Distance education courses child health course

Manifestations

The incubation period of typhoid bacteria is 1-3 weeks, usually 2 weeks. The patient presents with high fever (except in the malnourished), malaise, headache, lack of appetite, abdominal pain, constipation, vomiting with or without diarrhoea, mental dullness, delirium and confusion, meningeal irritation signs, cough, sore throat, nose bleeding (epistaxis), respiratory distress (if pneumonia develops), muscle and joint pains, sometimes jaundice.
In infants and young children, typhoid may present with vomiting and bloody diarrhoea. Typhoid may also present as encephalopathy with meningism, delirium, convulsions and coma. Sometimes it may present as septicaemia with drowsiness, shock and jaundice.
Signs

The signs of typhoid fever are mild abdominal distension, epistaxis, bradycardia, haemorrhage which may cause shock, hepatosplenomegaly.

Complications

If typhoid is not well managed, it can lead to the following complications:

• 
  Intestinal perforation;
  
• 
  intestinal haemorrhage;
  
• 
  convulsions in infants;
  
• 
  myocarditis;
  
• 
  arthritis;
  
• 
  osteomylitis especially in sickle cell disease;
  
• 
  meningitis;
  
• 
  pneumonia;
  
• 
  urinary tract infection;
  
• 
  glomerulonephritis;
  
• 
  acute tubular necrosis;
  
• 
  haemolytic anaemia;
  
• 
  hepatitis;
  
• 
  abscesses.
  

Investigations

Once typhoid is suspected, the investigations carried out include:

• Widal test,

• Blood culture,

• Stool culture,

• rectal swab culture, urine culture,

• and cerebrospinal fluid culture.

Blood culture is usually positive early in the disease and rarely positive after two weeks of infection.

Diagnosis:

Diagnosis is based on rising Widal test titre and isolation of salmonellae from any of the above specimens.

Management:

You should start treatment immediately on suspicion after collecting the laboratory specimens. The mainstays of management are:

• 
  Administration of antibiotics such as chloramphenicol 25mg/kg every 6 hours, given for 2-3 weeks. Other useful antibiotics are amoxycillin or cotrimoxazole;
  
• 
  Maintenance of fluid and electrolyte balance;
  
• 
  Isolation and barrier nursing;
  
• 
  Providing nutritious diet;
  
• 
  Surgery if bowel perforation occurs.
  

Prevention

Typhoid can be prevented with good sanitation and purification of water. You should advice the parents and caretakers to observe good personal hygiene and to cook food properly. Carriers should be identified, treated carriers and excluded from handling foods until the infection clears.

5. ACUTE OSTEOMYELITIS.

Acute osteomyelitis is the infection, usually bacterial, of the bone and the bone marrow. The infection usually occurs near the end of the long bones.

Causes

The most common bacteria causing osteomyelitis is Staphylococcus . But streptococci, Haemophilus influenzae, pneumococci, and salmonellae may cause osteomyelitis. In the newborn, E.coli, pseudomonas, proteus and klebsiella may also cause osteomyelitis.

Osteomyelitis usually arises as a result of the spread of the bacteria through the blood from a clinically unapparent focus of infection. This focus may be:

• 
  infected skin,
  
• 
  a boil,
  
• 
  dental abscess,
  
• 
  a wound with a retained foreign body
  

.

It is important to search carefully and locate the focus. Direct spread of bacteria from a wound of a compound fracture may also result in osteomyelitis.

Osteomyelitis occurs at any age but most commonly between the ages of 3-12 years.

ACTIVITY Write down the symptoms and signs of osteomyelitis. ____________________________________________________________ ____________________________________________________________ ____________________________________________________________

Clinical Manifestations

I hope your answer included the following clinical manifestations of osteomyelitis.

In infants, the clinical manifestations of osteomyelitis may be non-specific. They include irritability, refusal to feed, not moving a hand, arm or leg (pseudoparalysis)
Older children may complain of fever, pain or limp.

