medical microbiology

2010-03-14T22:09:00.000-07:00

Plants That Will Get Rid Of Mosquitoes
There are several plants you can plant in your yard or garden to get rid of mosquitoes. And these plants work very well.
1. Catnip
2. Rosemary
3. Marigolds
4. Citronella Grass also known as lemon grass.
5. Lemon Thyme
All of these plants will work very well to keep away mosquitoes. If you plant a combination of them you should not have any mosquito problems at all. Marigolds will also keep other insect pests out of your yard and garden.
Herbs 101
To get rid of flying insects including mosquitoes plant basil in pots on your porch and in your yard and garden. Most flying insects can not stand basil in any way. It will keep them completly away.
A Grass That Repels Mosquitoes
A very effective substance that repels mosquitoes is citronellla. Citronella can be found in lemon grass and in the natural oil found in the lemon grass it is much stronger than a store bought product. It is also called Thai Grass and should be available in your local garden supply store. It will mosquito proof your yard and garden.
Is A Bat House In Your Future
A small colony of bats will eat thousands of mosquitoes every night.
Get Bats In Your Belfry
If you don't have bats in your neighborhood you might consider purchasing a bat house. Most garden supply stores sell bat houses for about $25.00. Once the bats move in this will eliminate thousands of unwanted mosquitoes every night. Bats will not bother humans however, if you have a pool or birdbath they will swoop in for a drink every now and then.
The Mosquito Hunters
Toads Love To Eat Mosquitoes. So be sure to make any toads in your yard or garden welcome.
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Both toads and bats eat thousands of mosquitos a night. If you live in a area where toads occur and you want them in your yard build them a few toad houses. They love to live in clay flower pots so place a clay flower pot upside down and cut Mr Toad a hole near the top which is now the bottom and Mr Toad will move right in. Place your toad houses where they will not be disturbed. They love the cool dark toad house the clay flower pot provides to get away from the heat of the day.
Add small goldfish to your outdoor pool to take care of the mosquito larvae in it. Depending on how many gold fish you put in the pond you may never need to feed them. If you do need to feed them only feed them lightly so they will stay hungry for the mosquito larvae.
Biology of mosquito
Characteristics of mosquito:
· slender and long mouth parts
· scaly wings
· complete head for larvae
· a pair of spiracles on the dorsal part of the 8th abdominal segment of the larvae
Life cycle: complete metamorphosis with 4 stages (egg, larva, pupa and adult)
Egg:
· Adult mosquito generally lays eggs on water surface or its adjacent sites
· Development of eggs takes 2 to 3 days
Larva:
· Aquatic animal without leg
· With four stages of development
· Comes up to the water surface to take atmospheric air with its spiracle at the 8th segment
Pupa:
· Non-feeding aquatic form
· Has to come up to the water surface to breathe usually
· Life span is 2 to 3 days
Adult:
· Body can be divided as head, thorax and abdomen
· A pair of compound eyes and antennae as well as mouthparts on its head
· A pair of jointed legs on each segment of the thorax and a pair of wings
· The abdomen is composed of ten segments
Behaviour :
Mating: Female mosquito of many species mate 1 to 2 days after hatching. Female adults normally mate only once in its life.
Feeding: Normally only female adults feed on animal blood. Male adults feed on plant juice. Some species are anthropophilic and some are zoophilic.
Egg laying: Female mosquito of most species has to get blood meal for the development of eggs. Breeding place can be permanent stagnant water, flowing water, temporary stagnant water or containers.
Resting: Adult mosquito rests near breeding site for a few hours after hatching. Exophilic mosquito also rests indoors for a short period of time before and after feeding.
Dispersion: Adult mosquito disperses for feeding, finding suitable resting sites, mating and laying eggs. It can disperse through flight, air current or vehicles.
Hibernation: Some mosquitoes (for example most species of Anopheles and Culex) hibernate in winter at adult stage. Aedes over winter at egg stage.
Longevity: Generally male mosquitoes only survive one week but the females can live for two to three weeks.

Mosquito prevention
o Advice
o To the public
The public is advised:
§ To tidy up their premises and check for any accumulation of water inside their premises;
§ To remove all unnecessary water collection and eliminate the sources;
§ To change at least every week the water in flower vases and saucers of potted plants to prevent breeding of mosquitoes. The use of saucers should be avoided whenever possible;
§ To properly cover all containers that hold water to prevent mosquito from accessing the water;
§ To properly dispose articles that are able to contain water such as empty lunch boxes, cans and tyres;
§ To stop storing water along morning walk trails or Government land for irrigation;
§ To make large holes on tyres used as anti-bumping measure in garage to prevent water trapping or use mark(s) on the parking space to prevent bumping instead.
§ To contact the district pest control offices or PCAS of FEHD, or pest control companies for assistance in mosquito control or prevention.
§ To install mosquito screen on windows and doors.
§ To use mosquito net for sleeping if necessary.
§ To apply insect repellant on the clothes.
§ To wear light-coloured long-sleeved clothes and long trousers.
§ To avoid applying odour-producing cosmetics such as perfume/body lotion during outdoor activities.
To the management of construction sites
The management of construction sites is advised:
§ To assign a staff for the control and prevention of mosquito in the site;
§ To tidy up the construction site regularly, at least weekly and check for any accumulation of water inside the site;
§ To remove all unnecessary water collection and eliminate the source(s);
§ To cover all containers that hold water to prevent mosquito from accessing the water;
§ To render the vertical poles in scaffolding unable to hold water by making holes at the ends or filling them up with sand;
§ To dispose articles that are able to contain water such as empty lunch boxes, cans, disused articles and tyres into covered container(s) and remove these articles from the site regularly, at least weekly;
§ To carry out larviciding against mosquito breeding where the breeding sources or potential breeding grounds are inaccessible or could not be eliminated.
§ To contact the district pest control offices or PCAS of FEHD, or pest control companies for assistance in mosquito control or prevention.
Mosquito control
Adult Control
· to use mosquito trap for trapping the mosquito
· to use mosquito coil or aerosol to kill the mosquito directly
· to kill mosquito with electrical device designed for the purpose (Observe the safety precautions in using the device)
Larval Control
· to remove containers with water
· to clear stagnant water
· to pave/fill uneven ground and/or holes
· to apply larvicidal oil or pesticide to kill the larvae
· to keep fish which feeds on mosquito larvae
Figures

Anopheles species
Aedes species
Culex species
Fig. 1 Egg of different mosquito species

Culicines species
Anophelines species
Fig. 2 Posture of mosquito larva of different species in breathing

Fig. 3 A mosquito pupa

Fig. 4 Adult mosquito

What Is a Vaccine?

