JAUNDICE
Introduction
Jaundice, also known as icterus, is a condition which is characterised by a yellowish discolouration of the skin and the whites of the eyes. It is a symptom or clinical sign, not a disease by itself. The yellow colouration is caused by an excess amount of the bile pigment known as bilirubin in the body. Normally, bilirubin is formed by the breakdown of haemoglobin during the destruction of worn-out red blood cells. The pigment is then excreted by the liver into the bile via the bile ducts.
Cause and Pathogenesis
Excess amounts of bilirubin in the body can be caused by the overproduction of bilirubin, the failure of the liver cells to metabolise or excrete the bilirubin produced, or a blockage of the bile ducts. Overproduction of bilirubin may be caused by the destruction of an unusually large number of red blood cells, which occurs in a condition known as haemolytic anaemia. In this condition the liver cannot excrete the bilirubin which is formed more rapidly. This may occur in diseases such as,malaria, thalassemia, and haemolytic disease (due to destruction of the red blood cells) of the new-born . Often, mild jaundice occurs as a common and normal condition in new-born babies because at birth there is both a deficiency in the enzyme that helps to eliminate bilirubin and also an increased breakdown of red blood cells (RBC) in the body. In babies, the condition generally disappears within a few days after birth as the enzyme is formed in the body. Sometimes, deficiency of this enzyme can also cause jaundice in adults. Jaundice may also result from various diseases or conditions that can affect the liver, such as hepatitis, cirrhosis, or cancer. A blockage of the bile ducts, may cause jaundice. The ducts may be blocked by various factors including inflammation and infection (cholangitis), gallstones (cholelithiasis), or cancer of the pancreas or the common bile duct.
The clinical types of jaundice include haemolytic jaundice which is due to the breakdown of RBC; hepatocellular jaundice caused by hepatic pathology due to viruses, drugs, alcohol abuse, etc; and Cholestatic jaundice due to biliary tract obstruction.
There are various strains of hepatitis viruses including hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV). Viruses F and G also exist and may cause primary hepatitis. HAV is transmitted by contaminated food and water and by the faecal-oral route; HBV and HDV are transmitted by contact with bodily fluids, HCV by percutaneous exposure to blood, and HEV, by contaminated water and by the faecal-oral route. Hepatitis A is seen most often in children and young adults, but the incidence is rising among those who are HIV positive. Hepatitis B affects all age groups and is associated with blood transfusion. Hepatitis C accounts for most transfusion-related cases. It is seen in all age groups. Hepatitis D is seen in individuals who are susceptible to HBV or may be HBV carriers, such as haemophiliacs and IV drug users. The disease manifestation is severe in children. Hepatitis E is seen primarily among young adults in developing countries. It is most severe in pregnant women. Congenital non-haemolytic hyperbilirubinemia such as Gilbert's Syndrome also causes jaundice. Sometimes certain drugs such as chlorpromazine (an anti-psychotic drug) may inhibit bilirubin excretion by the liver, causing jaundice.
Symptoms and Signs
The main symptoms of jaundice are the characteristic yellowish colour of the skin, sclera (whites) of the eyes, nail beds and tongue. Other symptoms usually depend on the actual cause of the jaundice. In some types of jaundice, bilirubin is excreted in the urine, which becomes yellowish brown in colour. If the excretion of bile is obstructed, stools are almost white and the digestion of fat is consequently impaired. If the jaundice has been present for a long time, pruritis (intense itching) may occur. In jaundice, due to obstruction, lipid deposits on the skin such as xanthelesmas on the eyelids or xanthomas can develop. Some patients with jaundice may also have vomiting, and abdominal pain, malaise, severe weakness etc. Complications include hepatic failure with its attendant complications such as bleeding, vomiting of blood, accumulation of fluid in the abdomen (ascites), and a condition called hepatic encephalopathy where the patient has altered consciousness and later coma. Fulminant hepatic failure and hepatic coma may often be fatal even with treatment. Another complication of hepatitis is the development of cirrhosis (due to destruction of the liver cells) and also conditions such as chronic active hepatitis wherein the jaundice may persist for several months. The prognosis in these conditions may be poor although the results are better with prompt and effective treatment.
