Diphtheria (Greek "pair of leather scrolls") is an upper respiratory tract illness caused by

Corynebacterium diphtheriae, a facultative anaerobic Gram-positive bacterium. It is

characterized by sore throat, low fever, and an adherent membrane (a
pseudomembrane) on the tonsils, pharynx, and/or nasal cavity.[3 A milder form of
diphtheria can be restricted to the skin. Uncommon consequences include myocarditis
(about 20% of cases) [4] and peripheral neuropathy (about 10% of cases). [5]

Diphtheria is a contagious disease spread by direct physical contact or breathing the

aerosolized secretions of infected individuals. Historically quite common, diphtheria has
largely been eradicated in industrialized nations through widespread vaccination. In the
United States for example, there were 52 reported cases of diphtheria between 1980
and 2000; between 2000 and 2007 there were only three cases[6] as the DPT
(Diphtheria–Pertussis–Tetanus) vaccine is recommended for all school-age children.
Boosters of the vaccine are recommended for adults since the benefits of the vaccine
decrease with age without constant re-exposure; they are particularly recommended for
those traveling to areas where the disease has not been eradicated.

Signs and symptoms

The respiratory form has an incubation period of 2–5 days. The onset of disease is
usually gradual. Symptoms include fatigue, fever, a mild sore throat and problems
swallowing. Children infected have symptoms that include nausea, vomiting, chills, and a
high fever, although some do not show symptoms until the infection has progressed
further. In 10% of cases, patients experience neck swelling, informally referred to as "bull
neck." These cases are associated with a higher risk of death.

In addition to symptoms at the site of infection (sore throat), the patient may experience
more generalized symptoms, such as listlessness, pallor, and fast heart rate. These
symptoms are caused by the toxin released by the bacterium. Low blood pressure may
develop in these patients. Longer-term effects of the diphtheria toxin include
cardiomyopathy [7] and peripheral neuropathy (sensory type). [8] The cutaneous form of
diphtheria is often a secondary infection of a preexisting skin disease. Signs of
cutaneous diphtheria infection develop an average of seven days after the appearance
of the primary skin disease.

Clinical criteria

• Upper respiratory tract illness with sore throat

• Low-grade fever (>103°F is rare)
• An adherent pseudomembrane of the tonsil(s), pharynx, and/or nose.

Case classification

• Probable: a clinically compatible case that is not laboratory-confirmed and is not

epidemiologically linked to a laboratory-confirmed case
• Confirmed: a clinically compatible case that is either laboratory-confirmed or
epidemiologically linked to a laboratory-confirmed case
Epidemiology
Diphtheria is a serious disease, with fatality rates between 5% and 10%. In children
under 5 years and adults over 40 years, the fatality rate may be as much as 20%.[6]
Outbreaks, though very rare, still occur worldwide, even in developed nations such as
Germany and Canada. After the breakup of the former Soviet Union in the late 1980s,
vaccination rates in its constituent countries fell so low that there was an explosion of
diphtheria cases. In 1991 there were 2,000 cases of diphtheria in the USSR. By 1998,
according to Red Cross estimates, there were as many as 200,000 cases in the
Commonwealth of Independent States, with 5,000 deaths.[10] This was so great an
increase that diphtheria was cited in the Guinness Book of World Records as "most
resurgent disease".

In early May 2010, a case of diphtheria was diagnosed in Port-au-Prince, Haiti after the
devastating 2010 Haiti earthquake. The 15 year old male patient died while workers
searched for anti-toxin.[12]

Treatment
The disease may remain manageable, but in more severe cases lymph nodes in the
neck may swell, and breathing and swallowing will be more difficult. People in this stage
should seek immediate medical attention, as obstruction in the throat may require
intubation or a tracheotomy. Abnormal cardiac rhythms can occur early in the course of
the illness or weeks later, and can lead to heart failure. Diphtheria can also cause
paralysis in the eye, neck, throat, or respiratory muscles. Patients with severe cases will
be put in a hospital intensive care unit (ICU) and be given a diphtheria anti-toxin. Since
antitoxin does not neutralize toxin that is already bound to tissues, delaying its
administration is associated with an increase in mortality risk. Therefore, the decision to
administer diphtheria antitoxin is based on clinical diagnosis, and should not await
laboratory confirmation.[6]

