Giardiasis

Infectious agent:

Giardia lamblia is a flagellate protozoan which lives in the duodenum and jejunum.

Identification:

Clinical features :

Giardia infection is usually asymptomatic but may present as acute or chronic diarrhoea associated with abdominal cramps, bloating, nausea, vomiting, fever, fatigue and weight loss. Fat malabsorption may lead to steatorrhoea. Symptoms usually last one to two weeks or months. The rate of asymptomatic carriage may be high.

Method of diagnosis:

Stool microscopy for cysts or trophozoites can be used for diagnosis of Giardia however a negative test does not preclude infection.

Incubation period:

The incubation period is usually one to three weeks but it can be longer. It is on average seven to ten days.

Public health significance and occurrence:

Occurrence is worldwide and endemic in most regions. Over 800 cases are reported in Victoria each year. Infection is detected more frequently in children than adults. It is readily transmitted in institutions such as day care centres among children who are not toilet trained. Other risk factors for infection include travel to high risk areas, immunosuppression, male to male sexual intercourse and achlorhydria.

Reservoir:

Reservoirs include humans and animals as well as contaminated waters.

Mode of transmission:

Transmission occurs person to person and animal to person via hand to mouth transfer of cysts from infected faeces or faecally contaminated surfaces. Waterborne outbreaks may occur due to faecal contamination of public water supplies or recreational swimming areas.

Period of communicability:

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Food or water-borne Illness

Infectious agent:

The most frequent causes of food or water-borne illnesses are various bacteria, viruses and parasites. Refer to specific sections for detail on the more common agents. Non-infective agents:

• heavy metal poisoning, including, cadmium, copper, lead, tin and zinc

• fish toxins that are present in some shellfish or fish like paralytic shellfish poisoning or ciguatera

• plant toxins which occur naturally in some foods such as toxic fungi and green potato skins

• toxic cyanobacteria (blue green algae) overgrowth in water. Bacteria:

• toxin produced in food:

– Staphylococcus aureus

– Clostridium botulinum

– Bacillus cereus

• damage to gut wall and/or systemic infection:

– Salmonella spp.

– Shigella spp. – Clostridium perfringens

– Campylobacter spp.

– E. coli.

– Helicobacter pylori

– Vibrio cholerae/V. parahaemolyticus

– Yersinia enterocolitica

– S.typhi/Paratyphi

– Brucella spp.

– Listeria monocytogenes

Viruses:

• Hepatitis A and E viruses

• Noroviruses and other small round

structured viruses (SRSV)

• Rotavirus

Parasites:

• Cryptosporidium spp.

• Entamoeba histolytica

• Giardia lamblia

Identification:

Clinical features :

Symptoms vary with the causative agent and range from slight abdominal pain and nausea to retching, vomiting, abdominal cramps, fever and diarrhoea. Fever, chills, headache, malaise and muscular pains may accompany gastrointestinal symptoms. Vomiting, with or without diarrhoea, abdominal cramps and fever are common symptoms of viral disease or staphylococcal intoxication. Certain foodborne

illnesses can present with meningitis or septicaemia (listeriosis) or with neurological symptoms ((paralytic

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Erythema infection (human parvovirus infection or slapped cheek disease)

Infectious agent:

The causative agent is human parvovirus B19.

Identification:

Clinical features :

Asymptomatic infection with human parvovirus B19 is common. In children it causes a mild illness with

little or no fever but a striking redness of the cheeks, hence the alternative name of ‘slapped cheek disease’. There may also be a lacy pink rash on the trunk and limbs that fades within a week, but which

may recur over several weeks on exposure to heat or sunlight. Headache, itch or common cold-type symptoms may also occur. In adults the rash is often absent or atypical. They may have cold-type symptoms and sometimes painful or swollen joints lasting two or three days. Parvovirus affects the development of red blood cells. As a result several groups of people are at increased risk of developing complications:

• infection in the first half of pregnancy can cause foetal anaemia with hydrops foetalis. Foetal death occurs in less than ten per cent of these cases

• persons with haemolytic anaemia may develop transient aplastic crises, often in the absence of a rash

• immunosuppressed persons may develop severe chronic anaemia.

Method of diagnosis:

Diagnosis can be suspected on clinical grounds, particularly during outbreaks. However, confirmation depends on demonstrating the presence of specific IgM antibodies or seroconversion to specific IgG antibodies. Comparison of the current antibody status against prenatal screening serology for parvovirus is often useful in pregnancy. Specific IgM antibody titres decline two to three months after infection while IgG levels, which appear two weeks after infection, can persist indefinitely. Nucleic acid (PCR) testing and electron microscopy can also be used to confirm foetal infection.