Investigations and Diagnosis
Diagnosis of jaundice requires blood tests, which determine whether the liver is diseased, whether the bilirubin is metabolised normally by the liver cells, and if there is any abnormal breakdown and destruction of the red blood cells. Blood tests will also indicate any obstruction present. Hyperbilirubenaemia (increased serum levels of bilirubin) is present. The normal total of serum bilirubin is about 2-17 micro-mol/l(<1>enzyme-linked immunosorbent assay (ELISA) shows a rise in HAV antibodies. In HBV, serum antigen tests detect HBsAg, as well as a series of antibodies such as anti-HBe. A serum test for HCV can also be done. A liver biopsy may be done, for indications of cellular changes or pathology. Ultrasonogram can be done to examine the liver, gallbladder, and bile ducts to detect obstructions and locate gallstones. ERCP is done to detect abnormalities in the biliary tract and pancreas. Liver function tests are done to detect hepatic abnormalities. For some pancreatic pathologies, abdominal CT Scans or MRIs may be required.
Treatment and Prognosis
Treatment consists mainly of treating the underlying cause (if treatable) and in providing supportive therapy. The basic pathology or disease responsible for the jaundice should be diagnosed and treated. Obstructive jaundice can be relieved by removing the cause of the blockage such as gallstones, by surgical intervention. Haemolytic jaundice is treated by drugs that target the cause of the haemolysis (e.g., malaria), and by other therapy such as blood transfusion. It is important to stop the intake of the drugs or toxic chemicals or alcohol that may be responsible for the jaundice. Proper diet and nutritional supplements are also important in preventing the condition from worsening. Vitamin K injections may need to be given to prevent bleeding.
Prevention
The most important step in prevention of Hepatitis B infection is vaccination. Three doses of the vaccine need to be given at intervals of one month each or alternately two doses may be given at monthly intervals followed by the third dose at the sixth month. The immunity lasts for five years and booster doses are required after that period. It is important to avoid causes of liver disease such as alcohol abuse, drugs, and toxins. Prompt treatment of underlying hepatic disorders or pathology is essential to prevent or minimise permanent damage to the liver.
SMALLPOX
The Disease
Smallpox is a serious, contagious, and sometimes fatal infectious disease. There is no specific treatment for smallpox disease, and the only prevention is vaccination. The name smallpox is derived from the Latin word for “spotted” and refers to the raised bumps that appear on the face and body of an infected person.
There are two clinical forms of smallpox. Variola major is the severe and most common form of smallpox, with a more extensive rash and higher fever. There are four types of variola major smallpox: ordinary (the most frequent type, accounting for 90% or more of cases); modified (mild and occurring in previously vaccinated persons); flat; and hemorrhagic (both rare and very severe). Historically, variola major has an overall fatality rate of about 30%; however, flat and hemorrhagic smallpox usually are fatal. Variola minor is a less common presentation of smallpox, and a much less severe disease, with death rates historically of 1% or less.
Smallpox outbreaks have occurred from time to time for thousands of years, but the disease is now eradicated after a successful worldwide vaccination program. The last case of smallpox in the United States was in 1949. The last naturally occurring case in the world was in Somalia in 1977. After the disease was eliminated from the world, routine vaccination against smallpox among the general public was stopped because it was no longer necessary for prevention.
Where Smallpox Comes From
Smallpox is caused by the variola virus that emerged in human populations thousands of years ago. Except for laboratory stockpiles, the variola virus has been eliminated. However, in the aftermath of the events of September and October, 2001, there is heightened concern that the variola virus might be used as an agent of bioterrorism. For this reason, the U.S. government is taking precautions for dealing with a smallpox outbreak.