Antibiotics have not been demonstrated to affect healing of local infection in diphtheria
patients treated with antitoxin. Antibiotics are used in patients or carriers to eradicate C.
diphtheriae and prevent its transmission to others. The CDC recommends[9] either:

• Erythromycin (orally or by injection) for 14 days (40 mg/kg per day with a
maximum of 2 g/d), or
• Procaine penicillin G given intramuscularly for 14 days (300,000 U/d for patients
weighing <10 kg and 600,000 U/d for those weighing >10 kg). Patients with
allergies to penicillin G or erythromycin can use rifampin or clindamycin.

In cases that progress beyond a throat infection, diphtheria toxin spreads through the
bloodstream and can lead to potentially life-threatening complications that affect other
organs of the body, such as the heart and kidneys. The toxin can cause damage to the
heart that affects its ability to pump blood or the kidneys' ability to clear wastes. It can
also cause nerve damage, eventually leading to paralysis. 40% to 50% of those left
untreated can die.
Dengue fever (pronounced UK: /ˈdɛŋɡeɪ/, US: /ˈdɛŋɡiː/) and dengue hemorrhagic fever
(DHF) are acute febrile diseases which occur in the tropics, can be life-threatening, and
are caused by four closely related virus serotypes of the genus Flavivirus, family
Flaviviridae.[1] It is also known as breakbone fever, since it can be extremely painful.

Dengue is transmitted to humans by the Aedes (Stegomyia) aegypti or more rarely the
Aedes albopictus mosquito, both of which feed exclusively during daylight hours. [6]

Diagnosis
The diagnosis of dengue is usually made clinically. The classic picture is high fever with
no localising source of infection, a rash with thrombocytopenia and relative leukopenia -
low platelet and white blood cell count. Dengue infection can affect many organs and
thus may present unusually as liver dysfunction, renal impairment, meningo-encephalitis
or gastroenteritis.

1. Fever, headaches, eye pain, severe dizziness and loss of appetite.

2. Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding
from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea)
3. Thrombocytopenia (<100,000 platelets per mm³ or estimated as less than 3
platelets per high power field)
4. Evidence of plasma leakage (hematocrit more than 20% higher than expected, or
drop in hematocrit of 20% or more from baseline following IV fluid, pleural
effusion, ascites, hypoproteinemia)
5. Encephalitic occurrences.

Early symptoms include:

• Decreased appetite
• Fever
• Headache
• Joint aches
• Malaise
• Muscle aches
• Vomiting

Treatment
The mainstay of treatment is timely supportive therapy to tackle circulatory shock due to
hemoconcentration and bleeding. Close monitoring of vital signs in the critical period (up
to 2 days after defervescence - the departure or subsiding of a fever) is critical. Increased
oral fluid intake is recommended to prevent dehydration. Supplementation with
intravenous fluids may be necessary to prevent dehydration and significant concentration
of the blood if the patient is unable to maintain oral intake. A platelet transfusion may be
indicated if the platelet level drops significantly (below 20,000) or if there is significant
bleeding. The presence of melena may indicate internal gastrointestinal bleeding
requiring platelet and/or red blood cell transfusion.

Aspirin and non-steroidal anti-inflammatory drugs should be avoided as these drugs may
worsen the bleeding tendency associated with some of these infections. Patients may
receive paracetamol, acetaminophen, preparations to deal with these symptoms if dengue
is suspected.[26]

Blood transfusion

Dengue may also be transmitted via infected blood products (blood transfusions, plasma,
and platelets),[33][34] and in countries such as Singapore, where dengue is endemic, the risk
was estimated to be between 1.6 and 6 per 10,000 blood transfusions.[35]

What is Tuberculosis?
Tuberculosis or TB is an infectious disease caused by a bacteria called
Mycobacterium Tuberculosis. The bacteria can enter the body, usually the lungs, and
make a person sick by damaging the tissues that it reaches.