Incubation period:

The incubation period varies from four to twenty days.

Public health significance and occurrence:

Human parvovirus infection occurs worldwide and is a common childhood disease. Outbreaks occur during winter and spring with epidemics occurring every three to four years. Up to 50% of susceptible household contacts and 10–60% of child care or school contacts may be infected during outbreaks.

Reservoir:

Humans.

Mode of transmission:

The virus is transmitted by contact with infected respiratory secretions. It may be spread vertically from mother to foetus and rarely by transfusion of blood products..

Period of communicability:

Children with erythema infectiosum are most infectious before the onset of the rash and are probably not infectious after the rash appears. Patients with an aplastic crisis are infectious for a week after the onset of symptoms. Immunosuppressed persons with chronic anaemia due to infection may excrete virus for years.

Susceptibility and resistance:

Infection generally confers immunity. Serological surveys suggest 5–15% of preschool children and 50–60% of all adults are immune.

Control measures:

Preventive measures:

There is no vaccine available. All people who are non-immune to parvovirus, immunosuppressed, have

chronic haemolytic disorders, or who are pregnant are at increased risk of complications. These people should be advised of the risk that parvovirus infection may pose to them. They should avoid close contact

with children or adults in settings where parvovirus infection may occur such as schools, child care centres and health care facilities. Strict hand washing and separate eating utensils are also advised for these people.

Control of case:

There is no specific treatment required for uncomplicated infection. Specialist advice should be sought if a

patient with immunodeficiency or a blood disorder contracts parvovirus infection.

Control of contacts:

Intrauterine infection may rarely result in foetal hydrops or death if infection occurs within the first 20 weeks of pregnancy. Medical advice should be sought for pregnant women who have been in close contact with a case of parvovirus infection. Specific antibody testing should be performed to

determine the woman’s immune status to parvovirus.

Control of environment:

Not applicable.

Outbreak measures:

General public health measures include:

• advising high risk persons of relevant outbreaks

• advising patients and contacts to observe strict hand washing after coughing, sneezing and before eating.

.sources of information

·         The blue book: Guidelines for the control of infectious diseases

                                                          

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Donovanosis

Infectious agent:

Calymmatobacterium granulomatis, a gram-negative bacillus, the causative agents is now named Klebsiella granulomatis.

Identification:

Clinical features :

Donovanosis is a chronic, progressively destructive infection which affects the skin and mucous membranes of the external genitalia, inguinal and anal regions. Disseminated disease is uncommon but may be life threatening and so should be considered in patients from endemic areas. It presents initially as raised, ‘beefy’ nodules or sores. Lesions may extend peripherally with characteristic rolled edges. Local spread to pelvic and abdominal structures occurs and dissemination to distant sites can also occur.

Method of diagnosis:

The diagnosis is confirmed by demonstrating ‘Donovan bodies’ in Wright or Giemsa-stained smears of granulation tissue or by histological examination of biopsy specimens.

Incubation period:

The incubation period is weeks to months

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Diphtheria

Infectious agent:

Corynebacterium diphtheriae of the gravis, mitis or intermedius biotypes is an aerobic gram-positive bacillus. Toxin production results when the bacteria are infected by a bacteriophage containing

the diphtheria toxin gene tox.

Identification:

Clinical features :

Diphtheria is an acute bacterial infection caused by toxigenic strains of Corynebacterium diphtheriae. It primarily affects the tonsils, pharynx, nose and larynx. Other mucous membranes, skin, and rarely the vagina or conjunctivae can also be involved. The toxin causes local tissue destruction and membrane

formation. The characteristic lesion in the throat is an adherent greyish-white membrane that first occurs on the tonsils, but may spread up onto the palate and involve the pharynx and result in respiratory obstruction. The onset is insidious with early symptoms of malaise, sore throat, anorexia and low-grade fever. Patients with severe pharyngeal disease may develop neck swelling giving a characteristic ‘bull neck appearance’. Systemic absorption of the toxin can result in neuropathy and cardiomyopathy,

resulting in early death or later neurological complications. Laryngeal diphtheria can present as a slowly progressive croup which can result in death if the airway obstruction is not relieved. Non-toxigenic strains of C. diphtheria rarely cause local lesions but may cause infective endocarditis. Cutaneous diphtheria presents with lesions of variable appearance but which may resemble impetigo. Non-cutaneous diphtheria has a case

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Dengue virus disease

Dengue (pronounced DENgee) fever is a painful, debilitating mosquito-borne disease caused by any one of four closely related dengue viruses. These viruses are related to the viruses that cause West Nile infection and yellow fever.