2009-06-24T07:59:00.000-07:00

Chances are you never had diphtheria. You probably don’t know anyone who has suffered from this disease, either. In fact, you may not know what diphtheria is. Similarly, diseases like whooping cough (pertussis), measles, mumps, and German measles (rubella) may be unfamiliar to you. In the 19th and early 20th centuries, these illnesses struck hundreds of thousands of people in India each year, mostly children, and tens of thousands of people died. The names of these diseases were frightening household words. Today, they are all but forgotten. That change happened largely because of vaccines.
Chances are you’ve been vaccinated against diphtheria. You may even have been exposed to the bacterium that causes it, but the vaccine prepared your body to fight off the disease so quickly that you were unaware of the infection. Vaccines take advantage of your body’s natural ability to learn how to combat many disease-causing germs, or microbes, that attack it. What’s more, your body “remembers” how to protect itself from the microbes it has encountered before. Collectively, the parts of your body that remember and repel microbes are called the immune system. Without the immune system, the simplest illness—even the common cold—could quickly turn deadly.
On average, your immune system takes more than a week to learn how to fight off an unfamiliar microbe. Sometimes that isn’t soon enough. Stronger microbes can spread through your body faster than the immune system can fend them off. Your body often gains the upper hand after a few weeks, but in the meantime you are sick. Certain microbes are so powerful, or virulent, that they can overwhelm or escape your body’s natural defenses. In those situations, vaccines can make all the difference.
Traditional vaccines contain either parts of microbes or whole microbes that have been killed or weakened so that they don’t cause disease. When your immune system confronts these harmless versions of the germs, it quickly clears them from your body. In other words, vaccines trick your immune system to teach your body important lessons about how to defeat its opponents.
Vaccine Benefits
Once your immune system is trained to resist a disease, you are said to be immune to it. Before vaccines, the only way to become immune to a disease was to actually get it and, with luck, survive it. This is called naturally acquired immunity. With naturally acquired immunity, you suffer the symptoms of the disease and also risk the complications, which can be quite serious or even deadly. In addition, during certain stages of the illness, you may be contagious and pass the disease to family members, friends, or others who come into contact with you.
Vaccines, which provide artificially acquired immunity, are an easier and less risky way to become immune. Vaccines can prevent a disease from occurring in the first place, rather than attempt to cure it after the fact.
Benefits for You and Others
It is also much cheaper to prevent a disease than to treat it. Vaccines protect not only yourself but also others around you. If your vaccine-primed immune system stops an illness before it starts, you will be contagious for a much shorter period of time, or perhaps not at all. Similarly, when other people are vaccinated, they are less likely to give the disease to you. Vaccines protect not only individuals but entire communities. That is why vaccines are vital to the public health goal of preventing diseases.
If a critical number of people within a community are vaccinated against a particular illness, the entire group becomes less likely to get the disease. This protection is called community, or herd, immunity. On the other hand, if too many people in a community do not get vaccinations, diseases can reappear. In 1989, low vaccination rates allowed a measles outbreak to occur in the United States. The outbreak resulted in more than 55,000 cases of measles and 136 measles-associated deaths.

2008-12-29T18:03:00.000-08:00

wishing a happy new year to all readers

2008-12-17T19:47:00.000-08:00

TICKS

Ticks are found worldwide. They are blood-sucking, opportunistic parasites that can attach to the skin of a variety of vertebrate hosts. They have no segmentation and are dorsoventrally flat with four pairs of legs .

Although all stages of the tick life cycle can suck blood, it is normally the adult tick that poses a problem for humans. Human tick-associated diseases are most common in the summer months when the likelihood of contact increases during outdoor activities, usually in wooded areas. Being bitten by a tick is often painless and the presence of the tick may not be detected for some time. Often the tick poses no problem for the human host other than an erythromatous papule and it drops off after engorging on blood. Sometimes, the site of attachment may itch and become painful. Secondary infections of the wound site may occur, often as a result of the mouthparts remaining attached after the tick is removed.

Ticks can attach anywhere on the body but are frequently found at the hairline, around the ears, groin, armpits etc.
Whilst the bites of most ticks are inconsequential, they can carry a number of human disease agents including viruses, bacteria and protozoa. There are two families of ticks: the hard ticks (Ixodidae) and the soft ticks (Argasidae) .The Ixodidae attach to their host over a prolonged period of time (several days) while the Argasidae feed rapidly and then drop off. Consequently, they are frequently undetected.
Although most tick-associated problems arise from disease-causing organisms carried by the ticks, in one case – tick paralysis – the problem arises directly from toxins in the tick’s saliva.
Important disease-carrying ticks in the United States are:
Hard ticks:
Dog tick (Dermacentor variabilis) which is found east of the Rocky Mountains and in some areas of the Pacific coast states
Rocky Mountain Wood Tick (Dermacentor andersoni) . As its name suggests, it is found in the Rocky Mountains and also in southwest Canada
Deer Tick (Black-legged tick) (Ixodes scapularis) . This occurs in the north east and north central United States.
Western black legged tick (Ixodes pacificus) which is found in the Pacific coast states of the United States.
Brown dog tick (Rhipicephalus sanuguineus). Also known as the red dog tick . This is found world-wide (all over the US and also southeast Canada) and can complete its entire life cycle indoors. It primarily infests dogs but can feed on other mammals including man.
Lone star tick (Amblyomma americanum) , found in south eastern and south central United States.
Soft ticks:
Various species of Ornithodoros are found in the western United States. The family Argasidae is divided into four genera: Argas, Ornithodoros, Antricola, and Otobius .

DISEASES FOR WHICH HARD TICKS ARE CARRIERS
BACTERIAL DISEASES
ROCKY MOUNTAIN SPOTTED FEVER
There are several hundred reported cases of Rocky Mountain Spotted Fever each year in the United States (ranging, during the past half century, from a low of about 200 to more than 1200 in the early 1980’s). The numbers are again rising (figure 4). Most at risk are children under 15 years of age. Usually, cases occur in the summer because of higher numbers of ticks and more frequent contact of humans with ticks .
EpidemiologyThe causative agent, Ricketsia rickettsii, is carried by the Brown Dog tick and the Rocky Mountain Wood Tick (the two Dermacentor species in the United States). Contrary to its name, only a small proportion of cases are actually reported from the Rocky Mountain states. The highest number of cases in the United States occurs in the south-east and south central regions with the greatest incidence in Oklahoma and North Carolina.
Elsewhere in central and south America, Rhipicephalus sanguineus and Amblyomma cajennense carry Ricketsia rickettsii. The disease is known as fiebre manchada in Mexico; São Paulo fever or fiebre maculosa in Brazil; tick typhus or Tobia fever in Colombia.
SymptomsR. rickettsii is a small bacterium that grows inside cells, particularly endothelial cells that form the walls of small blood vessels . The disease is characterized by nausea, appetite-loss, fever, myalgia and headache. These are followed, 3 to 5 days after the tick bite, by the characteristic rash , which results from leakage of the blood vessels as a result of infected and dying endothelial cells.
Initially, the rash is formed of small, flat, pink, non-itchy macules (spots) on the wrists, forearms, and ankles . Subsequently, the macules become raised on the skin and there is pain (in the abdomen and joints) and diarrhea. The characteristic red rash, which occurs in up to 60% of patients, is found at the extremities (the palms and soles of feet). A minority of patients never progress to this stage. Laboratory tests show thrombocytopenia, hyponatremia and/or elevated levels of liver enzymes. Severe cases require hospitalization and can result in paralysis of the extremities and may even be life-threatening. Very severe sequelae include gangrene that may result in amputation, deafness, and incontinence.
TreatmentTreatment is by antibiotics (doxycycline). Since, if untreated, Rocky Mountain Spotted Fever can be fatal, treatment should be started as soon as this disease is suspected and before any diagnosis is confirmed by laboratory tests.
Laboratory detectionSerologic assays including indirect immunofluorescence microscopy.
PreventionClothes that cover body and anti-tick sprays (often containing DEET) are most often used. It is best to keep away from heavily tick-infested areas. If ticks are discovered on the body, they should be removed immediately using fingers or tweezers.