How do you get TB?

When a person with TB of the lungs coughs, shouts or sings, TB bacteria is

expelled into the air. The bacteria is carried within tiny, invisible droplets of moisture
that can float in the air for several hours. Any person who inhales these droplets can
become infected with TB. It does not matter if that person is rich or poor, educated
or illiterate, malnourished or obese. The person who breathes in the TB bacteria will
have TB infection.

TB is not caused by perspiration drying on one’s back, by over-exertion or

fatigue.

TB is not caused by smoking or pollution—although these clearly damage the

lungs.

TB is not caused by poor nutrition, - although this could make a person who
inhales a TB bacterium more likely to develop TB disease.

TB is not transmitted through food or drinks or using other utensils.

TB is acquired through exposure to someone sick with active TB of the

lungs.
What is TB infection?

If you have spent some time at home, in school, at work or elsewhere, with
someone who has active TB of the lungs, you may have unknowingly inhaled the TB
bacteria. If you have breathed in the TB germ, then you have been “infected” (you
have TB infection). This is different from TB disease. IN TB infection the TB bacilli do
not cause tissue damage. Unlike those with TB disease, persons with TB infection do
not have any symptoms. If their immune systems are normal, only one out of ten
persons with TB infection will later develop signs and symptoms of TB disease. The
other nine out of ten will have no manifestations of TB disease and will remain
healthy. If HIV infection, cancer, malnutrition, immunity-suppressing drugs or other
conditions have weakened their immune systems, the TB-infected persons will soon
develop active TB disease.

How do you know if you have TB infection?

If you have been in contact with someone diagnosed to have active

pulmonary TB, you can be tested for TB infection. The recommended test for TB
infection is the tuberculin skin test using the Mantoux method where the tuberculin
(or PDD) is injected into the skin. This is read after 48 to 72 hours. The skin tests
using the multiple-prong or prick devises are not recommended.

Your doctor must read the skin test and if this is found to be positive, he
must look for evidence of typical tissue damage caused by TB by ordering a chest x-
ray. If your tuberculin skin test is positive but you have no symptoms and your chest
x-ray is normal, then you have TB infection. If you have findings on chest x-ray
compatible with Tb and your skin test is positive, then you have TB disease
particularly if you have symptoms that suggest active pulmonary TB (see TB
disease).

Does TB infection have to be treated?

Not all persons with TB infection are given treatment by their physicians. Only
one out of ten persons with TB infection will eventually develop TB disease (become
sick with the symptoms of TB). Unfortunately it is impossible to identify which person
who becomes TB infected will be the one who later develops TB disease. But it is
possible to treat the person with TB infection with an anti-TB medication to eliminate
the changes of developing TB disease.

The medication used to treat infection (isoniazid or INH) can cause liver
toxicity particularly in older individuals. This must be weighed against the benefit of
treating TB infection (elimination of the 10% chance of developing TB disease).

Some individuals with TB infection may choose not to be treated. These

persons should be informed about the symptoms of TB disease and should be
instructed to visit physician for evaluation should they ever develop these symptoms.

What are the symptoms of TB disease?

• cough that does not go away for 3 weeks

 • coughing up blood
• prolonged fever
• night or afternoon sweats
• constant tiredness
• loss of weight and loss of appetite

Any person who develops these symptoms must be evaluated by their physician
for the possibility of TB disease.

What are the tests for TB disease?

1. Sputum examination for Acid-Fast Bacilli (AFB smear).

This is done by smearing a sample of coughed-up phlegm (sputum) on a glass
slide , treating this with special dyes and then examining the specimen under a
microscope. If TB bacilli are seen then the patient has active TB disease. It is
best to have three separate sputum specimens examined to increase the
likelihood of finding these bacilli. Unfortunately these Acid-Fast Bacilli are not
always seen on sputum examination even in persons with active lung TB.

