Acute pericarditis (Jempol)
According to a recent article, the most common causes of acute pericarditis includes:
(21%) Viral - adenovirus, enterovirus, cytomegalovirus, influenza virus, hepatitis B virus, and herpes simplex virus, etc
( 6%) Bacterial (other than tuberculosis)
( 6%) Uremia
( 4%) Tuberculosis
( 4%) Idiopathic
(remaining) trauma, drugs, post-AMI, myocarditis, dissecting aortic aneurysm, radiation
 Symptoms and Signs
Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and may be pleuritic in nature --- that is, sharp and worsens with inspiration, due to concomitant pleural inflammation. The pain may be alleviated with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction. As with any chest pain, other causes must also be ruled out, such as GERD, pulmonary embolism, muscular pain, etc.
Main article: chest pain
Pericardial rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur, which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium; however, even a large pericardial effusion does not necessarily present a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole, ventricular systole, and the filling phase of early ventricular diastole.
Fever may be present since this is an inflammatory process.
One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. This condition is fatal if not treated promptly.
Inflammatory markers. A CBC may show an elevated white count and a serum C-reactive protein may be elevated.
Molecular markers. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB) and cardiac troponin I (cTnI), both of which are also markers for myocardial injury. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances is related to inflammation of the myocardium. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L. Coronary angiography in those patients should indicated normal vascular perfusion. The elevation of these biomarkers are typically transient and should return to normal within a week. Persistence may indicated myopericarditis. Troponin levels increase in 35 - 50% of people with pericarditis.
Electrocardiogram (EKG). EKG changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes
stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.
stage 2 -- normalization of ST and PR deviations
stage 3 -- diffuse T wave inversions (may not be present in all patients)
stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted
Because the most common cause of ST elevation is an acute myocardial infarction, and since acute pericarditis can also be a short term complication after an acute myocardial infarction, steps must be taken to differentiate the two EKG readings.
Rarely, electrical alternans may be seen, depending on the size of the effusion.
Chest X-ray. Usually normal in acute pericarditis, but can reveal cardiomegaly (enlarged heart) if the pericardial effusion is more than 200 mL. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.
Echocardiogram. Usually normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.
Meningitis (Akademi JPJ Melaka)
Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs. Meningitis can be life-threatening because of the inflammation's proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.
The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia). Sometimes, especially in small children, only nonspecific symptoms may be present, such as irritability and drowsiness. If a rash is present, it may indicate a particular cause of meningitis; for instance, meningitis caused by meningococcal bacteria may be accompanied by a characteristic rash.
A lumbar puncture may be used to diagnose or exclude meningitis. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF), the fluid that envelops the brain and spinal cord. The CSF is then examined in a medical laboratory. The usual treatment for meningitis is the prompt application of antibiotics and sometimes antiviral drugs. In some situations, corticosteroid drugs can also be used to prevent complications from overactive inflammation. Meningitis can lead to serious long-term consequences such as deafness, epilepsy, hydrocephalus and cognitive deficits, especially if not treated quickly. Some forms of meningitis (such as those associated with meningococci, Haemophilus influenzae type B, pneumococci or mumps virus infections) may be prevented by immunization.
Signs and symptoms
 Clinical features
In adults, a severe headache is the most common symptom of meningitis – occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44–46% of all cases of bacterial meningitis. If none of the three signs is present, meningitis is extremely unlikely. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). Small children often do not exhibit the aforementioned symptoms, and may only be irritable and looking unwell. In infants up to 6 months of age, bulging of the fontanelle (the soft spot on top of a baby's head) may be present. Other features that might distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and abnormal skin color.
Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis. Other signs of meningism include the presence of positive Kernig's sign or Brudzinski's sign. Kernig's sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig's and Brudzinski's signs are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases. Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in patients reporting fever and headache. The patient is told to rapidly rotate his or her head horizontally; if this does not make the headache worse, meningitis is unlikely.
Meningitis caused by the bacterium Neisseria meningitidis (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash which may precede other symptoms. The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching: the redness does not disappear when pressed with a finger or a glass tumbler. Although this rash is not necessarily present in meningococcal meningitis, it is relatively specific for the disease; it does, however, occasionally occur in meningitis due to other bacteria. Other clues as to the nature of the cause of meningitis may be the skin signs of hand, foot and mouth disease and genital herpes, both of which are associated with various forms of viral meningitis.