TULAREMIA

This is also carried by the two Dermacentor species. Tularemia is caused by the bacterium Francisella tularensis, which is carried by rodents, rabbits and hares; as a result tularemia is otherwise known as rabbit fever. One of the several ways that humans can be infected is by being bitten by a tick that has acquired the bacterium after biting one of these animals; however, it can also be inhaled during the handling of infected rodents. There have been no reports to person-to-person transmission. Francisella tularensis is very infectious. Tularemia occurs all across the continental United States but is relatively rare, with about 200 cases being reported each year .
SymptomsThe symptoms of tularemia, which can be fatal if untreated, vary according to the route by which the infection was acquired; often the patient experiences swollen lymph glands, skin ulcers , inflammation of the eyes and throat, diarrhea. This may be followed by atypical pneumonia, pleuritis, and hilar lymphadenopathy. Inhaled tularemia results in rapid fever, chills, headache, myalgia, joint pain, dry cough, and progressive weakness. The pneumonia can result in respiratory distress and failure with blood in the sputum.
Diagnosis is initially from the symptoms but confirmatory laboratory tests using Gram or other stains or immunofluorescence microscopy are used to visualize the infecting bacteria.
TreatmentOral antibitotc treatment using streptomycin, gentamycin, tetracyclines (e.g. doxycycline) or fluoroquinolones, (e.g. ciprofloxacin) is the major form of therapy. Streptomycin or gentamicin can be used intravenously. There is a vaccine that is made from avirulent F. tularensis biovar palaearctica (type B). In addition, antibiotics can be used as post-exposure prophylaxis before the onset of symptoms if infection by F. tularensis is suspected.

Q FEVER

Various farm animals (cattle sheep goats etc) are the primary carriers of the bacterium Coxiella burnetii which causes Q fever. Spread to humans is usually via inhalation of dust containing dried urine, feces etc of infected animals. However, less commonly, the bacterium can be transmitted via the bite of Dermacentor ticks. Ingestion of contaminated milk can also lead to infection. C. burnetii infects macrophages and survives in the phagolysosome, where the bacteria multiply. The bacteria are released by lysis of the cells and phagolysosomes.SymptomsAcute Q feverMany patients, about half, show no signs of infection but in others after an incubation period of 1 - 2 weeks, there is a sudden onset of fever, headache, general malaise, myalgia, sore throat, chills, sweats, non-productive cough, nausea, vomiting, diarrhea, abdominal pain, and chest pain. The patient may also appear confused. Many patients go on to the symptoms of pneumonia and hepatitis but most recover in a month or two without treatment although acute Q fever has a mortality rate of 1-2%.
Chronic Q feverIf the patient fails to resolve the infection, chronic Q fever results. This can occur a few months after primary infection but can also occur many years later. Endocarditis of the aortic heart valves is the major problem that arises. This usually occurs in people with heart valve disease but also at risk are transplant, cancer and kidney disease patients. The chronic form of Q fever has a fatality rate of about 60 - 70%.
DiagnosisSerology to determine the presence of antibodies against Coxiella burnetii is used.
TreatmentAntibiotics such as doxycyline are used to treat acute Q fever. For chronic Q fever, two protocols have been investigated: doxycycline along with quinolones for at least 4 years and doxycycline with hydroxychloroquine for 1.5 to 3 years.
There is a vaccine used in Australia for persons who may come in contact with C. burnettii but it is not commercially available in the United States.

EHRLICHOSIS
HUMAN EHRLICHOSIS

Human ehrlichosis is carried by Dermacentor variabilis and by Amblyomma americanum and is caused by a number of bacteria of the Ehrlichia family, in the United States principally by Ehrlichia chaffeensis. These bacteria are small gram-negative organisms that infect leukocytes . As with many tick-borne diseases, incidence follows vector distribution with higher incidence during the summer months when tick populations and contact with them are higher. The number of cases has been increasing .
SymptomsAfter an incubation of period of a week to 10 days, the patient presents with myalgia, headache and general malaise. There can also be nausea, vomiting, diarrhea, cough, joint pains and the patient may be confused. Sometimes, there is a rash but this is normally only in pediatric cases. If left untreated, more severe manifestations of the infection can occur, including prolonged fever, renal failure, disseminated intravascular coagulopathy, meningoencephalitis, adult respiratory distress syndrome, seizures, or coma. Mortality rate at this stage is 2 - 3%. More at risk are immune-suppressed patients.
DiagnosisMicroscopy using blood smears or serology to detect anti-Ehrlichia antibodies can be used.
TreatmentAntibiotics such as doxycycline are the recommended treatment.

HUMAN GRANULOCYTIC EHRLICHIOSIS
Human granulocytic ehrlichiosis is caused by a species of Ehrlichia similar to species found in animals (Ehrlichia equi and Ehrlichia phagocytophila) and is transmitted by blacklegged ticks (Ixodes scapularis) and western blacklegged ticks (Ixodes pacificus).