The signs of osteomyelitis include:

• 
  tenderness on pressure over the involved bone, usually at the metaphysis (end of the shaft),
  
• 
  swelling over the subperiosteal abscess,
  
• 
  redness,
  
• 
  regional lymphadenitis,
  
• 
  septic arthritis of the nearby joint or sympathetic effusion of the nearby joint.
  

Investigations:

The investigations done are blood culture, Gram staining of the needle aspirate of the abscess, full blood count and X-ray of the affected part.

Diagnosis

The diagnosis is based on the clinical findings, blood culture, and X-ray findings. Early in the illness, X-ray may shows only soft tissue swelling. Subperiosteal calcification becomes evident after 10 -14 days.

Treatment

Osteomyelitis is treated with:

• 
  Intravenous flucloxacillin 50 mg/kg every 6 hours, or higher doses intramuscularly where intravenous drug cannot be given, for 1-2 weeks and continued orally for a total of 6 weeks;
  
• 
  Rest;
  
• 
  Paracetamol for relieving the pain;
  
• 
  Elevation of the limb;
  
• 
  Support in a partial plaster;
  
• 
  Physiotherapy is offered in the recovery phase;
  
• 
  Aspiration of the abscess or joint.
  

Complications

Osteomyelitis may be complicated by:

• 
  Septic arthritis;
  
• 
  Chronic osteomyelitis;
  
• 
  Septic meningitis or epidural abscess;
  
• 
  Pathological fractures;
  
• 
  Flexion contractures.
  
• 
  Arrest of growth of the limb
  

Differential Diagnosis

A number of conditions are considered in the differential diagnosis of osteomyelitis. These are:

• 
  sickle cell disease,
  
• 
  septic arthritis,
  
• 
  cellulitis,
  
• 
  local abscess,
  
• 
  acute rheumatic fever,
  
• 
  incomplete fracture,
  
• 
  leukaemia,
  
• 
  bone tumours and
  
• 
  secondary metastasis.
  

Next, let us learn about septic arthritis.

6. SEPTIC ARTHRITIS

Septic arthritis is infection of a joint by bacteria.

What Causes Septic Arthritis?

Septic arthritis is caused most commonly by Staphylococcus pyogenes. Other bacteria which cause septic arthritis are gonococcus, streptococci, haemophilus influenzae, pneumococci, meningococci, and salmonellae.

The bacteria in the blood may reach a joint and cause septic arthritis. The bacteria may also reach the joint by direct extension from a neighbouring osteomyelitis. Direct extension through the epiphyseal centre is most likely to occur in infancy. This is because in infancy vessels from the metaphysis penetrate through the growth plate.

Clinical Manifestations:

Symptoms of septic arthritis include fever, irritability, and apprehension. The signs of septic arthritis are pallor, tachycardia, fluctuation, swelling, tenderness, redness (except the hip because it is hidden), limitation of movement, muscle spasm in a position of flexion and intense pain on movement.

Investigations

The investigations include obtaining a joint aspirate for culture and Gram staining, blood culture, and X-ray.

Diagnosis

Diagnosis is based on finding of bacteria on Gram staining of the aspirate, and isolation of the bacteria in the blood or joint aspirate cultures. Early in the infection X-ray shows soft tissue swelling and increased joint space. After 10-14 days, the X-ray shows osteoporosis, bone erosion and decrease of the joint space.

Management

Septic arthritis is managed with high intravenous antibiotics as in osteomyelitis for at least 4 weeks. If there is no improvement in 24 hours of starting the antibiotics, surgical decompression is done to prevent the destruction of the articular cartilage, necrosis of the epiphysis and dislocation which may cause permanent disability in the hip and shoulder. The other joints are decompressed with daily aspirations with large bore needle. Traction is applied to maintain good functional position. Physiotherapy is done to rebuild the muscle and regain mobility. Oral therapy is started when there is marked improvement.

Complications.

• 
  A disabling ankylosis (stiffening of the joint) may occur in neglected cases.
  
