Gram positive cocci arranged in chains or pairs.
They cause pyogenic infections with a characteristic tendency to spread unlike staph(which typically localize)
Billroth called them streptococci (Strepto meaning twisted or coiled)
They cause Non Suppurative lesions, acute rheumatic fever & glomerulonephritis.
Streptococci are first divided into obligate anaerobes & facultative anaerobes.
Streptococci are classified on basis of hemolytic properties; Alpha , Beta , Gamma.
Most pathogenic strepto fall into group Beta & called as hemolytic strepto cocci.
Alpha strepto cocci are generally commensals in throat and produce opportunistic infections called as viridance group(green).
Gamma strepto cocci include fecal strepto cocci.
MORPHOLOGY
Gram positive cocci in chains , 0.5 – 1 um in diameter.
They are non motile and non sporing.
Group C strains have some capsules.
CULTURE
Aerobic and facultative anaerobe.
Grows best at 37 degrees C (range – 22 to 42 degree C)
They have exact nutritive requirements, growth occurring in media with blood ,serum or sugars.
Colonies are small (0.5 to 1 mm) circular ,semi transparent & low convex with a wide zone of beta hemolysis.
Hemolysis is promoted by 10% CO2.
Virulent strains form “matt” colonies,
Avirulent strains form glossy colonies.
RESISTANCE
Delicate organisms and inactivated by heat at 56 degree C for 30 minutes.
They survive in dust for several weeks if protected from sunlight.
It is rapidly inactivated by antiseptics.
Its more resistant to crystal violet than many other bacteria.
They do not develop resistance to drugs. (unlike staph)
They are sensitive to bacitracin.
ANTIGENIC STUCTURE
1) Capsular Hyaluronic Acid
2)Group Specific Polysaccharide Antigen
3)Type Specific Antigen
M,T&R proteins
TOXINS AND OTHER VIRULENCE FACTORS
Hemolysins
There are two types of hemolysins: O and S
Streptolysin O:
Lyses red cells ,cytotoxic for neutrophils platelets and cardiac tissue.
It is antigenic and antistreptolysin O appears in sera post streptococal infection.
Estimation (ASO titre) standard serological procedure for the retrospective diagnosis.
ASO titre > 200 units suggest either recent or recurrent streptococcal infection.
Streptolysin S:
Oxygen stable.
Responsible for haemolysis in blood agar.
It is a protein but not antigenic.
Pyrogenic exotoxin (erythrogenic, dick, scarlatinal toxin)
Three types of streptococcal pyrogenic exotoxin (S P E) A,B & C
SPE ‘s are SUPERANTIGENS (induce massive release of cytokines causing fever, shock & tissue damage)
Streptokinase(Fibrinolysin)
It breaks down fibrin barrier around lesions and spreads the infection.
Streptokinase IV given as RX in early myocardial infarction and other thromboembolic disoders.
Deoxyribonucleases(stretodornase,DNAase)
Stretodornase liquefies the thick pus.
This property apply therapeutically in liquefying thick exudates as in empyema.
There are four types of DNAases A,B,C &D.
Nicotinamide adenine dinucleotidase (NADase, formerly diphosphopyridine nucleotidase, DPNase)
It is leucotoxic.
It is antigenic.
Hyaluronidase
Breaks down hyaluronic acid of tissues and spread the infection along intercellular spaces.
It is semingly self destructive process.
It is antigenic.
Serum opacity factor (SOP
PATHOGENICITY
Streptococcus pyogenes is intrinsically much more dangerous organism than staph aureus and has much greater tendency to spread in the tissues.
It is more likely to give septicaemia.
Carriers(5% )of general population carry S pyogenes in resp tract , mouth & skin.
Carrier rate is higher in children between 1 to 15 years of age.
Carriers and patients with acute infections are the sources of infection.