Transmission
Generally, direct and fairly prolonged face-to-face contact is required to spread smallpox from one person to another. Smallpox also can be spread through direct contact with infected bodily fluids or contaminated objects such as bedding or clothing. Rarely, smallpox has been spread by virus carried in the air in enclosed settings such as buildings, buses, and trains. Humans are the only natural hosts of variola. Smallpox is not known to be transmitted by insects or animals.
A person with smallpox is sometimes contagious with onset of fever (prodrome phase), but the person becomes most contagious with the onset of rash. At this stage the infected person is usually very sick and not able to move around in the community. The infected person is contagious until the last smallpox scab falls off.
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* Smallpox may be contagious during the prodrome phase, but is most infectious during the first 7 to 10 days following rash onset.
MALARIA
Introduction
Malaria is one of the major scourges of mankind in the developing world. It is estimated to affect more than 500 million people causing between one and three million deaths every year. Though, to a large extent, it has been eradicated from large parts of North America and Europe, it is rampant in most areas of the tropics. Travellers to the tropics have to specially safeguard themselves against the risk of malaria.
Cause and Pathogenesis
Malaria is caused due to infection by the protozoan Plasmodium species. It is transmitted by the bite of the infected Anopheles mosquito. Four major species of Plasmodia are implicated in the causation of malaria in humans and these are Plasmodium Vivax, Plasmodium Ovale, Plasmodium Malariae and Plasmodium Falciparum. Among these species, it is Plasmodium Falciparum that is the most dangerous and that is responsible for most of the deaths resulting from malaria. Infection begins when the infected female Anopheles mosquito bites the human. The microscopic forms of the parasite are carried through the patient's blood stream until they reach the liver. There they invade the liver cells and begin to reproduce. The swollen liver cells eventually burst discharging the merozoite forms of the parasite into circulation and this is when the symptoms of the infection start to become apparent.
Once inside the bloodstream the merozoites invade the red blood cells and start to grow. They consume and degrade the ntracellular proteins inside the red cell, especially the haemoglobin, eventually causing the infected red cells to rupture.
Symptoms and Signs
The early symptoms of malaria are non-specific. The patient usually feels ill and has headache, fatigue, muscle pains and vague abdominal discomfort. These symptoms are followed by fever. The fever in classical malaria is a sequence of paroxysms of fever spikes, chills and rigors with sweating occurring at regular intervals. Physical examination reveals a few findings like a palpable spleen and mild anaemia with some patients having a mildly enlarged, palpable liver. Altered consciousness occurs in Falciparum malaria and may be an ominous sign as are convulsions. The involvement of the nervous system is seen in cerebral malaria, which is caused by Plasmodium Falciparum and is the most lethal form of malaria. kidney failure is also seen sometimes in Falciparum Malaria.
Investigations and Diagnosis
The diagnosis of malaria depends upon the demonstration of the asexual forms of the parasite in the peripheral blood smears of the individual. There are now a number of newer methods of demonstrating the parasite in the blood. The Quantitative Buffy Coat (QBC) technique is now in extensive use. However, in endemic areas it is not always possible to demonstrate the parasite in the blood smears and several patients get treated for malaria on the basis of their clinical symptoms and signs. Supportive evidence for malaria may come in the form of mild anaemia, raised erythrocyte sedimentation rate and increased levels of C-Reactive protein. In severe cases, many of the biochemical parameters in blood are altered.
Treatment and Prognosis
Once the diagnosis of malaria has been made on the basis of a positive blood smear or strong clinical suspicion, then treatment should be started without delay. Chloroquine remains the mainstay in the treatment of malaria. The other drugs that are often used include Mefloquine, Tetracyclines, Primaquine, Pyrimethamine, Proguanil and Quinine. Newer drugs like Halofantrine, Artesunate and Qinghaosu are being used for cases of Chloroquine-resistant malaria. Except for the Falciparum malaria, patients who receive adequate treatment for the other forms, most often have an uneventful recovery. However, resistance to the conventional drugs is increasing and is a major cause for worry.