Infectious agent:

Dengue virus (DENV) has four related but distinct serotypes: 1, 2, 3 and 4. Dengue virus has been recognised since the latter part of the 18th century as causing epidemics in tropical and subtropical parts throughout the world. Dengue was first recognised in Townsville late in the 19th century and early in the 20th century. Outbreaks occurred in an area from the coast of Western Australia to the Northern Territory and down through high rainfall areas of Queensland and New South Wales. At that time Aedes aegypti  mosquitoes were widely distributed in northern Australia and occurred as far south as the Victorian border in eastern Australia and south of Perth in Western Australia. By the 1970s Aedes aegypti were restricted to a small area of northern Queensland. Epidemic dengue returned to north Queensland in 1981–82. Other outbreaks occurred there in the 1990s, a time when Aedes aegypti mosquitoes were spreading westwards from Queensland to the Northern Territory border and towards  the New South Wales border.

Identification:

Clinical features :

Dengue fever (break bone fever):

Dengue fever classically presents as an acute febrile illness of sudden onset. It is extremely debilitating with fever lasting three to five days, myalgia (particularly backache), arthralgia, retro-orbital pain, anorexia, gastrointestinal disturbance, rash and increased vascular permeability. There is a high subclinical rate of

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Cytomegalovirus infection

Cytomegalovirus (CMV) is a virus found around the world. It is related to the viruses that cause chickenpox and infectious mononucleosis (mono). Between 50 percent and 80 percent of adults in the United States have had a CMV infection by age 40. Once CMV is in a person's body, it stays there for life. CMV is spread through close contact with body fluids. Most people with CMV don't get sick and don't know that they've been infected. But infection with the virus can be serious in babies and people with weak immune systems. If a woman gets CMV when she is pregnant, she can pass it on to her baby. Usually the babies do not have health problems. But some babies can develop lifelong disabilities.A blood test can tell whether a person has ever been infected with CMV. Most people with CMV don't need treatment. If you have a weakened immune system, your doctor may prescribe antiviral medicine. Good hygiene, including proper hand washing, may help prevent infections.

Infectious agent:

Cytomegalovirus (CMV) also designated as Human herpesvirus 5, is a member of the subfamily betaherpesvirus of the family herpesviridae. Other members of the herpesvirus group include herpes

simplex virus types 1 and 2, varicella zoster virus (which causes chickenpox), and Epstein-Barr virus (which causes infectious mononucleosis/glandular fever). These viruses share a characteristic ability to remain dormant within the body over a long period.

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Cryptosporidiosis

Cryptosporidiosis (crypto) is an illness caused by a parasite. The parasite lives in soil, food and water. It may also be on surfaces that have been contaminated with waste. You can become infected if you swallow the parasite.The most common symptom of crypto is watery diarrhea. Other symptoms include

• Dehydration
• Weight loss
• Stomach cramps or pain
• Fever
• Nausea
• Vomiting

Most people with crypto get better with no treatment, but crypto can cause serious problems in people with weak immune systems such as in people with HIV/AIDS. To reduce your risk of crypto, wash your hands often, avoid water that may be infected, and wash or peel fresh fruits and vegetables before eating.

Infectious agent:

Cryptosporidium parvum is a coccidian protozoon.

Identification:

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Cryptococcal infection(cryptococcosis)

Cryptococcus is a type of fungus that is found in the soil worldwide, usually in association with bird droppings. The major species of Cryptococcus that causes illness in human is Cryptococcus neoformans. Another less common species that can also cause disease in humans, Cryptococcus gattii, has been isolated from eucalyptus trees in tropical and sub-tropical regions

Infectious agent:

Cryptococcus neoformans, an encapsulated yeast-like fungus. There are two principal variants:C. neoformans var. neoformans (serotypes A & D) and C. neoformans var. gattii (serotypes B & C).

Identification:

Clinical features :

Cryptococcal infection usually presents as sub-acute or chronic meningoencephalitis with headache and altered mental state. Lung involvement may cause symptoms of lower respiratory tract infection or may be asymptomatic. Skin, bone and other organs are less frequently infected

Method of diagnosis:

Encapsulated budding forms of the fungus may be seen in the CSF, urine or pus using Indian ink staining. Cryptococcal antigens may also be detected in the CSF and serum. The diagnosis is confirmed by culture (CSF, blood, sputum or andurine) or by histopathology (Mayer’s mucicarmine

staining). Pulmonary cryptococcosis in non-HIV infected persons usually manifests as a nodule which must be distinguished from a malignancy. Malignancies may co-exist.