Showing posts with label The Microbiological Diseases. Show all posts
Showing posts with label The Microbiological Diseases. Show all posts
Monday, February 15, 2010
Sunday, February 14, 2010
Laboratory Diagnosis of Syphilis
Laboratory Diagnosis of Syphilis
Diagnosis of syphilis is based on microscopy and serology. At the first antenatal visit, all women in UK are screened for sexually transmitted diseases including syphilis and HIV. The serological tests are repeated at three monthly intervals in cases of anogenital ulceration if the initial tests are negative. All infants born to seropositive mothers should be examined at birth and at monthly intervals for 3 months until it is confirmed that serological tests are and remain negative.
Microscopy
Microscopic demonstration of T. pallidum from the lesions or infected lymph nodes in early syphilis depends on the following three tests:
Dark-field microscopy: if a lesion such as chancre is present, dark-field microscopy should be attempted to visualize the characteristic motile spirochetes in the exudates collected from the lesion. The sensitivity rate[5] is up to 97%, so failure to find the organism does not exclude a diagnosis of syphilis. (For an explanation of sensitivity and specificity, please see Lalkhen and McCluskey.[8])
Direct fluorescent antibody (DFA) test: this uses the indirect fluorescent technique with killed T. pallidum as antigen. The organisms are fixed on a slide to which serum is added. The antibody in the serum unites with treponemes and is made visible with fluorescent stain.[1]
Polymerase chain reaction (PCR) test: it may be useful for the detection of primary syphilis with sensitivity up to 98.6%.
Serological Tests
Non-treponemal Tests. These tests detect the cross-reaction of antibody to syphilis with cardiolipin. The result is reported as reactive or non-reactive; a reactive test is accompanied by a quantitative titre and should be confirmed with a treponemal test. False positive non-treponemal tests may occur in patients who are pregnant, i.v. drug users, those with systemic inflammatory diseases such as systemic lupus erythematosus, or after a recent viral infection.[3]
VDRL (venereal disease research laboratory) test: this is simple and inexpensive and is the preferred test worldwide.
RPR (rapid plasma reagin) test: this is used for screening purposes and is the least technically demanding test as no microscope is needed. It uses carbon-containing cardiolipin antigen and requires a minimal quantity of blood.
Treponemal Tests. These tests specifically detect antibodies against T. pallidum and are positive for life in the vast majority of infected patients regardless of stage or treatment history.[3]
TPHA (T. pallidum haemagglutination assay) or TPPA (T. pallidum particle agglutination assay): these are very valuable and simple tests using an indirect haemagglutination method with red cells or by gelatine particles. Together with VDRL, it is probably the best combination for routine use. False positive reactions occur in up to 2%.[1]
EIA (enzyme immuno assay): treponemal enzyme immunoassay is the screening test of choice and can detect IgG and IgM antibodies as it is positive in earlier stages of syphilis. A positive test is then confirmed with the TPHA/TPPA or VDRL/RPR tests.
FTA-ABS (fluorescent treponemal antibody absorption) assay: this uses the indirect fluorescent technique with killed T. pallidum as an antigen. The organisms are fixed on a slide to which serum is added. The antibody in the serum unites with treponemes. The test has been made more specific by absorbing the group antibodies. This is the most sensitive and specific test available. It becomes positive earlier during the initial stage of primary syphilis. However, it is not suitable for assessing the activity, as the positive test persists long after successful treatment.[1]
Neurological involvement[9] is confirmed by a positive VDRL, raised cell count (>5/mm2), and raised protein (40 mg dl–1) in the CSF obtained by lumbar puncture. Chest X-ray, electrocardiography, echocardiography, cardiac catheterization, and biopsy of gumma can reveal involvement of other systems.
Diagnosis of syphilis is based on microscopy and serology. At the first antenatal visit, all women in UK are screened for sexually transmitted diseases including syphilis and HIV. The serological tests are repeated at three monthly intervals in cases of anogenital ulceration if the initial tests are negative. All infants born to seropositive mothers should be examined at birth and at monthly intervals for 3 months until it is confirmed that serological tests are and remain negative.