Cerebral malaria is a medical emergency and even with the best of treatment there is a substantial mortality rate.
Prevention
Prevention is the area on which the maximum focus should be. Steps to reduce the frequency of mosquito bites in endemic areas are important. Use of suitable clothing, insect repellents, bed nets etc. are recommended. Widespread use of the bed nets and repellents has been shown to reduce the incidence of malaria. Efforts are taken to reduce the population of mosquitoes in endemic areas. However, Chemoprophylaxis is often recommended for people who travel to malaria-endemic areas. Chloroquine is most often the drug of choice for Chemoprophylaxis except in areas of known chloroquine-resistance where drugs like Mefloquine or Doxycycline are used.
MEASLES
Introduction
Measles, a disease recognised for over two thousand years, is a highly contagious, acute infection caused by the rubella virus. It usually occurs in children. It is seen in every country of the world. Before the use of vaccines, epidemics of measles occurred every two to five years. Cough, cold, fever and a skin rash that begins several days before the initial symptoms characterise the illness. Recovery from measles is usual, but serious complications of the respiratory and central nervous system may occur.
Cause and Pathogenesis
Measles virus belongs to the Morbillivirus group of the Paramyxovirus family. Humans are the only natural host for wild measles virus. The virus is easily destroyed but remains in the droplet form in air for several hours, especially under conditions of low relative humidity. It is spread by direct contact with droplets from respiratory secretions of infected persons. It is one of the most communicable of infectious diseases and is most infectious when cough and cold is at its peak. The virus invades the respiratory lining membrane and then enters the blood stream. It causes inflammation of the respiratory tract and may predispose to secondary bacterial pneumonia.
Symptoms and Signs
The incubation period is one to two weeks and is often longer in adults. The illness begins with symptoms of malaise, fever, loss of appetite, conjunctivitis, cough and cold lasting several days. This is followed by bluish-grey spots in the oral cavity (Koplik's spots) and then a diffuse skin rash beginning on the face and proceeding down the body to involve the extremities. The rash lasts for five days and then peeling of the skin occurs. Several days after the appearance of the rash, the fever abates. The most common complications of measles involve the respiratory tract and the nervous systems. Bacterial super-infection can also cause middle ear infection or pneumonia in severe cases. Encephalitis may be acute or chronic, after measles infection. Transient hepatitis can also occur.
Severe measles can occur in persons who are immunocompromised such as those, being treated for malignancy or those with AIDS. Malnourished children in developing countries may also develop severe measles. In pregnant women, however, measles (rubeola) unlike German measles (rubella) does not cause any congenital anomalies.
Investigations and Diagnosis
Classic measles is diagnosed when a child develops along with cough, cold, conjunctivitis, Koplik's spots and a skin rash. Leucopenia (a low white blood cell count) is common. Virus isolation in the laboratory is technically difficult. A four-fold increase in the measles antibody titre in acute and convalescent serum samples is considered diagnostic.
Treatment and Prognosis
The disease is usually self-limited, and supportive therapy such as antipyretics and fluids are indicated. Bacterial super-infection should be promptly treated with appropriate antimicrobials. Prophylactic antibiotics are not known to be of value and are not recommended.
Prevention
Measles can be prevented by administrating a live vaccine long before an anticipated exposure. It is now recommended that all healthy children be administered live measles vaccines at fifteen months of age. A second dose given in childhood, usually as a measles-mumps-rubella (MMR) is now routine. The first vaccine can be given between six and nine months of age in situations where the incidence of measles is high before the age of one year. Transient fever and rash develop about one week after vaccination in 5 - 15 percent of children. Live measles vaccine is contra-indicated in persons with defects in the cell-mediated immunity and in pregnant women.