LYME DISEASE

Lyme disease is caused by the spirochete bacterium, Borrelia burgdorferi , which typically infects small mammals in the northeast and north central United States. It is transmitted to humans by Ixodid black legged ticks (deer ticks). There are over 20,000 cases per year in the United States making it the most common tick-borne disease in North America. The disease was first described from the town of Old Lyme in Connecticut but is found on both the east and west coasts and in the Mississippi valley . In Europe, a similar disease is caused by Borrelia garinii or Borrelia afzelii.
Symptoms
Fever, headache and malaise and a characteristic rash named erythemia migrans , which can occur in a few days but sometimes only after a few weeks, are typical of Lyme Disease. The rash (which is usually not painful) often has a bull’s eye appearance since as it grows (up to 30 cm across) the central region clears. If left untreated, the infection spreads and can result in Bell’s Palsy (partial paralysis of muscles in one or both sides of the face), meningitis, heart palpitations and severe joint pain. These symptoms usually resolve in a few weeks but after several months about 60% of patients will get severe joint swelling and arthritis. A small minority may also get neurologic symptoms (tingling of the extremities, shooting pains, numbness)
TreatmentEarly administration with antibiotics (doxycycline, amoxicillin, or cefuroxime axetil) is recommended. Some patients continue with neurological and muscle pain problems even after antibiotic treatment. It is not known what causes these but they may be autoimmune in nature.
DiagnosisVarious laboratory tests include Elisa, western blot

SOUTHERN TICK-ASSOCIATED RASH ILLNESS
This rash is similar to that seen in Lyme disease. The causative organism is not known but it is not Borrelia burgdorferi, the Lyme disease agent. The lone star tick, Amblyomma americanum, is the transmission vector.
SymptomsMalaise, fever, myalgia, arthralgia and a “bulls eye” rash at the site of the tick bite. There are no chronic neurological symptoms as are seen with Lyme disease

TreatmentThe usual oral antibiotics are used and the symptoms quickly resolve.

PROTOZOA
BABESIOSIS
Babesiosis is carried by species of Ixodes including the deer tick (Ixodes scapularis) in the north and mid-west of the United States and in other countries, including Europe. Babesia microti is the usual causative organism and is a hemoprotozoan (i.e. it circulates in the bloodstream). Normally, the two hosts of Babesia microti are ticks and peromyscus mice (Peromyscus leucopus). The tick infects the mice with sporozoites, which reproduce asexually in erythrocytes. These escape to the blood stream where they may form male and female gametes that are taken up by the tick during a blood meal. In the tick, the gametes fuse and go through a sporogonic cycle to form more sporozoites. Humans can also acquire sporozoites when bitten by an infected tick and are usually dead-end hosts but babesiosis has been transmitted to other humans via blood transfusions .
In most cases, infection is asymptomatic but after a week to a month, symptoms can appear. These include fever, chills, sweating, myalgias and fatigue. In severe cases, hepatosplenomegaly and hemolytic anemia can occur. Normally, the patient recovers, although severe cases occur in immuno-compromised patients and the elderly.
Disease cause by another protozoan, Babesia divergens, can cause more severe and sometimes fatal cases of babesiosis.
DiagnosisDiagnosis is by serology, immunofluorescence microscopy and by direct observation of the parasite in blood smears in which “Maltese Cross”-like inclusions in erythrocytes are seen . These consist of four budding merozoites attached together.

TreatmentUsual antibiotics used are clindamycin plus quinine or atovaquone plus azithromycin.

VIRUSES
CRIMEAN-CONGO HEMORRHAGIC FEVER
This is caused by a Nairovirus, a member of the Bunyaviridae. It is found in Eastern Europe and throughout the Mediterranean areas of southern Europe, the Middle East, Africa, northwestern China, central and south Asia. Ixorid ticks (genus Hyalomma) spread the virus, which is also carried by numerous species of domestic and wild animals. Person to person transmission through infected blood and other body fluids has been documented.
SymptomsInitially, the patient presents with headache, high fever, back pain, joint pain, stomach pain, and vomiting. There may be flushing, red eyes and throat and small red spots called petechiae on the palate. Hemorrhage ensues after a few days and lasts for a few weeks. this is indicated by severe bruising, nosebleeds, and failure to stop bleedings after a cut or injection. Slow recovery often ensues but mortality can be as high as 50%.

TreatmentSince this is a viral disease, treatment is largely supportive with particular attention to electrolyte balance. Ribavirin has been used. An inactivated vaccine has been used in Eastern Europe.

COLORADO TICK FEVER
This is sometimes confused with a mild case of Rocky Mountain Spotted Fever but Colorado Tick Fever is caused by a coltivirus, a member of the reoviruses. They are endemic to north western North America and are found in Ixodid ticks. The virus distribution closely matches that of its vector, Dermacentor andersoni.
Person-to-person transmission can occur by blood. Prolonged viremia observed in humans and rodents is due to the intraerythrocytic location of virions, which protects them from immune clearance.
SymptomsInfection results in abrupt fever, chills, headache, retro-orbital pain, photophobia, myalgia, abdominal pain, and malaise. Sometimes fever can be diphasic or triphasic, usually lasting for 5 to 10 days. Severe forms of the disease that involve infection of the central nervous system or hemorrhagic fever, pericarditis, myocarditis, and orchitis have been rarely observed, mainly in children. Severity is sufficient to result in hospitalization of approximately 20% of patients. There has been evidence of transmission from mother to child.

FAR EASTERN TICK-BORNE ENCEPHALITIS (Also known as Russian spring-summer encephalitis or Taiga encephalitis)This is caused by a flavivirus which is spread by ixodid ticks (Ixodes persulcatus, I. ricinus and I. cookie). Small animals are the reservoir and the virus is endemic to the former Soviet Union and parts of eastern and central Europe.

SymptomsAbout two weeks after infection, there is a mild influenza-like disease that normally resolves in a few days but which can be followed by meningitis and meningoencephalitis in about one third of cases. In some cases, there may be partial paralysis and mortality may be as high as 25%.

TreatmentSupportive care is normal. There is a vaccine of killed virus that is available in Europe.

POWASSAN ENCEPHALITIS
This is a rare disease caused by a flavivirus carried by Ixodid ticks. There has been less than one case per year reported in the United States but mortality is high. It is widespread in North America and is found in small animal populations including woodchucks.
SymptomsAfter a relatively long incubation period of up to one month, the patient may present with a sore throat, dizziness, headache and confusion. This can proceed to general malaise, vomiting, respiratory distress, fever and convulsions, which then lead to paralysis and possibly coma. Because the virus attacks brain tissue, survivors can have severe neurological problems.
TreatmentSupportive care is indicated.