Microscopy
Microscopic demonstration of T. pallidum from the lesions or infected lymph nodes in early syphilis depends on the following three tests:
Dark-field microscopy: if a lesion such as chancre is present, dark-field microscopy should be attempted to visualize the characteristic motile spirochetes in the exudates collected from the lesion. The sensitivity rate[5] is up to 97%, so failure to find the organism does not exclude a diagnosis of syphilis. (For an explanation of sensitivity and specificity, please see Lalkhen and McCluskey.[8])
Direct fluorescent antibody (DFA) test: this uses the indirect fluorescent technique with killed T. pallidum as antigen. The organisms are fixed on a slide to which serum is added. The antibody in the serum unites with treponemes and is made visible with fluorescent stain.[1]
Polymerase chain reaction (PCR) test: it may be useful for the detection of primary syphilis with sensitivity up to 98.6%.
Serological Tests
Non-treponemal Tests. These tests detect the cross-reaction of antibody to syphilis with cardiolipin. The result is reported as reactive or non-reactive; a reactive test is accompanied by a quantitative titre and should be confirmed with a treponemal test. False positive non-treponemal tests may occur in patients who are pregnant, i.v. drug users, those with systemic inflammatory diseases such as systemic lupus erythematosus, or after a recent viral infection.[3]
VDRL (venereal disease research laboratory) test: this is simple and inexpensive and is the preferred test worldwide.
RPR (rapid plasma reagin) test: this is used for screening purposes and is the least technically demanding test as no microscope is needed. It uses carbon-containing cardiolipin antigen and requires a minimal quantity of blood.
Treponemal Tests. These tests specifically detect antibodies against T. pallidum and are positive for life in the vast majority of infected patients regardless of stage or treatment history.[3]
TPHA (T. pallidum haemagglutination assay) or TPPA (T. pallidum particle agglutination assay): these are very valuable and simple tests using an indirect haemagglutination method with red cells or by gelatine particles. Together with VDRL, it is probably the best combination for routine use. False positive reactions occur in up to 2%.[1]
EIA (enzyme immuno assay): treponemal enzyme immunoassay is the screening test of choice and can detect IgG and IgM antibodies as it is positive in earlier stages of syphilis. A positive test is then confirmed with the TPHA/TPPA or VDRL/RPR tests.
FTA-ABS (fluorescent treponemal antibody absorption) assay: this uses the indirect fluorescent technique with killed T. pallidum as an antigen. The organisms are fixed on a slide to which serum is added. The antibody in the serum unites with treponemes. The test has been made more specific by absorbing the group antibodies. This is the most sensitive and specific test available. It becomes positive earlier during the initial stage of primary syphilis. However, it is not suitable for assessing the activity, as the positive test persists long after successful treatment.[1]
Neurological involvement[9] is confirmed by a positive VDRL, raised cell count (>5/mm2), and raised protein (40 mg dl–1) in the CSF obtained by lumbar puncture. Chest X-ray, electrocardiography, echocardiography, cardiac catheterization, and biopsy of gumma can reveal involvement of other systems.
The Microbiological Disease Syphilis in Pregnancy-Clasification
Introduction
For several decades, syphilis has been out of sight, mind, and memory, but the incidence in the Western world is now on the rise again and it could once more become a major health concern. This change has followed the rapidly rising number of human immunodeficiency virus (HIV) positive individuals worldwide, together with the advent of health tourists, economic migrants, asylum seekers, and the easy availability of low-cost travel.
Just as syphilis has all but disappeared as an entity in the working memory of most anaesthetists, it has suddenly re-emerged as a co-existing condition in women presenting for Caesarean section.
