Saturday, 29 March 2014
Monday, 3 March 2014
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:
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
Sunday, 2 March 2014
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
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
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
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
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.
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:
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.
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
Saturday, 1 March 2014
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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