TICK-BORNE ENCEPHALITIS (Also known as biphasic meningoencephalitis, central European tick-borne encephalitis, Czechoslovak tick-borne encephalitis, diphasic milk fever or viral meningoencephalitis)
This disease results from infection by tick-borne encephalitis virus, which is a member of the Flaviviridae.
SymptomsTick-borne encephalitis starts as mild influenza-like symptoms with fever accompanied by leuko- and thrombocytopenia. This resolves within a few days. However, about one third of patients develop meningitis and meningoencephalitis. This can, in a few cases, be followed by paralysis. The European form of the disease has a mortality rate of under 5%. Most patients recover but about a third may have long-lasting neurological problems.
TreatmentSupportive is indicated. There is an experimental killed vaccine in Europe. In Sweden TBE vaccination is recommended for residents of and regular visitors to TBE endemic areas.
KYASANUR FOREST DISEASE
This disease is similar to Russian spring-summer encephalitis and is also caused by flaviviruses. It is found only in the Kyasanur forest of Northern India. The disease occurs during the dry season as its tick vector (Haemaphyalis spinigera) begins to feed on humans. Local carriers are shrews and monkeys.
LOUPING ILL VIRUS
This is found in the British Isles and is caused by a flavivirus that is carried by pheasants and sheep, among other animals. It can infect many hosts via the tick vector, Ixodes ricinus. It causes mild encephalitis that gives the infected animal an unusual gait (hence its name). However, it can kill livestock and humans not given proper supportive care.

DISEASE CAUSED DIRECTLY BY HARD TICKS
TICK PARALYSIS
In addition to being carriers of disease-causing microorganisms, some ticks (Amblyomma americanum and the two Dermacentor species) can cause tick paralysis. This is a rare disease caused by toxin in the saliva of the tick and results in an acute, ascending, flaccid paralysis caused by reduced acetyl choline or motor neuron action potentials. The paralysis, which is not associated with pain, starts a few days after the bite and comes on gradually over a period of days. The paralysis resolves surprisingly rapidly, usually within a day of the removal of the tick but if the tick is not removed the mortality rate, as a result of respiratory paralysis, can be as high as 10%. Tick paralysis can be confused with other acute neurologic disorders or diseases (e.g., Guillain-Barré syndrome or botulism).

DISEASE FOR WHICH SOFT TICKS ARE CARRIERS
BACTERIA
TICK-BORNE RELAPSING FEVER
Tick-borne relapsing fever is a rare disease (about 25 cases per year in the United States) and is caused by several spirochete bacterial species of the Borelia family. The transmission agents are soft ticks of the genus Ornithodoros. Soft ticks (family Argasidae) differ in many ways from the so-called hard ticks (family Ixodidae), but the most important is that they take brief meals from their host and then drop off. The bite is usually painless. Thus, they are far less likely to be found than the hard ticks that stay attached while feeding for hours. In the wild, these ticks are found in nesting materials when not feeding on their animal host. All stages of the life cycle can take blood meals.
The individual Borrelia species that cause tick-borne relapsing fever are usually associated with specific Ornithodoros tick vectors. B. hermsii is transmitted to humans by Ornithodoros hermsi, B. parkerii is transmitted by Ornithodoros parkeri and B. turicatae is transmitted by Ornithodoros turicata. Each tick is associated with a preferred environment and hosts. Ornithodoros hermsi is found at higher altitudes (1500 – 8000 feet) where it is associated usually with ground squirrels, tree squirrels and chipmunks. Ornithodoros parkeri occurs at lower elevations and inhabit caves and the burrows of ground squirrels, prairie dogs and burrowing owls. Ornithodoros turicata occurs in caves and ground squirrel, prairie dog or burrowing owls burrows in the plains regions of the Southwest United States.
SymptomsInitially, the patient experiences arthralgia, myalgia, headache, chills and fever. This is followed by nausea, cough, photophobia, and dizziness. The patient may be confused. There is often a rash. The incubation period before the onset of the first symptoms is about a week (though it can be shorter or longer). After the onset of disease, symptoms last a few days and then resolve. After a week or two, the symptoms reoccur and in the absence of treatment, recurrence continues for several more episodes. As the fever resolves, the patient may go through a crisis in which first there is a high fever accompanied by confusion and delirium. This “chill phase” lasts up to half an hour. Then there is the “flush phase” in which the temperature drops accompanied by profuse sweating and sometimes a drop in blood pressure.
DiagnosisMicroscope smears of blood, bone marrow or cerebrospinal fluid stained with Giemsa or acridine orange. Serologic testing is also available.
TreatmentAntibiotics are used and symptoms resolve a few days. There can, however, be long-term sequelae including heart and kidney problems, peripheral nerve involvement, ophthalmia, and abortion. Without treatment mortality may be up to 10% of patients.

CHIKUNGUNYA VIRUS IN INDIA

2008-10-21T00:21:00.000-07:00

CHIKUNGUNYA VIRUS IN INDIA

Chikungunya is a relatively rare form of viral fever caused by an alpha virus (RNA Virus) that is spread by the bite of an infected Aedes aegypti mosquito. The virus is classified under arboviruses which are transmitted by arthropod vectors.

The name is derived from the Makonde word meaning “ that which bends up” in reference to the stooped posture developed as a result of the arthritic symptoms of the disease. The disease was first described in 1952 following an outbreak on the Makonde plateau along the border between Tanganyika and Mozambique.

Chikungunya virus was first isolated from Indian subcontinent in 1963 from Calcutta, since then there have been several reports of Chikungunya virus infection in different parts of India. The last outbreak of Chikungunya virus infection occurred in India in 1971. subsequently the virus had ‘disappreared’ from the subcontinent. However, recent reports of large scale outbreak of fever caused by Chikungunya virus infection in several parts of South India have confirmed the reemergence of this virus.

The symptoms of this infection include abrupt onset of fever, chills, headache and severe joint pain with or without swelling (usually the smaller joints), low back pain and rash. The symptoms are most often clinically indistinguishable from those observed in dengue fever. Therefore it is very important to clinically distinguish Dengue from Chikungunya virus infection. Unlike Dengue Hemorrhagic manifestations are relatively rare and as a rule shock is not observed in Chikungunya virus infection. Most often Chikungunya is a self limiting febrile illness. However, neurological complications such as meningoencephalitis and mother to child transmission has been observed.

The precise reasons for the reemergence of Chikungunya in the Indian subcontinent in not known. Although it is well recognized that reemergence of viral infection are due to a variety of social, environmental, behavioral and biological changes. The challenge faced during this large outbreak in the country has been the lack of rapid diagnostic facilities. Although, the National Institute of Virology at Pune, has been a great help in determining the etiology of the outbreak, relying on one institute in the country to render diagnostic help for case management would be a foolish task. It would be therefore desirable to ensure that several virology laboratories in the country are enrolled and networked to deliver rapid diagnosis in large outbreak such as this as well other emerging viral infections like Chandipura and Avian Influenza.