• 
  Sinus formation
  

7. RHEUMATIC FEVER

Rheumatic fever is a generalized inflammatory disease of the connective tissue, characterized by fever, joint pains, and heart disease with less frequent involvement of the skin, nervous system and the subcutaneous tissues. Rheumatic fever has a tendency to recur and is due to an immune reaction following Group A beta haemolytic streptococcal throat infection.

Epidemiology

Rheumatic fever is common among the children of the poor, where there is overcrowding and delay in the treatment of throat infections. Rheumatic fever is extremely rare under 2 years of age. Most cases of rheumatic fever occur in children aged 5-15 years.

Cause

Acute rheumatic fever is related to a previous Group A beta haemolytic streptococcal throat infection. The interval between the throat infection and the attack of acute rheumatic fever varies from 4- 6 weeks.

Clinical Manifestations

The clinical manifestations of rheumatic fever include:

• 
  fever
  
• 
  polyarthralgia (discomfort in the joints without objective evidence of pain, redness or swelling)
  
• 
  migratory polyarthritis involving the large joints (knees, ankles, elbow and the wrist). The affected joints are painful, red, hot, and swollen for about 24 hours. After the recovery of one group of joints, the attack moves on to other groups of joints. This movement of the attack from one group of joints to the other explains the description of the arthritis as migratory. The polyarthritis lasts 1-4 weeks and subsides without leaving any residual damage in the affected joints.
  
• 
  Carditis, the most serious manifestation of rheumatic fever, involves the inflammation of all the layers of the heart wall simultaneously. The inflammation of the pericardium (outer coating of the heart) is called pericarditis. The inflammation of the myocardium (heart muscle) is called myocarditis. The inflammation of the endocardium (internal lining of the heart wall) is called endocarditis. The involvement of the heart is revealed by the occurrence of new mitral and aortic murmurs and cardiomegaly. Very severe rheumatic heart disease may lead to heart failure. The heart lesions may remain and worsen with every recurrence of the acute rheumatic fever.
  
• 
  Subcutaneous nodules are several tender swellings 0.5-2cm in diameter. These nodules are found on the extensor surfaces of the bone prominences of the knees, elbows, shoulders, scapulae, the occiput and the spinal processes. The subcutaneous nodules occur in less than 15% of the cases and are indicators of a severe disease.
  
• 
  Sydenham chorea is characterized by jerky, involuntary and irregular movements of the limbs and face, emotional instability, inattentiveness, clumpsiness and crying out loudly. The movements are usually bilateral but may also be unilateral. The chorea is worsened by stress and disappears when the child is asleep. Sydenham chorea is rare and affects girls more commonly than boys. After several weeks or months, spontaneous remission occurs.
  
• 
  Erythema marginatum consists of non-pruritic macules or patches with central pallor and a well defined irregular margin on the trunk and the proximal parts of the limbs. Erythema marginatum occurs in 10 % of the cases of acute rheumatic fever.
  

The laboratory findings include acute phase reactants (leukocytosis, raised erythrocyte sedimentation rate, and elevated C-reactive protein), evidence of a preceding streptococcal infection (elevated or rising antistreptolysin titre, isolation of streptococci from throat swab culture, and positive streptozyme test) and prolonged PR interval in the Electrocardiogram (ECG).

Diagnosis

No single clinical feature or laboratory test can establish the diagnosis of rheumatic fever. The diagnosis of rheumatic fever is made using some selected clinical features, the major and minor criteria published by Jones.

The five major criteria are:

• 
  migratory polyarthritis;
  
• 
  carditis;
  
• 
  Sydenham chorea;
  
• 
  Subcutaneous nodules; and
  
• 
  erythema marginatum.
  

The minor criteria include:

• 
  fever;
  
• 
  Polyarthralgia in the absence of polyarthritis as a major criterion;
  
• 
  prolonged PR interval on the electrocardiogram;
  
• 
  Acute phase reactants (leukocytosis, raised erythrocyte sedimentation rate, and elevated C-reactive protein);
  
• 
  evidence of a preceding streptococcal infection (elevated or rising antistreptolysin titre, isolation of streptococci from throat swab culture, and positive streptozyme test).
  