Passive immunisation with antibodies is recommended for those at high risk of developing severe measles and for those who have been exposed to the infection. For example, children with malignant disease and those with defects in cell-mediated immunity. To be effective, passive immunisation must be given within six days after an exposure.
DENGUE FEVER
Introduction
Dengue fever is a disease caused by infection with a type of virus called Flavivirus. There are four different subtypes of this virus producing varying manifestations of the disease. The disease is spread through the bites of mosquitoes belonging to the Aedes egypti species. The disease is essentially a tropical one and is endemic in large parts of Latin and South America. Of late, its incidence has been on the increase in Asian countries such as India.
Cause and Pathogenesis
Dengue fever is transmitted to humans by the bite of the infected Aedes egypti mosquito. The Aedes mosquito breeds in relatively fresh water, lives close to human habitations and bites during the day. The incubation period between the bite and the onset of symptoms is usually two to seven days. The Aedes mosquito is also responsible for the spread of diseases such as yellow fever and Chikungunya virus fever.
Symptoms and Signs
A large number of infections may be sub-clinical, that is, the patients may not even be aware that they have had the disease. The infection usually manifests itself as fever with severe body pain or myalgia. There may be an associated rash over parts of the body. The body pain is so intense that this disease has been called break-bone fever. Quite often, the disease makes no further progress and the patients recover. However, some patients may develop involvement of either of the two dreaded syndromes in Dengue - bleeding (called DHF or Dengue Hemorraghic Fever) or involvement of the brain with altered consciousness (encephalitis). Fatalities are higher among patients in whom these complications are present. Joint pain is another symptom though there may not be true arthritis. Associated symptoms include severe headache, vomiting, and photophobia. Examination of the patient may reveal few findings such as a rash and pain on palpation of the muscles. These symptoms usually last for a period of two to five days and most patients who do not have complications recover completely. The risk of complications appears to be greater in children, particularly the risk of bleeding and DHF with its high fatality rate. Some patients may also go into shock, a condition known as Dengue Shock Syndrome (DSS). This too carries a higher risk of mortality.
Investigations and Diagnosis
The diagnosis of dengue is based on the clinical presentation, knowledge of the area in which the person lives, and laboratory investigations. Blood tests may show a low white blood cell count, a low platelet count, and elevation of certain enzymes. The definitive diagnosis is, however, made by isolating the virus in the blood of the individual during the acute phase of the disease or by detecting antibodies to the virus in the blood. Antigen detection is also possible. A rise in the antibody titre is a useful method of diagnosis. Investigations also need to be done to rule out other likely causes of fever such as malaria and leptospirosis.
Treatment and Prognosis
Treatment is usually supportive and symptomatic. Analgesics, anti-pyretics, and broad-spectrum antibiotics are used during the acute phase to minimise the risk of secondary infection. In cases of bleeding, blood transfusions are required. Shock, if present, needs to be aggressively treated with fluids, oxygen, and close monitoring. Most patients will recover without any sequel. The overall mortality rate with effective treatment is close to 1% but this may be higher in children.
Prevention
Control and elimination of mosquito population is the best method of prevention. A vaccine is in the late stages of development but is still not available for commercial use on a large scale. Control of the mosquito population reduces the incidence of dengue, yellow fever, and certain other rare fevers that are also transmitted by the same species of mosquito.
Source Dr. V.Ramasubramaniam MBBS, MD, MRCP.
Dr.V.Ramasubramaniam is an Assistant Professor of Medicine and heads the Division of Infectious Diseases at the Sri Ramachandra Medical College and Research Institute
CONJUNCTIVITIS
Introduction
Conjunctivitis, commonly known as "pink eye," is an inflammation of the membrane (conjunctiva) that covers the eye and lines the inner surface of the eyelid. There are four main causes of conjunctivitis.
One cause involves the introduction of either bacterial or viral microorganisms into the eye. These may be transmitted to the eye by contaminated hands, washcloths or towels, cosmetics (particularly eye makeup), false eyelashes or extended wear contacts.