Leptospirosis (Pati, Butterworth)
Leptospirosis is caused by a spirochaete bacterium called Leptospira spp. that has at least 5 serovars of importance in the United States and Canada causing disease in dogs (Icterohaemorrhagiae, Canicola, Pomona, Grippotyphosa, and Bratislava) There are other (less common) infectious strains. It should however be noted that genetically different leptospira organisms may be identical serologically and vice versa. Hence, an argument exists on the basis of strain identification. The traditional serologic system is seemingly more useful from a diagnostic and epidemiologic standpoint at the moment (which may change with further development and spread of technologies like PCR).
Leptospirosis is transmitted by the urine of an infected animal, and is contagious as long as it is still moist. Although rats, mice and voles are important primary hosts, a wide range of other mammals including dogs, deer, rabbits, hedgehogs, cows, sheep, raccoons, possums, skunks, and even certain marine mammals are also able to carry and transmit the disease as secondary hosts. Dogs may lick the urine of an infected animal off the grass or soil, or drink from an infected puddle. There have been reports of "house dogs" contracting leptospirosis apparently from licking the urine of infected mice that entered the house. The type of habitats most likely to carry infective bacteria are muddy riverbanks, ditches, gulleys and muddy livestock rearing areas where there is regular passage of either wild or farm mammals. There is a direct correlation between the amount of rainfall and the incidence of leptospirosis, making it seasonal in temperate climates and year-round in tropical climates.
Leptospirosis is also transmitted by the semen of infected animals. Abattoir workers can contract the disease through contact with infected blood or body fluids.
Humans become infected through contact with water, food, or soil containing urine from these infected animals. This may happen by swallowing contaminated food or water or through skin contact. The disease is not known to be spread from person to person and cases of bacterial dissemination in convalescence are extremely rare in humans. Leptospirosis is common among watersport enthusiasts in specific areas as prolonged immersion in water is known to promote the entry of the bacteria. Surfers are especially at high risk in areas that have been shown to contain the bacteria and can contract the disease by swallowing contaminated water, contacting water with the eyes and nose, or entrance through open wounds. Occupational risk factors include veterinarians, slaughter house workers, farmers, sewer workers, and architects and other building workers working on derelict buildings. An outbreak in an inner city environment has been linked to contact with rat urine.
Rubella (Pelajar di Pulau Pinang)
Rubella, commonly known as German measles, is a disease caused by the rubella virus. The name "rubella" is derived from the Latin, meaning little red. Rubella is also known as German measles because the disease was first described by German physicians in the mid-eighteenth century. This disease is often mild and attacks often pass unnoticed. The disease can last one to three days. Children recover more quickly than adults. Infection of the mother by Rubella virus during pregnancy can be serious; if the mother is infected within the first 20 weeks of pregnancy, the child may be born with congenital rubella syndrome (CRS), which entails a range of serious incurable illnesses. Spontaneous abortion occurs in up to 20% of cases.
Rubella is a common childhood infection usually with minimal systemic upset although transient arthropathy may occur in adults. Serious complications are very rare. Apart from the effects of transplacental infection on the developing fetus, rubella is a relatively trivial infection.
Acquired (i.e. not congenital) rubella is transmitted via airborne droplet emission from the upper respiratory tract of active cases. The virus may also be present in the urine, feces and on the skin. There is no carrier state: the reservoir exists entirely in active human cases. The disease has an incubation period of 2 to 3 weeks.
In most people the virus is rapidly eliminated. However, it may persist for some months post partum in infants surviving the CRS. These children are a significant source of infection to other infants and, more importantly, to pregnant female contacts.
It should not be confused with rubeola, which was a historical name for measles.
In humans, leptospiral infection causes a wide range of symptoms, and some infected persons may have no symptoms at all. Leptospirosis is a biphasic disease that begins with flu-like symptoms (fever, chills, myalgias, intense headache). The first phase resolves, and the patient is briefly asymptomatic until the second phase begins. This is characterized by meningitis, liver damage (causing jaundice), and renal failure; because of the wide range of symptoms the infection is often wrongly diagnosed. This leads to a lower registered number of cases than there really are. Symptoms of leptospirosis include high fever, severe headache, chills, muscle aches, and vomiting, and may include jaundice, red eyes, abdominal pain, diarrhea, and/or a rash. The symptoms in humans appear after a 4-14 day incubation period.
In animals, the incubation period (time of exposure to first symptoms) is anywhere from 2 to 20 days. In dogs, the liver and kidney are most commonly damaged by leptospirosis. Vasculitis can occur, causing edema and potentially disseminated intravascular coagulation (DIC). Myocarditis, pericarditis, meningitis, and uveitis are also possible sequelae.  One should strongly suspect leptospirosis and include it as part of a differential diagnosis if the sclerae of the dog's eyes appear jaundiced (even slightly yellow), though the absence of jaundice does not eliminate the possibility of leptospirosis, and its presence could indicate hepatitis or other liver pathology rather than leptospirosis. Vomiting, fever, failure to eat, reduced urine output, unusually dark or brown urine, and lethargy are also indications of the disease.