PRINCE.C.P
Lecturer in Microbiology

GLOBAL WARMING

2008-10-14T09:19:00.000-07:00

WHAT IS GLOBAL WARMING?
Carbon dioxide and other gases warm the surface of the planet naturally by trapping solar heat in the atmosphere. This is a good thing because it keeps our planet habitable. However, by burning fossil fuels such as coal, gas and oil and clearing forests we have dramatically increased the amount of carbon dioxide in the Earth’s atmosphere and temperatures are rising.
The vast majority of scientists agree that global warming is real, it’s already happening and that it is the result of our activities and not a natural occurrence. The evidence is overwhelming and undeniable.
We’re already seeing changes. Glaciers are melting, plants and animals are being forced from their habitat, and the number of severe storms and droughts is increasing.
The number of Category 4 and 5 hurricanes has almost doubled in the last 30 years.
Malaria has spread to higher altitudes in places like the Colombian Andes, 7,000 feet above sea level.
The flow of ice from glaciers in Greenland has more than doubled over the past decade.
At least 279 species of plants and animals are already responding to global warming, moving closer to the poles.
If the warming continues, we can expect catastrophic consequences.
Deaths from global warming will double in just 25 years -- to 300,000 people a year.
Global sea levels could rise by more than 20 feet with the loss of shelf ice in Greenland and Antarctica, devastating coastal areas worldwide.
Heat waves will be more frequent and more intense.
Droughts and wildfires will occur more often.
The Arctic Ocean could be ice free in summer by 2050.
More than a million species worldwide could be driven to extinction by 2050.
There is no doubt we can solve this problem. In fact, we have a moral obligation to do so. Small changes to your daily routine can add up to big differences in helping to stop global warming. The time to come together to solve this problem is now – TAKE ACTION

malayalam kavitha

2008-10-02T10:25:00.000-07:00

കക്കൊസില് തൂറാം

പട്ടരുകുട്ടി തൂറാന്‍ പോയി
കുണ്ടിയിന്മേല്‍ തേള്‍ കുത്തി
പട്ടരുകുട്ടി കരഞ്ഞു പോയി
പാവം പാവം പട്ടരുകുട്ടി .

prion diseases

2008-10-02T10:00:00.000-07:00

This video will help you to have an idea about prion diseases.watch it !

Entamoeba histolytica

2008-10-01T20:53:00.000-07:00

Several protozoan species in the genus Entamoeba infect humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba, associated with intestinal and extra intestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.
Life Cycle:
Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ( : noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ( : intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ( : extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).
Geographic Distribution:Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.
Clinical Features:A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions).
Laboratory Diagnosis:Entamoeba histolytica must be differentiated from other intestinal protozoa including: E. coli, E. hartmanni, E. gingivalis, Endolimax nana, and Iodamoeba buetschlii (the nonpathogenic amebas); Dientamoeba fragilis (which is a flagellate not an ameba); and the possibly pathogenic Entamoeba polecki. Differentiation is possible, but not always easy, based on morphologic characteristics of the cysts and trophozoites. The nonpathogenic Entamoeba dispar, however, is morphologically identical to E. histolytica, and differentiation must be based on isoenzymatic or immunologic analysis. Molecular methods are also useful in distinguishing between E. histolytica and E. dispar and can also be used to identify E. polecki. Microscopic identification of cysts and trophozoites in the stool is the common method for diagnosing E. histolytica. This can be accomplished using:
§ Fresh stool: wet mounts and permanently stained preparations (e.g., trichrome).
§ Concentrates from fresh stool: wet mounts, with or without iodine stain, and permanently stained preparations (e.g., trichrome). Concentration procedures, however, are not useful for demonstrating trophozoites.
In addition, E. histolytica trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
Diagnostic findings:
§ Microscopy
§ Immunodiagnosis
§ Molecular methods for discriminating between E. histolytica and E. dispar
§ Morphologic comparison with other intestinal parasites
§ Bench aid for E. histolytica

Treatment:For asymptomatic infections, iodoquinol, paromomycin, or diloxanide furoate (not commercially available in the U.S.) are the drugs of choice. For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess), the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanide furoate

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EMERGING AND RE-EMERGING INFECTIOUS DISEASES

2008-09-01T10:18:00.000-07:00

Emerging infectious diseases are diseases of infectious origin whose incidence in humans have increased within the past decades or threatens to increase in the near future. The reappearance of a previously known infection after a period of disappearance or decline in incidence is known as re-emergence. Factors such as environmental degradation, rapid population growth, poverty, increased international travel, microbial adaptation of antibiotics, and development of insecticidal resistance and the collapse of public health systems may contribute to the emergence or re-emergence of a disease. Despite the discovery of antibiotics and vaccines, the world continues to be vulnerable to new, emerging, and re-emerging microbial diseases. New diseases in India include HIV/AIDS and a new strain of cholera (V. cholerae 0139) that emerged in 1992. Tuberculosis, malaria, dengue hemorrhagic fever and dengue shock syndrome, Japanese encephalitis, meningococcal meningitis, and hepatitis B .The outbreak of a plague epidemic in India in 1994 and the resurgence of Kala-Azar and epidemics of Leptospirosis are examples of the re-emergence of once-controlled infectious diseases. Preventive efforts and policies to ensure adequate supplies of appropriate medicines, and establishment of national and regional surveillance and diagnostic facilities for combating infectious disease threats should be established.

prion diseases

2008-08-21T10:32:00.000-07:00

PRION DISEASES-AN OVERVIEW
Prince. C.P
Department of Microbiology
Mother Theresa Institute of Health Sciences
Puducherry

Infectious diseases are caused by microorganisms like bacteria, viruses, fungi, protozoan parasites and helminthic parasites.
Recent research by Stanley.B.Prusiner and others discovered the existence of a new group of infectious agents which are responsible for some rare fatal diseases. These agents do not belong to any of the classical pathogens, as they do not posses a nucleic acid (RNA/DNA) and are just infectious protein molecules. They are called as Prions.
Prions are small Self replicating proteinaceous infectious particles which can resist inactivation procedures like sterilization and can modify nucleic acids.
Prions are resistant to denaturation by proteases, heat, radiation, and formalin treatments, although their infectivity can be reduced by such treatments.
Prion diseases are often called Transmissible Spongiform Encephalopathies because of the post mortem appearance of the brain with large vacuoles in the cortex and cerebellum.
Prion diseases have Common features like long incubation periods (years), characteristic spongiform changes associated with neuronal loss and failure to induce inflammatory response-no antibodies are produced against prions.
Prion diseases in animals
Scrapie: sheep
TME (transmissible mink encephalopathy): mink
CWD (chronic wasting disease): mule -deer, elk
BSE (bovine spongiform encephalopathy): cows
Prion diseases in man
CJD: Creutzfeld-Jacob Disease
GSS: Gerstmann-Straussler-Scheinker syndrome
FFI: Fatal familial Insomnia
Kuru
Alpers Syndrome

These diseases are characterized by loss of motor control, dementia, paralysis, wasting and eventually death, typically following pneumonia.
The first Prion disease identified was Kuru, which was found among the Fore tribe of Papua New Guinea. .Kuru is transmitted among this tribe due to their practice of cannibalism .They eat their relative’s dead body.
Prion proteins induce abnormal folding of normal cellular Prion proteins (PrP) in the brain, leading to brain damage. When infectious PrP-sc enters into nervous tissues it interacts with normal PrP-c of the brain cells and converts them into Prp-sc. This leads into the accumulation of PrP-sc in brain cells.
Diagnosis is mainly based on symptoms. Other useful methods are 1.Electroencephalography — often has characteristic triphasic spikes
2. Cerebrospinal fluid analysis for 14-3-3 protein
3. MRI of the brain
No treatment is available today. The search for viable treatment is going on. Preventive measures like strict quarantine laws and mass slaughtering of infected animals are useful to control the spread of infection.
Prion research in future may provide the clarification for the doubts about origin of life and pathogenesis of diseases like Alzhmer’s and Parkinsonism.