ACTIVITY Write down the usage of the above criteria for making diagnosis of acute rheumatic fever: _____________________________________________________________________ _____________________________________________________________________ _____________________________________________________________________

Now compare your answer with the information in the following discussion.

.

The diagnosis of rheumatic fever is based on the presence of two major criteria or one major criterion and two minor criteria, together with evidence of a preceding streptococcal infection.

Complications.

The development of rheumatic valvular heart disease is the major complication of acute rheumatic fever.

Treatment:

After taking the throat swab, the first intramuscular dose of benzyl penicillin is given. The intramuscular injections or oral penicillin are then continued for 10 days. Children with painful joints and carditis often lie still. As they recover, they are not allowed to walk until the joint involvement has subsided, heart size diminished and rapid pulse diminished. Thereafter, the children are progressively allowed more activity. If there has been heart failure, the convalescence may be more prolonged and activity is restricted until the evidence of rheumatic activity has been absent for 2 weeks.

Anti-inflammatory treatment

The anti-inflammatory treatment is effected with salicylates 100mg/kg/24 hours divided in 4 doses for 3-5 days followed by 75mg/kg/24 hours divided in 4 doses for 4-6 weeks. Patients with carditis or congestive cardiac failure are also given predisone, 2mg/kg/24 hours divided in 4 doses for 2-3 weeks. Thereafter, predisone is tapered over a period of 2 weeks by giving 5mg/24 hours every 2-3 days. While predisone is being withdrawn, salicylates are given. Mild rebounds after the discontinuation of the anti-inflammatory drugs are left alone. Those with severe rebounds are given salicylates or steroids once more.

Congestive cardiac failure is treated with digoxin, diuretics, fluid and salt restriction and oxygen. The slow dose of digoxin is 0.04 -0.06 mg/kg in 4 doses. The maintenance digoxin dosage is 0.01 mg/kg in two divided doses. Furosemide 2 mg/kg intravenously per dose is given when there is pulmonary oedema.

Prevention of rheumatic fever.
a) Primary prevention.

Primary prevention means treatment of the streptococcal upper respiratory infection with antibiotics to prevent the first attack of rheumatic fever. Antibiotic therapy started up to the 9^th day of the onset of symptoms of the upper respiratory infection can prevent rheumatic fever.

b) Secondary prevention.

Secondary prevention means prevention of infection of upper respiratory tract with group A beta haemolytic streptococci in persons who have had an attack of rheumatic fever. The preferred method of secondary prevention is regular monthly intramuscular injections of benzathine penicillin G, 1.200,000 units. Patients with rheumatic carditis need a lifelong secondary prophylaxis. The individuals with no carditis continue with secondary prophylaxis until early twenties provided that at least 5 years will have passed since the last attack of rheumatic fever.

Before dental or surgical procedures, patients with rheumatic carditis also need additional antibiotics to prevent infective endocarditis. The secondary prophylaxis of rheumatic fever is not enough for preventing infective endocarditis. The additional antibiotics (gentamycin, amoxycillin, cephalexin, azithromycin or erythromycin) are given within half an hour before the procedure.

I hope you now understand how to diagnose and treat rheumatic fever. Remember that it can be prevented by treating a sore throat early with antibiotics. So advice parents not to ignore a child with a sore throat but to bring them for treatment as early as possible.

Before you proceed to read the next section, do the following activity.

ACTIVITY Write down the features of nephrotic syndrome: __________________________________________________________ _________________________________________________________ _________________________________________________________

8. NEPHROTIC SYNDROME.

Nephrotic syndrome is a disease characterized by oedema, heavy loss of proteins in the urine, low albumin in the blood and high levels of lipids in the blood due to many causes. The nephrotic syndrome frequency peaks between 5 and 8 years.