Incidence of Syphilis
The 1999 WHO estimates suggest an annual rate for syphilis of ~12 million active infections. The risk of contracting syphilis through a sexual contact with a person with primary or secondary syphilis is 30–50%. More than 80% of women with syphilis are in reproductive age; therefore, there is a serious risk of vertical transmission to the fetus.[6] Worldwide, a million pregnancies are adversely affected each year by syphilis because of maternal infection. About 270 000 babies are born with congenital syphilis, 460 000 pregnancies end in abortion or perinatal death, and 270 000 babies are born prematurely or with low birth weight.[7]
Aetiology[1]
Treponema pallidum is the causative organism for syphilis. It is a delicate, motile spirochete bacterium. Humans are its only natural source. Syphilis is usually transmitted by sexual contact through exposure to mucocutaneous syphilitic lesions that contain infectious spirochetes. The infecting organism in body fluid gains access through microscopic abrasions in skin or mucosal surfaces, and begins to replicate locally. After inoculation, the incubation period is around 3 weeks (10–90 days), at the end of which a primary sore develops at the site of infection, usually the genitalia.
Classification
Syphilis is classified[2] as congenital or acquired. There are four stages of syphilis: primary, secondary, latent, and late (tertiary).
Primary Syphilis
The first development is a chancre at the site of inoculation, classically in the anogenital region which is a painless, solitary, round indurated ulcer with a bright red margin.[1] Chancres appear on average about 3 weeks after sexual contact and heal in 3–6 weeks. However, with a small inoculum, this incubation period may be as long as 90 days. One of the common sites for lesions is the cervix; therefore, the clinical manifestations of primary syphilis may go unnoticed by the patient and her partner.[3]
Secondary Syphilis
Untreated patients will progress to secondary syphilis after the signs for primary syphilis resolve (within 4–10 weeks[3]). The lesions are numerous, variable, and affect many systems. A symmetrically distributed, maculopapular, non-irritating rash is found on the palms and the soles with painless lymphadenopathy. The highly infectious condyloma lata are found on warm and moist areas such as genitalia, perianal region, perineum, and axillae. Both meningism and headache can occur, especially at night. Their cause can be confirmed by the presence of an elevated cell count and elevated proteins in cerebrospinal fluid. Less common accompaniments to secondary syphilis include alopecia, laryngitis, mild hepatitis, nephrotic syndrome, bone pain, and uveitis.
Latent Syphilis
The natural history of untreated secondary syphilis is marked by spontaneous resolution after a period of 3–12 weeks, leaving the patient entirely free of symptoms. This naturally attained asymptomatic state is called latency.[4] The latency is arbitrarily subdivided into early (<2 yr from the onset of the infection) and late (>2 yr) stages. During this time, the patient remains serologically positive for syphilis. Approximately 60% of patients remain latent for the rest of their lives. In the early latent stage, 25% will relapse with a secondary syphilitic manifestation, whereas the likelihood of such relapses in the late latent stage is small.[1]
Late Syphilis (Tertiary Syphilis)
Tertiary syphilis develops in 30–40% of untreated patients. The three main manifestations of late syphilis are cardiovascular, gummatous, and neurosyphilis. Cardiovascular syphilis usually occurs 15–30 yr after primary syphilis and may occur in any large vessel. It is characterized, by an aortitis, aortic incompetence, coronary ostial stenosis (presenting as angina), and aortic medial necrosis causing aortic aneurysm. Gummatous syphilis is granulomatous locally destructive lesions that usually occur 3–12 yr after inoculation. They can occur in almost any tissue. Neurosyphilis presents with a variety of syndromes including general paresis, tabes dorsalis, syphilitic meningitis, and meningovascular syphilis. The incubation period is 5–12 yr.[5]
Syphilis in Pregnancy
Antenatal syphilis poses a significant threat to the pregnancy and fetus. T. pallidum readily crosses the placenta, resulting in fetal infection. Vertical transmission can occur at any time during pregnancy and at any stage of syphilis.[6] Risk of transmission correlates with the extent of spirochetal presence in the circulation. Vertical transmission of syphilis is more common in primary (50%) and secondary syphilis (50%), compared with early latent (40%), late latent (10%), and tertiary syphilis (10%). Seventy to one hundred per cent of infants born to untreated infected mothers are infected. Pregnancies complicated by syphilis may result in intrauterine growth restriction, non-immune hydrops fetalis, stillbirth, preterm delivery, and spontaneous abortion in up to 50% of pregnancies. Women who had documented treatment for syphilis in the past do not need treatment during current or subsequent pregnancies.