2. Chest x-rays
This may be helpful in cases when the Acid-Fast Bacilli are not seen on sputum
examination. However, chest x-rays with findings suggestive of TB are not definitive
proof that the disease is really TB. There are other diseases that may mimic the
appearance of TB on chest x-rays. It also frequently difficult to judge if the lung
disease is active or not by chest x-ray.

3. TB culture of sputum or other specimen

This is done by growing the TB bacteria in the laboratory but this is expensive
and may require up to 8 weeks for final results.

What is the best way to prevent the spread of tuberculosis?

The best way to prevent the spread of tuberculosis is to treat and care all
patients with active pulmonary tuberculosis. The vaccination for TB known as BCG
may prevent children from developing the most severe forms of TB.

Malaria is a mosquito-borne infectious disease caused by a eukaryotic protist of the

genus Plasmodium. It is widespread in tropical and subtropical regions, including parts of
the Americas (22 countries), Asia, and Africa. Each year, there are approximately 350–
500 million cases of malaria,[1] killing between one and three million people, the majority
of whom are young children in sub-Saharan Africa.[2] Ninety percent of malaria-related
deaths occur in sub-Saharan Africa. Malaria is commonly associated with poverty, and
can indeed be a cause of poverty[3] and a major hindrance to economic development.

Five species of the plasmodium parasite can infect humans; the most serious forms of the
disease are caused by Plasmodium falciparum. Malaria caused by Plasmodium vivax,
Plasmodium ovale and Plasmodium malariae causes milder disease in humans that is not
generally fatal. A fifth species, Plasmodium knowlesi, is a zoonosis that causes malaria in
macaques but can also infect humans.[4][5]
Signs and symptoms

Typical fever patterns in Malaria.

Symptoms of malaria include fever, shivering, arthralgia (joint pain), vomiting, anemia
(caused by hemolysis), hemoglobinuria, retinal damage,[10] and convulsions. The classic
symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then
fever and sweating lasting four to six hours, occurring every two days in P. vivax and P.
ovale infections, while every three days for P. malariae.[11] P. falciparum can have
recurrent fever every 36–48 hours or a less pronounced and almost continuous fever. For
reasons that are poorly understood, but that may be related to high intracranial pressure,
children with malaria frequently exhibit abnormal posturing, a sign indicating severe
brain damage.[12] Malaria has been found to cause cognitive impairments, especially in
children. It causes widespread anemia during a period of rapid brain development and
also direct brain damage. This neurologic damage results from cerebral malaria to which
children are more vulnerable.[13][14] Cerebral malaria is associated with retinal whitening,
[15]
which may be a useful clinical sign in distinguishing malaria from other causes of
fever.[16]

Causes
Malaria parasites

Malaria parasites are members of the genus Plasmodium (phylum Apicomplexa). In

humans malaria is caused by P. falciparum, P. malariae, P. ovale, P. vivax and P.
knowlesi.[22][23] P. falciparum is the most common cause of infection and is responsible for
about 80% of all malaria cases, and is also responsible for about 90% of the deaths from
malaria.[24] Parasitic Plasmodium species also infect birds, reptiles, monkeys,
chimpanzees and rodents.[25] There have been documented human infections with several
simian species of malaria, namely P. knowlesi, P. inui, P. cynomolgi,[26] P. simiovale, P.
brazilianum, P. schwetzi and P. simium; however, with the exception of P. knowlesi,
these are mostly of limited public health importance.[27]

Malaria parasites contain apicoplasts, an organelle usually found in plants, complete with
their own functioning genomes. These apicoplast are thought to have originated through
the endosymbiosis of algae[28] and play a crucial role in various aspects of parasite
metabolism e.g. fatty acid bio-synthesis.[29] To date, 466 proteins have been found to be
produced by apicoplasts[30] and these are now being looked at as possible targets for novel
anti-malarial drugs.