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Croup or bronchiolitis and its treatment

Croup:

Croup, or acute laryngotracheobronchitis, is the most common infectious cause of sudden upper airway obstruction in children and of stridor in febrile children. Croup accounts for more than 15% of pediatric respiratory illnesses.Children aged 6 months to 6 years--especially boys--are affected most often: the peak incidence occurs during the second year of life. About 2% of all preschoolers have croup every year, and recurrence is common. Croup can develop at any time of the year, although it classically presents in late autumn and winter.

Although croup can be caused by bacteria (eg, Staphylococcus aureus, Haemophilus influenzae, Corynebacterium diphtheriae, and Mycoplasma pneumoniae) and atypical agents, most cases are viral. The leading cause of croup, isolated from more than 80% of positive cultures, is parainfluenza virus (types 1, 2, and 3). Other viruses that can cause croup include adenovirus, influenza A and B viruses, respiratory syncytial virus (RSV), and rubeola virus.

The time and manner in which the child presents may yield general clues to the cause of the viral croup. For example, parainfluenza viruses predominate in the fall, whereas RSV croup peaks in the midwinter. The most severe illness is caused by influenza A virus infection.

Bronchiolitis:

Bronchiolitis is one of the most common and serious viral infections to affect the small and medium airways of the lower respiratory tract in young children.Almost 85% of all reported cases of bronchiolitis are caused by RSV. However, parainfluenza virus, adenovirus, influenza A virus, and rhinovirus can also be responsible. Bronchiolitis targets young children, particularly those aged 2 to 6 months. Most children are infected by age 3; roughly 10% have clinically

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What is Creutzfeldt-Jakob disease (CJD) , how can u diagnose and treat it

Introduction:

Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, invariably fatal brain disorder. It affects about one person in every one million people per year worldwide; in the United States there are about 300 cases per year. CJD usually appears in later life and runs a rapid course. Typically, onset of symptoms occurs about age 60, and about 90 percent of individuals die within 1 year. In the early stages of disease, people may have failing memory, behavioral changes, lack of coordination and visual disturbances. As the illness progresses, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur.

There are three major categories of CJD:

• In sporadic CJD, the disease appears even though the person has no known risk factors for the disease. This is by far the most common type of CJD and accounts for at least 85 percent of cases.
• In hereditary CJD, the person has a family history of the disease and/or tests positive for a genetic mutation associated with CJD. About 5 to 10 percent of cases of CJD in the United States are hereditary.
• In acquired CJD, the disease is transmitted by exposure to brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through casual contact with a CJD patient. Since CJD was first described in 1920, fewer than 1 percent of cases have been acquired CJD.

CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges under a microscope. CJD is the most common of the known human TSEs. Other human TSEs include kuru, fatal familial insomnia (FFI), and Gerstmann-Straussler-Scheinker disease (GSS). Kuru was identified in

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Diabetes its tyes and treatment

Diabetes is a disorder of metabolism—the way our bodies use digested food for growth and energy. Most of the food we eat is broken down into glucose, the form of sugar in the blood. Glucose is the main source of fuel for the body.
After digestion, glucose passes into the bloodstream, where it is used by cells for growth and energy. For glucose to get into cells, insulin must be present. Insulin is a hormone produced by the pancreas, a large gland behind the stomach.
When we eat, the pancreas automatically produces the right amount of insulin to move glucose from blood into our cells. In people with diabetes, however, the pancreas either produces little or no insulin, or the cells do not respond appropriately to the insulin that is produced. Glucose builds up in the blood, overflows into the urine, and passes out of the body in the urine. Thus, the body loses its main source of fuel even though the blood contains large amounts of glucose.

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Circadian rhythm sleep disorder And Treatment

Circadian rhythm sleep disorders are a family of sleep disorders affecting the timing of sleep.


People with circadian rhythm sleep disorders are unable to sleep and wake at the times required for normal work, school, and social needs.

They are generally able to get enough sleep if allowed to sleep and wake at the times dictated by their body clocks.

Unless they have another sleep disorder, their sleep is of normal quality.

Humans have biological rhythms, known as circadian rhythms, which are controlled by a biological clock and work on a daily time scale.

Due to the circadian clock, sleepiness does not continuously increase as time passes.

Instead, the drive for sleep follows a cycle, and the body is ready for sleep and for wakefulness at different times of the day.


Types of circadian rhythm sleep disorders


Two of these disorders are extrinsic (from Latin extrinsecus, from without, on the outside) or circumstantial:
Jet lag, which affects people who travel across several time zones.
Shift work sleep disorder, which affects people who work nights or rotating shifts.