Minor conjunctivitis can accompany a viral cold or flu. Although bacterial and some of the viral infections (particularly herpes) are not very common, they are potentially serious. Both types of infection are contagious.
Irritants are another cause of conjunctivitis. Offenders of this type include air pollutants, smoke, soap, hairspray, makeup, chlorine, cleaning fluids, etc.
Seasonal allergic response to grass and other pollens can cause some individuals to acquire conjunctivitis.
Pink eye may be more serious if you: have a condition that decreases your ability to fight infection (impaired immune system), have vision in only one eye or you wear contact lenses.
Symptoms
Various combinations of the following symptoms may be present: itching, redness, sensitivity to light, feeling as if something is in the eye, swelling of the lids and/or discharge from the eyes. The consistency of possible discharge may range from watery to pus-like, depending on the specific cause of the conjunctivitis.
Duration
It usually takes from a few days to two weeks for most types of conjunctivitis to clear. Conjunctivitis due to an allergy may continue as long as the offending pollen is present. Under such conditions, symptoms are likely to recur each year.
Diagnosis
Diagnosis consists of physical examination of the eye by the clinician. If a discharge is present, a culture for bacteria may be warranted.
Treatment
Treatment varies depending on the cause. Medications in the form of ointments, drops or pills may be recommended to help kill the germ infecting the eye, relieve allergic symptoms and/or decrease discomfort. In the case of conjunctivitis due to a viral cold or flu, the practitioner may recommend that you be patient and let it run its course.
OTHER MEASURES THAT SHOULD BE FOLLOWED:
- Apply cool compresses to the infected eye(s) three to four times per day for 10-15 minutes using a clean washcloth each time. This should help reduce itching and swelling and provide some comfort.
- Wash your hands frequently and keep them away from your eyes in order to reduce or prevent recontamination.
- Avoid rubbing your eyes to decrease irritation of the area.
- Wear sunglasses if your eyes are sensitive to the light.
- Avoid exposure to the irritants that may be causing the conjunctivitis.
- Dispose of old eye makeup if the culture for bacteria is positive.
- Use a clean pillowcase each night. (Pillowcase can be changed every other day and turned over nightly).
- Avoid wearing contact lenses while you are using medications or if your eyes are uncomfortable. Cleanse contact lenses thoroughly.
Although many kinds of conjunctivitis are hard to prevent, there are measures that can be taken to decrease your risk of reacquiring or spreading it to someone else. These are listed below:
- Do not share eye makeup or cosmetics of any kind with anyone.
- Avoid sharing washcloths or towels.
- Wash hands frequently and keep away from the eyes.
- Wear protective goggles (i.e., for swimming or working) if you must be exposed to chemicals that are irritating.
- Do not use medication (eye drops, ointment, etc.) that has been prescribed for someone else.
- Avoid swimming in non-chlorinated pools or stagnant lakes or ponds.
- Do not save medication - dispose of it when treatment is completed.
If any of the following problems should occur, notify your clinician:
- Visual changes
- Severe eye pain
- Pain when moving eyes
- Fever
- No improvement with medication within 48-72 hours
- Drainage continues after you have completed full course of medication
- Roommates or other family members develop symptoms
- Eyes become very sensitive to light
- Wash your hands before touching your eyes or your medications.
- Gently, pull your lower lid down with your finger.
- Look up toward the ceiling.
- To instill drops: Drop medicine inside center of your lower lid. Do not drop it on your eyeball. Close your eyes gently without squeezing the lids shut. Blink to distribute medication over the eye. To instill ointment: Starting in the corner of your eye closest to the nose, squeeze a thin ribbon of ointment along the inside of the lower lid. Close eyes gently without squeezing the lids shut. Roll eyes to distribute the medication over them.
- Remove excess solution or ointment outside your eye with a clean tissue, using a separate tissue for each eye.
- Wash hands after you have finished your medication, to avoid transmitting the infection to others.
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