Congenital Syphilis
In spite of a downward trend in the incidence of syphilis, congenital syphilis, an infection passed from mother to child through the placenta during fetal development or birth, remains a great concern. An infected woman’s potential to infect her fetus remains for many years, although the risk of infecting a fetus declines gradually during the course of untreated illness. After 8 yr, there is little risk, even in the untreated mother. Nearly half of all children infected with syphilis during gestation die shortly before or after birth.
Infants who survive develop early-stage and late-stage symptoms of syphilis, if not treated. Early-stage symptoms include irritability, failure to thrive, non-specific fever, a rash and condyloma lata on the borders of the mouth, anus, and genitalia. Some of these lesions may resemble the wart-like lesions of adult syphilis. A small percentage of infants have a watery nasal discharge (sniffles) and a saddle nose deformity resulting from destruction of the cartilage of the nose. Bone lesions are common, especially in the upper arm (humerus). Later signs appear as tooth abnormalities (Hutchinson teeth), bone changes (sabre shins), neurological involvement, blindness, and deafness.
For several decades, syphilis has been out of sight, mind, and memory, but the incidence in the Western world is now on the rise again and it could once more become a major health concern. This change has followed the rapidly rising number of human immunodeficiency virus (HIV) positive individuals worldwide, together with the advent of health tourists, economic migrants, asylum seekers, and the easy availability of low-cost travel.
Just as syphilis has all but disappeared as an entity in the working memory of most anaesthetists, it has suddenly re-emerged as a co-existing condition in women presenting for Caesarean section.
Incidence of Syphilis
The 1999 WHO estimates suggest an annual rate for syphilis of ~12 million active infections. The risk of contracting syphilis through a sexual contact with a person with primary or secondary syphilis is 30–50%. More than 80% of women with syphilis are in reproductive age; therefore, there is a serious risk of vertical transmission to the fetus.[6] Worldwide, a million pregnancies are adversely affected each year by syphilis because of maternal infection. About 270 000 babies are born with congenital syphilis, 460 000 pregnancies end in abortion or perinatal death, and 270 000 babies are born prematurely or with low birth weight.[7]
Aetiology[1]
Treponema pallidum is the causative organism for syphilis. It is a delicate, motile spirochete bacterium. Humans are its only natural source. Syphilis is usually transmitted by sexual contact through exposure to mucocutaneous syphilitic lesions that contain infectious spirochetes. The infecting organism in body fluid gains access through microscopic abrasions in skin or mucosal surfaces, and begins to replicate locally. After inoculation, the incubation period is around 3 weeks (10–90 days), at the end of which a primary sore develops at the site of infection, usually the genitalia.
Classification
Syphilis is classified[2] as congenital or acquired. There are four stages of syphilis: primary, secondary, latent, and late (tertiary).