Intrinsic type

Four of them are intrinsic (from Latin intrinsecus, on the inside, inwardly), "built-in":
Delayed sleep phase disorder (DSPD), aka delayed sleep phase syndrome (DSPS), characterized by a much later than normal timing of sleep onset and offset and a period of peak alertness in the middle of the night.
Advanced sleep phase syndrome (ASPS), characterized by difficulty staying awake in the evening and difficulty staying asleep in the morning.
Non-24-hour sleep-wake syndrome (Non-24), in which the affected individual's sleep occurs later and later each day, with the period of peak alertness also continuously moving around the clock from day to day.
Irregular sleep-wake rhythm, which presents as sleeping at very irregular times, and usually more than twice per day (waking frequently during the night and taking naps during the day) but with total time asleep typical for the person's age.

Treatment for circadian rhythm sleep disorders

Possible treatments for circadian rhythm sleep disorders include:
Behavior therapy or advice about sleep hygiene where the patient is told to avoid naps, caffeine, and other stimulants. They are also told to not be in bed for anything besides sleep and sex
Bright light therapy is used to advance or delay sleep, depending on how the circadian rhythm is shifted. Patients are exposed to high-intensity light (up to 10,000 lux) for a duration of 30–60 minutes at a time, the time of day depending on whether an advance or a delay is required.
Blue blocking glasses therapy is used to block blue wavelength light from reaching the eye during evening hours so that melatonin production is increased.
Medications such as melatonin and modafinil (Provigil), or other short term sleep aids or wake-promoting agents can be beneficial; the former is a natural neurohormone responsible partly and in tiny amounts for the human body clock. Tasimelteon has been proven effective in Phase III trials.
Sleep phase chronotherapy progressively advances or delays the sleep time by 1–2 hours per day

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Discovery Points to New Approach to Fight Dengue Virus

Researchers have discovered that rising temperature induces key changes in the dengue virus when it enters its human host, and the findings represent a new approach for designing vaccines against the aggressive mosquito-borne pathogen.

The researchers found that the dengue virus particles swell slightly and take on a bumpy appearance when heated to human body temperature, exposing "epitopes," or regions where antibodies could attach to neutralize the virus.

The discovery is significant because it could help to explain why vaccines against dengue have been ineffective, said Michael G. Rossmann, Hanley Distinguished Professor of Biological Sciences at Purdue University.

Scientists have been designing vaccines targeting the virus's smooth appearance found at the cooler temperatures of mosquitoes and ticks.

"The bumpy form of the virus would be the form present in humans, so the optimal dengue virus vaccines should induce antibodies that preferentially recognize epitopes exposed in that form," Rossmann said.

The findings are detailed in a research paper appearing online this week in Proceedings of the National Academy of Sciences.



The researchers used a technique called cryo-electron microscopy to see the three-dimensional structure of the virus at temperatures ranging from 28-37 degrees Celsius (37 degrees Celsius is 98.6 degrees Fahrenheit, or human body temperature). Findings showed that the virus has a smooth appearance while at the cooler temperatures found in mosquito or tick vectors, but then it morphs into the bumpy form at warmer temperatures before fusing to the host cell and delivering its genetic material.



"These findings were a big surprise," said Richard J. Kuhn, professor and head of Purdue's Department of Biological Sciences and director of the Bindley Bioscience Center. "No one expected to see the virus change its appearance as it moves from the mosquito to humans."



The paper was co-authored by postdoctoral researcher Xinzheng Zhang; lab manager Ju Sheng; postdoctoral researcher Pavel Plevka; Kuhn; Michael S. Diamond, a researcher at Washington University School of Medicine; and Rossmann.



Findings also could apply to related infections in the flavivirus family, which includes a number of dangerous insect-borne diseases such as West Nile, yellow fever, tick-borne encephalitis and Japanese encephalitis.



Dengue (pronounced DEN-gē) is a leading cause of serious illness and death among children in some Asian and Latin American countries, causing 50 million to 100 million infections per year. Globally, dengue has grown dramatically in recent decades, placing about half the world's population at risk of infection.



The researchers determined that the bumpy form of the virus is more efficient at infecting mammalian cells. The team was able to measure the virus's infectivity using a laboratory procedure where cells are infected in a culture dish. The bumpy shape is an intermediate stage before the virus becomes unstable, releasing its genetic material. The virus is made of subunit molecules that separate when the virus particle expands into its bumpy form, revealing exposed membrane surfaces between the subunits where antibodies might bind.



The work is funded by the National Institutes of Health and Purdue through university support for a structural biology electron microscope facility



( from universities, journals, and other research organizations )

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