poisoning. Mees’ lines (transverse white striae of the fingernails), hyperkeratosis, hyperpigmentation, sensory and motor polyneuritis and distal weakness also seen.

Diagnosis: Radiopaque sign on abdominal X-ray; ECG shows QRS broadening, QT prolongation, ST depression, T-wave flattening; 24-h urinary arsenic 50 µg/day; (no seafood x 24 h); if recent exposure, serum arsenic 7 ?g/100ml. High arsenic in hair or nails.

Treatment: In acute poisoning ipecac is given to induce vomiting. Gastric lavage (remove stomach content) and activated charcoal is given along with symptomatic treatment. Dimercaprol is given every 4 hourly at the dose of 3-5 mgs/kg intramuscularly for two days and every 6 hourly for 1 day, than twice a day for 10 days. Alternative to dimercaprol is oral succimer.

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Posted by - October 13, 2008 at 1:50 am

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Anaplasmosis: Human Granulocytotropic Anaplasmosis

Human Granulocytotropic Anaplasmosis (HGA) is caused by A. phagocytophilum. In 2006 more than 3257 cases of HGA were reported to the CDC, Atlanta. The distribution of cases is similar to that for Lyme disease because of the shared Ixodes scapularis tick vector. Most of the cases were reported from upper midwestern and northeastern United States. White-tailed deer & white footed mice in the United States and red deer in Europe are natural reservoirs.

Signs and symptoms: The incubation period of Human Granulocytotropic Anaplasmosis is 4-8 days. After the incubation period the following symptoms like fever, malaise, myalgia (muscle pain) and headache appear. Some patients may develop nausea, vomiting, confusion and rash.

Severe complications like adult respiratory distress syndrome (ARDS), a toxic shock syndrome, and opportunistic infections, which may be life-threatening, can develop. Case fatality rate is very less about 0.5% and up to 7% patients may require intensive care.

Diagnosis: PCR testing of blood from patients with active disease before initiation of therapy is sensitive and specific. Other non specific findings like thrombocytopenia, leukopenia, or elevation in serum alanine or aspartate aminotransferase are seen.

Treatment: Doxycycline 100 mg orally twice daily is the drug of choice for treatment of HGA. Rifampin can be used successfully in children and pregnant women. Most of the patients respond within 24 to 48 hours.

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Posted by - October 9, 2008 at 3:50 am

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Ehrlichiosis: Human Monocytotropic Ehrlichiosis

Human Monocytotropic Ehrlichiosis (HME) is caused by Ehrlichia chaffeensis. In the year 2006 more than 2657 cases were reported to the Centers for Disease Control and Prevention (CDC), Atlanta, USA. But active prospective studies indicate an incidence of as high as 414 cases per 100,000 populations in some regions of the United States. White tailed deer is the major reservoir and Lone Star tick (A. americanum), the main vector feed on them (all life stages feed on white tailed deer).

Clinical manifestations: Illness develops after about 8 days (incubation period). The organisms spread through blood pool which is created by the feeding tick. Clinical manifestations are fever (97% of cases), headache (80% of cases), malaise (82% of cases) and myalgia (57% of cases). Symptoms like nausea, vomiting, and diarrhea, cough and rash are less frequent.

Severe complications include toxic shock like or septic shock like syndromes, adult respiratory distress syndrome (ARDS), cardiac failure, meningoencephalitis, hepatitis and hemorrhage. In immunocompromised patients an overwhelming infection may be seen.

Human Monocytotropic Ehrlichiosis can be severe. 62% of patients with documented cases are hospitalized, and about 3% die.

Diagnosis: HME can be fatal; so empirical antibiotic therapy based on clinical diagnosis is required. Diagnosis is suggested by fever with a known tick exposure during the preceding 3 weeks, thrombocytopenia and/or leukopenia, and increased serum aminotransferase activities. HME can be confirmed by PCR amplification of E. chaffeensis nucleic acids in blood which is obtained before the start of antibiotic therapy. It should be differentiated from Human Granulocytotropic Anaplasmosis (HGA).

Treatment: Treatment is with doxycycline 100 mg given orally or intravenously twice daily or tetracycline 250–500 mg given orally every 6 hourly and continued for 3-5 day after symptoms subside.  

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Posted by - October 5, 2008 at 12:38 pm

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Typhus: Indian Tick Typhus

Indian tick typhus is usually wrongly diagnosed as Rocky Mountain Spotted Fever (RMSF) due to its similarity with RMSF. In 1925 Megaw identified it as distinct entity. Before that it used to be diagnosed as RMSF.

The causative agent is Rickettsia conorii, which is a member of spotted fever group of rickettsiae. The tick is the reservoir of infection. Transmission of tick to tick is through transplacental mode. Incubation period is 3-7 days.