Causes

In 90% of the cases, the cause of nephrotic syndrome is unknown. The type whose cause is unknown is called idiopathic nephrotic syndrome. In the remaining 10%, the nephrotic syndrome is secondary to acute glomerulonephritis, purpura, lupus erythematosus, drugs, hepatitis, acquired immunodeficiency syndrome, syphilis, malaria, schistosomiasis hydatid disease, and diabetes mellitus. There is also a congenital form of nephrotic syndrome.

All types of nephrotic syndrome are characterized by increased permeability of the glomerular membrane to proteins. This increased permeability of the glomerular membrane to proteins leads to heavy loss of proteins in the urine. The protein loss is at a greater rate than the liver can produce the serum proteins. This imbalance between protein loss and the production leads to low levels of albumin in the blood. In turn, low albumin in the blood leads to oedema.

Clinical Manifestations

There is gradual appearance of oedema over a period of days or weeks. The oedema first appears in the face early in the morning and progresses to the feet later in the day. Other symptoms are loss of appetite, lethargy, passage of little urine (oliguria) and abdominal swelling and pain due to ascites.

The signs of nephrotic syndrome are oedema, ascites, and pleural effusion.
Investigations

The investigations include determinations of serum protein, proteins in urine, serum cholesterol.

Diagnosis

Nephrotic syndrome is based on the clinical features and finding of gross proteinuria (40 mg /hr/m² ).

Management

Patients with severe oedema, pleural effusion, ascites or genital oedema are hospitalized. Sodium intake is restricted until oedema resolves. If oedema is severe, fluid intake is also restricted. In some instances of severe oedema, 25% human albumin 1g/kg/ 24 hours is given intravenously. Predinisone is given at a dose of 60mg/m² /24 hours divided in 3 or 4 doses. Usually after 2 weeks of predinisone administration, response to predinisone occurs. The response to predinisone is indicated by cessation of proteinuria. The nephrosis is steroid resistant if the child continues to have proteinuria after a month of treatment with predinisone.

After five days of protein free urine, the dosage of predinisone is reduced to 60 mg/m² to a maximum of 60 mg every other day with breakfast. This alternate day regime of predinisone is continued for 3 – 6 months to maintain the remission. After such a period of alternate predinisone therapy, the drug may be stopped abruptly.
Relapses may occur. A relapse is recurrence of oedema and proteinuria and is treated as above..
Complications

The complications of nephrotic syndrome include:

• 
  infections and pneumonia for immunoglobulin loss and increased catabolism;
  
• 
  pulmonary embolism, arterial and venous thrombosis for increased tendency to form clots in the blood (hypercoagulability);
  
• 
  iron resistant microcytic anaemia for loss of transferrin, the protein which transports iron in the body;
  
• 
  rickets for loss of cholecalciferol binding protein, the protein which transports the active form of vitamin D in the body.
  
  
  

The increased tendency to form clots in the blood, also known as Hypercoagulability, is partly due loss of antithrombin III (an anticoagulant protein) in the urine. It is also caused by increased levels of fibrinogen in the blood, increased tendency of the platelet to collect into a mass (aggregability), and damaged ability to break down the fibrin (fibrinolysis). Fibrin is the main component of the blood clot.

Prognosis:

Many of the children with steroid sensitive idiopathic nephrotic syndrome have repeated relapses until recovery toward the end of the second decade of life. The recovery is indicated by passage of urine without proteins for at least 5 years. In the other types, full recovery does not occur and the disease progresses to end stage renal failure.

Prevention

There is no known way of preventing idiopathic nephrotic syndrome. The secondary nephrotic syndrome can be prevented by:

• 
  preventing the primary diseases: hepatitis, acquired immunodeficiency syndrome, syphilis, malaria, schistosomiasis and hydatid disease;
  
• 
  avoiding such drugs as captopril, troxidone and mercurial diuretics and penicillamine;
  
• 
  Carefully controlling diabetes mellitus in childhood.
  