Primary Syphilis
The first development is a chancre at the site of inoculation, classically in the anogenital region which is a painless, solitary, round indurated ulcer with a bright red margin.[1] Chancres appear on average about 3 weeks after sexual contact and heal in 3–6 weeks. However, with a small inoculum, this incubation period may be as long as 90 days. One of the common sites for lesions is the cervix; therefore, the clinical manifestations of primary syphilis may go unnoticed by the patient and her partner.[3]
Secondary Syphilis
Untreated patients will progress to secondary syphilis after the signs for primary syphilis resolve (within 4–10 weeks[3]). The lesions are numerous, variable, and affect many systems. A symmetrically distributed, maculopapular, non-irritating rash is found on the palms and the soles with painless lymphadenopathy. The highly infectious condyloma lata are found on warm and moist areas such as genitalia, perianal region, perineum, and axillae. Both meningism and headache can occur, especially at night. Their cause can be confirmed by the presence of an elevated cell count and elevated proteins in cerebrospinal fluid. Less common accompaniments to secondary syphilis include alopecia, laryngitis, mild hepatitis, nephrotic syndrome, bone pain, and uveitis.
Latent Syphilis
The natural history of untreated secondary syphilis is marked by spontaneous resolution after a period of 3–12 weeks, leaving the patient entirely free of symptoms. This naturally attained asymptomatic state is called latency.[4] The latency is arbitrarily subdivided into early (<2 yr from the onset of the infection) and late (>2 yr) stages. During this time, the patient remains serologically positive for syphilis. Approximately 60% of patients remain latent for the rest of their lives. In the early latent stage, 25% will relapse with a secondary syphilitic manifestation, whereas the likelihood of such relapses in the late latent stage is small.[1]
Late Syphilis (Tertiary Syphilis)
Tertiary syphilis develops in 30–40% of untreated patients. The three main manifestations of late syphilis are cardiovascular, gummatous, and neurosyphilis. Cardiovascular syphilis usually occurs 15–30 yr after primary syphilis and may occur in any large vessel. It is characterized, by an aortitis, aortic incompetence, coronary ostial stenosis (presenting as angina), and aortic medial necrosis causing aortic aneurysm. Gummatous syphilis is granulomatous locally destructive lesions that usually occur 3–12 yr after inoculation. They can occur in almost any tissue. Neurosyphilis presents with a variety of syndromes including general paresis, tabes dorsalis, syphilitic meningitis, and meningovascular syphilis. The incubation period is 5–12 yr.[5]
Syphilis in Pregnancy
Antenatal syphilis poses a significant threat to the pregnancy and fetus. T. pallidum readily crosses the placenta, resulting in fetal infection. Vertical transmission can occur at any time during pregnancy and at any stage of syphilis.[6] Risk of transmission correlates with the extent of spirochetal presence in the circulation. Vertical transmission of syphilis is more common in primary (50%) and secondary syphilis (50%), compared with early latent (40%), late latent (10%), and tertiary syphilis (10%). Seventy to one hundred per cent of infants born to untreated infected mothers are infected. Pregnancies complicated by syphilis may result in intrauterine growth restriction, non-immune hydrops fetalis, stillbirth, preterm delivery, and spontaneous abortion in up to 50% of pregnancies. Women who had documented treatment for syphilis in the past do not need treatment during current or subsequent pregnancies.
Congenital Syphilis
In spite of a downward trend in the incidence of syphilis, congenital syphilis, an infection passed from mother to child through the placenta during fetal development or birth, remains a great concern. An infected woman’s potential to infect her fetus remains for many years, although the risk of infecting a fetus declines gradually during the course of untreated illness. After 8 yr, there is little risk, even in the untreated mother. Nearly half of all children infected with syphilis during gestation die shortly before or after birth.
Infants who survive develop early-stage and late-stage symptoms of syphilis, if not treated. Early-stage symptoms include irritability, failure to thrive, non-specific fever, a rash and condyloma lata on the borders of the mouth, anus, and genitalia. Some of these lesions may resemble the wart-like lesions of adult syphilis. A small percentage of infants have a watery nasal discharge (sniffles) and a saddle nose deformity resulting from destruction of the cartilage of the nose. Bone lesions are common, especially in the upper arm (humerus). Later signs appear as tooth abnormalities (Hutchinson teeth), bone changes (sabre shins), neurological involvement, blindness, and deafness.
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