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biological weapons

2008-08-21T10:23:00.000-07:00

BIOLOGICAL WARFARE-A THREAT TO HUMANKIND
Prince.C.P
Lecturer in Microbiology
Mother Theresa Institute of Health Sciences
Gorimedu
Pondicherry-605006
cpprincepni@yahoo.co.in

Biological weapons deliver toxins and microorganisms, such as viruses and bacteria, so as to deliberately produce disease among people, animals, and agriculture. Biological attacks can result in destruction of crops, temporarily diseasing of a small community, and killing large numbers of people.
The act of bioterrorism can range from a simple threat to the actual use of these biological weapons, also referred to as agents. A number of nations have or are seeking to acquire biological warfare agents, and there are concerns that terrorist groups may also acquire the technologies and expertise to use these destructive agents.
Biological agents may be used for an isolated assassination, as well as to cause death to thousands. If the environment is contaminated, a long-term threat to the population could be created.
History of Biological Warfare
The use of biological agents is not a new concept, and history is filled with examples of their use. Biological warfare has been practiced repeatedly throughout history. Before the 20th century, the use of biological agents took three major forms:
1. Deliberate poisoning of food and water with infectious material
2. Use of microorganisms, toxins or animals, living or dead, in a weapon system
3. Use of biologically inoculated fabrics.
Olden times:
* Scythian archers infected their arrows by dipping them in decomposing bodies or in blood mixed with manure as far back as 400 BC.
* Persian, Greek, and Roman literature from 300 BC quotes examples of dead animals used to contaminate wells and other sources of water.
*During the battle of Tortona in the 12th century AD, Barbarossa used the bodies of dead and decomposing soldiers to poison wells.
*During the siege of Kaffa in the 14th century AD, the attacking Tatar forces hurled plague-infected corpses into the city in an attempt to cause an epidemic within enemy forces.
*In 1710, when the Russians besieging Swedish forces at Reval in Estonia catapulted bodies of people who had died from plague.
*During the French and Indian War in the 18th century AD, British forces under the direction of Sir Jeffrey Amherst gave blankets that had been used by smallpox victims to the Native Americans in a plan to spread the disease.
Modern times:
#During World War I, the German Army developed anthrax, glanders, cholera, and a wheat fungus specifically for use as biological weapons. They allegedly spread plague in St. Petersburg, Russia, infected mules with glanders in Mesopotamia, and attempted to do the same with the horses of the French Cavalry.
#The Geneva Protocol of 1925 was signed by 108 nations. This was the first multilateral agreement that extended prohibition of chemical agents to biological agents. Unfortunately, no method for verification of compliance was addressed.
#During World War II, Japanese forces operated a secret biological warfare research facility in Manchuria that carried out human experiments on prisoners. They exposed more than 3000 victims to plague, anthrax, syphilis, and other agents in an attempt to develop, observe and study the disease. Some victims were executed or died from their infections.
# in 1942, the United States formed the War Research Service. Anthrax and botulinum toxin initially were investigated for use as weapons. Sufficient quantities of botulinum toxin and anthrax were stockpiled by June 1944 to allow unlimited retaliation if the German forces first used biological agents.
# The British also tested anthrax bombs on Gruinard Island off the northwest coast of Scotland in 1942 and 1943 and then prepared and stockpiled anthrax-laced cattle cakes for the same reason.
#The United States continued research on various offensive biological weapons during the 1950s and 1960s. From 1951-1954, harmless organisms were released off both coasts of the United States to demonstrate the vulnerability of American cities to biological attacks. This weakness was tested again in 1966 when a test substance was released in the New York City subway system.
#During the Vietnam War, Viet Cong guerrillas used needle-sharp punji sticks dipped in feces to cause severe infections after an enemy soldier had been stabbed.
#in 1979, an accidental release of anthrax from a weapons facility in Sverdlovsk, USSR, killed at least 66 people. The Russian government claimed these deaths were due to infected meat, and maintained this position until 1992, when Russian President Boris Yeltsin finally admitted to the accident.
Bioterrorism and biowarfare today:
A number of countries have continued offensive biological weapons research and use. Additionally, since the 1980s, terrorist organizations have become users of biological agents.
@In 1985, Iraq began an offensive biological weapons program producing anthrax, botulinum toxin, and aflatoxin. During Operation Desert Storm, the coalition of allied forces faced the threat of chemical and biological agents. Following the Persian Gulf War, Iraq disclosed that it had bombs, Scud missiles, 122-mm rockets, and artillery shells armed with botulinum toxin, anthrax, and aflatoxin. They also had spray tanks fitted to aircraft that could distribute agents over a specific target.
@In September and October of 1984, 751 people were intentionally infected with Salmonella, an agent that causes food poisoning, when followers of the Bhagwan Shree Rajneesh contaminated restaurant salad bars in Oregon.
@In 1994, a Japanese sect of the Aum Shinrikyo cult attempted an aerosolized (sprayed into the air) release of anthrax from the tops of buildings in Tokyo.
@In 1995, 2 members of a Minnesota militia group were convicted of possession of ricin, which they had produced themselves for use in retaliation against local government officials.
@In 1996, an Ohio man attempted to obtain bubonic plague cultures through the mail.
@In 2001, anthrax was delivered by mail to US media and government offices. There were 4 deaths.
@In December 2002, 6 terrorist suspects were arrested in Manchester, England; their apartment was serving as a "ricin laboratory." Among them was a 27-year-old chemist who was producing the toxin. Later, on January 5, 2003, British police raided 2 residences around London and found traces of ricin, which led to an investigation of a possible Chechen separatist plan to attack the Russian embassy with the toxin; several arrests were made.
@On February 3, 2004, 3 US Senate office buildings were closed after the toxin ricin was found in mailroom that serves Senate Majority Leader Bill Frist's office.
Biological agents involved in bioterrorism
There are more than 1200 biological agents that could be used to cause illness or death; relatively few possess the necessary characteristics to make them ideal candidates for biological warfare or terrorism agents. The ideal biological agents are relatively easy to acquire, process, and use. Only small amounts (on the order of pounds and often less) would be needed to kill thousands of people in a metropolitan area. Biological warfare agents are easy to hide and difficult to detect or protect against. They are invisible, odorless, tasteless, and can be spread silently.
Although the list of potential agents is long, only a handful of pathogens are thought to have the ability to cause a maximum credible event to paralyze a large city or region of the country, causing high numbers of deaths, wide-scale panic, and massive disruption of commerce. Diseases like anthrax, smallpox, and plague, notorious for causing large outbreaks, still head that list. In addition, other agents, such as botulinum toxin, hemorrhagic fever viruses, and tularemia, have potential to do the same.
Many other pathogens can cause illness and death, and the threat list will always be dynamic. We must, therefore, have the appropriate surveillance system and laboratory capability to identify other pathogens.