9. VIRAL HEPATITIS

Hepatitis is inflammation of the liver most commonly caused by the hepatitis viruses. These viruses are so called because of their special preference for the liver cells for multiplication.

Causes

As mentioned above, the hepatitis viruses are the commonest causes of hepatitis. The hepatitis viruses which to-date have been identified are hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus, hepatitis E virus, and Hepatitis G virus. Commonly used abbreviations of these viruses are HAV, HBV, HCV, HDV, HEV, and HGV. As yet hepatitis F virus has not been identified. All the hepatitis viruses have a special liking for the liver cells.

The disease caused by each of the hepatitis virus is called after that particular virus. Thus we speak of hepatitis A, hepatitis B etc. Other viruses, such as cytomegalovirus, Epstein-Barr virus, rubella virus and enteroviruses, may also cause hepatitis.

A. Hepatitis A

Hepatitis A is the infection of the liver by hepatitis A virus. Hepatitis occurs all over the world but most cases are found in the developing countries. Hepatitis A virus is most commonly transmitted by the faecal oral route. Rarely, hepatitis A virus is transmitted through the blood products or through the skin. The incubation period of hepatitis A averages 4 weeks with a range of 2 to 6 weeks. From the liver, the virus reaches the blood, bile and the stools. Maximum faecal excretion of hepatitis A virus occurs late in the incubation period with a minimum occurrence after the onset of the symptoms. Up to two thirds of all the cases are asymptomatic. Two thirds of the symptomatic cases are without jaundice.

Clinical manifestations

Fever, anorexia, nausea, vomiting, diarrhoea and headache may precede jaundice by one week. In infants and young children, these symptoms may also pass unnoticed. The symptoms are more likely to appear in older children. The jaundice is associated with liver enlargement and tenderness. The peak of the jaundice occurs one to two weeks after the onset and then begins to subside. Darkening of the urine may precede the jaundice. The stools may become light or clay coloured.

Hepatitis A outbreak in the asymptomatic infants and young children is recognized when the symptoms appear in several children in a school.

Diagnosis:

A history of contact, detection of anti-HAV IgM (immunoglobulin M) antibodies, elevated aminotransferases especially the alanine aminotrasferase, and elevated conjugated and unconjugated bilirubin.

Complications

99 % of the children recover. In very rare occasions, fulminant hepatitis does occur. Aplastic anaemia is another rare complication.

Treatment

There are no specific measures. Light diet at the start of the illness is preferable. Low fat diet is offered during the period of jaundice.

.
Fulminant hepatitis has a very high fatality. The prognosis is particularly poor if coma with deepening of jaundice and ascites develop. Incomplete resolution leads to prolonged hepatitis or chronic cholestatic hepatitis but not cirrhosis. 6 to 10 weeks after resolution, benign relapses may occur for several months in 10% to 15% of the cases.
Prevention

Hepatitis A can be prevented through isolation of cases, careful hand washing, careful handling of the stools, diapers and other contaminated clothes. Isolation is necessary because the patient remains contagious for 7 days after the appearance of jaundice. An inactivated hepatitis A virus vaccine is available. But this vaccine can be administered only in children aged above 2 years of age.

B) Hepatitis B
Hepatitis B is caused by hepatitis B virus. This virus possesses three antigens: hepatitis B surface antigen, hepatitis B core antigen, and hepatitis B e antigen. The abbreviations for these antigens are HBsAg, HBcAg and HBeAg respectively.
Epidemiology:

Hepatis B virus, too, has a world-wide distribution. But most cases are found in the developing countries. High concentrations of hepatitis B virus occur in the blood, serum, serous exudates, saliva, vaginal fluids, and semen. Hepatitis B virus is most commonly transmitted vertically from an infected mother to her baby before birth (intrauterine infection) or during labour and birth (perinatal infection) and later by blood, blood products or other body fluids through contact with contaminated needles, skin piercing, tattoos intravenous drug abuse, haemodialysis or through sexual contact. The lower the age at the time of infection is, the higher the risk of developing chronic HBV infection. Chronic infection is defined by being HBsAg positive for six months. Finding HBsAg in a patient is diagnostic and indicative of infectivity. Presence of HBe antigen indicates infectivity. On the other hand, the appearance of anti-HBs antibodies indicates recovery (termination of viral multiplication), non-infectivity and immunity. Hepatitis B virus is transmitted through the blood products or the skin. The incubation period of hepatitis B is averages 4 months range of 2 to 6 months.