Complications include meningitis, extreme fatigue, hearing loss, respiratory distress, and renal interstitial tubular necrosis, which results in renal failure and often liver failure (the severe form of this disease is known as Weil's disease, though it is sometimes named Weil Syndrome). Cardiovascular problems are also possible.
Signs and symptoms
After an incubation period of 14–21 days, the primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days. Other symptoms include low grade fever, swollen glands (post cervical lymphadenopathy), joint pains, headache and conjunctivitis. The swollen glands or lymph nodes can persist for up to a week and the fever rarely rises above 38 oC (100.4 oF). The rash disappears after a few days with no staining or peeling of the skin. Forchheimer's sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate.
Rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40. The older the person is the more severe the symptoms are likely to be. Up to one-third of older girls or women experience joint pain or arthritic type symptoms with rubella. The virus is contracted through the respiratory tract and has an incubation period of 2 to 3 weeks. During this incubation period, the carrier is contagious but may show no symptoms.
 Congenital rubella syndrome
Main article: Congenital rubella syndrome
Rubella can cause congenital rubella syndrome in the newly born. The syndrome (CRS) follows intrauterine infection by Rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects. It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anaemia and hepatitis. The risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed. Many mothers who contract rubella within the first critical trimester either have a miscarriage or a still born baby. If the baby survives the infection, it can be born with severe heart disorders (PDA being the most common), blindness, deafness, or other life threatening organ disorders. The skin manifestations are called "blueberry muffin lesions." 
Main article: Rubella virus
The disease is caused by Rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome. The virus is transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. It is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them.
Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are be involved in virus infection or non-resolution of the disease. 
 Diagnosis of acquired rubella
Rubella virus specific IgM antibodies are present in people recently infected by Rubella virus but these antibodies can persist for over a year and a positive test result needs to be interpreted with caution. The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.
Swine Flu (Sg Buloh)
Swine influenza (also called swine flu, hog flu and pig flu) refers to influenza caused by those strains of influenza virus, called swine influenza virus (SIV), that usually infect (is endemic in) pigs. As of 2009 these strains are all found in Influenza C virus and the subtypes of Influenza A virus known as H1N1, H1N2, H3N1, H3N2, and H2N3. Swine influenza is common in pigs in the midwestern United States (and occasionally in other states), Mexico, Canada, South America, Europe (including the United Kingdom, Sweden, and Italy), Kenya, Mainland China, Taiwan, Japan and other parts of eastern Asia.
Transmission of swine influenza virus from pigs to humans is not common and does not always cause human influenza, often only resulting in the production of antibodies in the blood. The meat of the animal poses no risk of transmitting the virus when properly cooked. If transmission does cause human influenza, it is called zoonotic swine flu. People who work with pigs, especially people with intense exposures, are at increased risk of catching swine flu. In the mid-20th century, identification of influenza subtypes became possible, this allows accurate diagnosis of transmission to humans. Since then, fifty confirmed transmissions have been recorded, Rarely, these strains of swine flu can pass from human to human. In humans, the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.
The 2009 flu outbreak in humans, known as "swine flu", is due to a new strain of influenza A virus subtype H1N1 that contains genes closely related to swine influenza. The origin of this new strain is unknown. However, the World Organization for Animal Health (OIE) reports that this strain has not been isolated in pigs. This strain can be transmitted from human to human, and causes the normal symptoms of influenza.
Pigs can become infected with human influenza, and this appears to have happened during the 1918 flu pandemic and the 2009 flu outbreak.
Of the three genera of influenza viruses that cause human flu, two also cause influenza in pigs, with Influenzavirus A being common in pigs and Influenzavirus C being rare. Influenzavirus B has not been reported in pigs. Within Influenzavirus A and Influenzavirus C, the strains found in pigs and humans are largely distinct, although due to reassortment there have been transfers of genes among strains crossing swine, avian, and human species boundaries.
Influenza C viruses infect both humans and pigs, but do not infect birds. Transmission between pigs and humans have occurred in the past. For example, influenza C caused small outbreaks of a mild form of influenza amongst children in Japan, and California. Due to its limited host range and the lack of genetic diversity in influenza C, this form of influenza does not cause pandemics in humans.
Swine influenza is known to be caused by influenza A subtypes H1N1, H1N2, H3N1, H3N2, and H2N3. In pigs, three influenza A virus subtypes (H1N1, H3N2, and H1N2) are the most common strains worldwide. In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants, containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.