The mode of transmission: Man is only accidental host. Man acquires infection by tick bite. Contamination of skin by crashed tick can also be a mode of transmission. The transmission cycle is as follows:


Tick —–Tick ——- Tick —–Tick

                  |                 |

                Dog            Man


               Tick ——-Man

Signs and symptoms: The patient generally gives history of tick bite and if examined carefully a lesion or eschar is seen at the site of the bite. After 3-7 days (incubation period) there is acute onset of fever (which may be for 2 to 3 weeks), headache and malaise. On the third day a maculopapular rash may appear. But unlike rashes of other rickettsial diseases the rash appear in the extremities like wrists and ankles first and them spreads it to the rest of the body.

Treatment: Broad spectrum antibiotics like tetracycline, doxycycline and chloramphenicol are the drug of choice for the treatment of Indian tick typhus. 

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Posted by - October 4, 2008 at 2:24 pm

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Typhus: Scrub Typhus

Scrub typhus is the commonest type of typhus in men. Scrub typhus is caused by O. tsutsugamushi. It is maintained by transovarian transmission in trombiculid mites. After hatching, infected larval mites known as chigger, which is the only stage that feeds on a host, inoculate organisms into the skin. Scrub typhus is endemic in eastern and southern Asia, northern Australia, and islands of the western Pacific and Indian Oceans.

The mode of transmission is as follows:


Mite to Rats & mice to Mite to  Rats & mice




Signs & Symptoms: The symptoms can be from mild self limiting disease to fatal. Incubation period of scrub typhus is 6–21 days. Fever, headache, cough, myalgia, and gastrointestinal symptoms are common. The classic symptom includes an eschar where the chigger feeds, regional lymphadenopathy, and a maculopapular rash, but only rarely seen. Severe cases include encephalitis and interstitial pneumonia which are due to vascular injury. The case-fatality rate for untreated classic cases is 7%.

Diagnosis:  Diagnosis is mainly by clinical symptoms. IFA (immuno fluorescent assay), indirect immunoperoxidase, and enzyme immunoassays are the laboratory diagnosis techniques.

Treatment: Doxycycline 100 mg twice a day for 7 -15 days or chloramphenicol 500 mg four times a day orally for 7–15 days is the treatment of choice.

Some cases of scrub typhus as seen in Thailand are caused by doxycycline or chloramphenicol resistant strains. These doxycycline or chloramphenicol resistant cases of scrub typhus are treated with rifampin, azithromycin or clarithromycin.

Prevention: Good personal hygiene is required for prevention. Clearing of vegetation where rats and mice live and application of insecticides like lindane, chlordane to ground and vegetation to control the mite. No vaccine is available at present.

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Posted by - October 3, 2008 at 12:56 pm

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Typhus: Epidemic (Louse-Borne) Typhus

Epidemic or louse borne typhus is transmitted by Rickettsia prowazekii. The infection is transmitted from man to man by infected louse (Pediculus corporis, P. capitis). Lice acquire R. prowazekii when they ingest blood from a rickettsemic patient. Pediculus corporis lives in clothing under poor hygienic conditions and usually in impoverished cold areas. The rickettsiae multiply in the midgut of the louse and are shed in the louse’s feces. The infected louse leaves a febrile patient and deposits infected feces on its new host during its blood meal and the new host autoinoculates the organisms by scratching.

Epidemic or louse borne typhus can cause devastating outbreaks during war and disasters. In humans the organism can persist for many years with out any symptoms and the disease can manifest itself as Brill-Zinsser disease and can be transmitted by louse to other humans.

Signs & Symptoms:  Incubation period is about 1 week. Onset of illness is abrupt, with severe headache and fever. Fever rises rapidly to 38.8°–40.0°C (102°–104°F). Cough is prominent (70% of patients get). Myalgia (muscle pain) if present is severe. There is characteristic “crouching” posture. Rash can be seen on the upper trunk, on the fifth day, and then becomes generalized and involve the entire body except the face, palms, and soles. But more than half of the patients do not develop rash. Photophobia, dry, brown, and furred tongue, skin necrosis and gangrene of the digits, confusion and coma are other symptoms.

Fatality is 7–40% in untreated cases.

Diagnosis: Epidemic or louse borne typhus is sometimes misdiagnosed as typhoid fever in tropical countries. It can be diagnosed by the serologic or immunohistochemical diagnosis of a single case or by detection of R. prowazekii in a louse found on a patient.

Treatment: Doxycycline (200 mg/d, given in two divided doses) is the treatment of choice. If there is vomiting or patient is unconscious doxycycline can be given intravenously. Treatment is continued for 2-3 days after symptoms subside, though single 200 mg doxycycline is sufficient.

During pregnancy chloramphenicol early in pregnancy or, if necessary, doxycycline late in pregnancy is the treatment of choice.

Prevention: The best way to prevent is to maintain good personal hygiene. Clothes should be washed and changed regularly. Insecticides can be used every 6 weeks to control the louse population.

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Posted by - October 2, 2008 at 12:53 pm

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