Symptoms

Hepatitis B presents with:

• 
  Gastrointestinal upset, lethargy, and malaise;
  
• 
  Jaundice in only 25% from the eighth week of exposure and lasting for 4 weeks;
  
• 
  Liver enlargement and tenderness. Sometimes the liver is not palpable below the costal margin. Gentle striking of the rib cage with a closed fist over the liver may then elicit the liver tenderness;
  
• 
  Splenomegaly and lymph nodes enlargement are common;
  
• 
  Macular rash, maculopapular rash, urticarial lesions and arthritis may precede jaundice.
  

Diagnosis

The diagnosis of hepatitis B is based on the presence of HBs antigen in the blood, anti-HBc IgM antibodies together with elevated alanine and aspartate aminotransferases and bilirubin (both conjugated and unconjugated). Presence of HBs antigen alone signifies infection or a carrier state.

Treatment

A patient with hepatitis is given:

• 
  Rest
  
• 
  Nutritious diet,
  
• 
  Alpha interferone 5-6 million units/m² body surface area three times a day for 4 to 6 months.
  

Prognosis:

10 % of the cases develop chronic hepatitis. Chronic hepatitis B predisposes to cirrhosis and hepatocellular carcinoma more in adults than in children.

Prevention

Hepatitis B is prevented by:

• 
  Immunization with Hepatitis B vaccine;
  
• 
  avoiding sharing of needles;
  
• 
  Proper disposal of needles;
  
• 
  Screening of blood for Hepatitis B surface antigen;
  
• 
  Careful sterilization of instruments;
  
• 
  Wearing gloves during withdrawal of blood .
  

C) Hepatitis C

Hepatitis C is the infection of the liver by hepatitis C virus. This virus has numerous subtypes and subspecies and is transmitted in the same way as the hepatitis B virus. In hepatitis C, seroconversion (change from a negative ELISA to a positive one) may take as long as 6 months to develop.

Clinical Manifestations

The clinical manifestations of hepatitis C are similar to those of other hepatitis viruses. There may be manifestations of small vessels vasculitis, cerebritis, membranoproliferative glomerulonephritis and peripheral neuropathy.

Diagnosis:

The diagnosis is based on detecting IgG antibodies.

Recombinant immunoblot assay (RIBA) detects antibodies to multiple hepatitis C virus antigens. Polymerase chain reaction becomes positive in three days.
Treatment:

A combination of alpha interferone and ribavirin has been recommended.

Complications:

There is a low risk of developing fulminant hepatitis but there is a high risk of developing cirrhosis and hepatocellular carcinoma.

Prevention:

There is no vaccine available. To minimize further liver damage, the patients should be given hepatitis A and hepatitis B vaccines.

D) Hepatitis D.

Hepatitis D virus is the smallest animal virus. Because it is incomplete, HDV alone cannot multiply or cause an infection. To be able to multiply and cause infection, HDV must associate HBV. From the excess of hepatitis B surface antigen, HDV acquires an envelop. This explains why hepatitis D occurs only in subjects with hepatitis B. The HDV and HBV infections occur either simultaneously (coinfection) or the HDV infects a subject already having a chronic HBV infection (superinfection).
Epidemiology:

HDV is transmitted in the same ways as hepatitis B virus but the vertical transmission is rare. The incubation period of a coinfection of HDV and HBV is 90 days. The incubation period after superinfection HDV on HBV infection is 1-2 months.