Biological agents involved in bioterrorism or biocrimes

Traditional biological warfare agents
Agents associated with biocrimes and bioterrorism
Pathogens
Bacillus anthracis
Ascaris suum

Brucella suis
Bacillus anthracis

Coxiella burnetii
Coxiella burnetiib

Francisella tularensis
Giardia lamblia

Smallpox
HIV

Viral encephalitides
Rickettsia prowazekii

Viral hemorrhagic fevers
(typhus)

Yersinia pestis
Salmonella typhimurium

Salmonella typhi

Shigella species

Schistosoma species

Vibrio cholerae

Viral hemorrhagic fevers (Ebola)

Yellow fever virus

Yersinia enterocolitica

Yersinia pestis
Toxins
Botulinum
Botulinum

Ricin
Cholera endotoxin

Staphylococcal enterotoxin B
Diphtheria toxin

Nicotine

Ricin

Snake toxin

Tetrodotoxin
Anti-crop agents
Rice blast

Rye stem rust

Wheat stem rust

Diseases considered for weaponization:
Anthrax, ebola, Marburg virus, plague , cholera , tularemia , brucellosis, Q fever , machupo, Coccidioides mycosis , Glanders , Melioidosis , Shigella , Rocky Mountain spotted fever, typhus , Psittacosis, yellow fever, Japanese B encephalitis , Rift Valley fever , and smallpox .
Naturally-occurring toxins that can be used as weapons include ricin, botulism toxin, saxitoxin, and many mycotoxins.
The organisms causing these diseases are known as select agents. Their possession, use, and transfer should be regulated law.

Delivery of biological agents
Biological warfare agents can be disseminated in various ways:
Through the air by aerosol sprays: To be an effective biological weapon, airborne germs must be dispersed as fine particles. To be infected, a person must breathe a sufficient quantity of particles into the lungs to cause illness.
Used in explosives (artillery, missiles, and detonated bombs): The use of an explosive device to deliver and spread biological agents is not as effective as the delivery by aerosol. This is because agents tend to be destroyed by the blast, typically leaving less than 5% of the agent capable of causing disease.
Put into food or water: Contamination of a city's water supplies requires an unrealistically large amount of an agent as well as introduction into the water after it passes through a regional treatment facility.
Absorbed through or injected into the skin: This method might be ideal for assassination, but is not likely to be used to cause mass casualties.
Detection
Biological agents could either be found in the environment using advanced detection devices including microbiological assays or after specific testing or by a doctor reporting a medical diagnosis of an illness caused by an agent.
Animals may also be early victims and shouldn't be overlooked.
Early detection of a biological agent in the environment allows for early and specific treatment and time enough to treat others who were exposed with protective medications. Doctors must be able to identify early victims and recognize patterns of disease. If unusual symptoms, a large numbers of people with symptoms, dead animals, or other inconsistent medical findings are noted, a biological warfare attack should be suspected. Doctors report these patterns to public health officials.
Protective measures
Protective measures can be taken against biological warfare agents. These should be started early (if enough warning is received) but definitely once it is suspected that a biological agent has been used.
1. Use Personal Protective Equipments:
Masks: Currently, available masks such as the military gas mask or high-efficiency particulate air (HEPA) filter masks used for tuberculosis exposure filter out most biological warfare particles delivered through the air. However, the face seals on ill-fitting masks often leak. For a mask to fit properly, it must be fitted to a person's face.
Clothing: Most biological agents in the air do not penetrate unbroken skin, and few organisms stick to skin or clothing. After an aerosol attack, the simple removal of clothing eliminates a great majority of surface contamination. Thorough showering with soap and water removes 99.99% of the few organisms that may be left on the victim's skin.
2. Medical protection:
Health care providers treating victims of biological warfare may not need special suits but should use latex gloves and take other precautions such as wearing gowns and masks with protective eye shields. Victims would be isolated in private rooms while receiving treatment.
Antibiotics: Victims of biological warfare might be given antibiotics orally (pills) or through an IV, even before the specific agent is identified.
Vaccinations: Currently, protective vaccines are available for anthrax, botulinum toxin, tularemia, plague, Q fever, and smallpox. The widespread immunization of nonmilitary personnel has not been recommended by any governmental agency so far. Immune protection against ricin and staphylococcal toxins may also be possible in the near future.
Anti-agriculture Biological warfare
Biological warfare can also specifically target plants to destroy crops or defoliate vegetation. The United States and Britain discovered plant growth regulators (i.e., herbicides) during the Second World War, and initiated an Herbicidal Warfare program that was eventually used in Malaya and Vietnam in counter insurgency. Though herbicides are chemicals, they are often grouped with biological warfare as bioregulators in a similar manner as biotoxins.Scorched earth tactics or destroying livestock and farmland were carried out in the Vietnam War and Eelam War in Sri Lanka.
The United States developed an anti-crop capability during the Cold War that used plant diseases (bioherbicides, or mycoherbicides) for destroying enemy agriculture. Diseases such as wheat blast and rice blast were weaponized in aerial spray tanks and cluster bombs for delivery to enemy water sheds in agricultural regions to initiate epiphytotics (epidemics among plants).
In 1980s Soviet Ministry of Agriculture had successfully developed variants of foot-and-mouth disease and rinderpest against cows, African swine fever for pigs, and psittacosis to kill chicken. These agents were prepared to spray them down from tanks attached to airplanes over hundreds of miles.
Attacking animals is another area of biological warfare intended to eliminate animal resources for transportation and food.
In summary, we know that biological pathogens have been used for biological warfare and terrorism, and their potential for future use is a major concern. Therefore we must be prepared to respond appropriately if they are used again. The technology and intellectual capacity exist for a well-funded, highly motivated terrorist group to mount such an attack.
Beware! We do not know who are our enemy and friend; it can be George Bush or Saddham Hussein!