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STI CHLAMYDIA LVG


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CHLMYDIA IS classified according to MOMP of which there are 18 serovariants..?
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1)A,B, Ba, C: TRACHOMA 2) D-K(B,C): GENITAL INFECTION 3)L(L1-L3) LYMPHOGRANULOMA VENEREUM LVG. women with infection with serotype G are increases risk of developing cervical cancer.

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CHLMYDIA IS classified according to MOMP of which there are 18 serovariants..?
1)A,B, Ba, C: TRACHOMA 2) D-K(B,C): GENITAL INFECTION 3)L(L1-L3) LYMPHOGRANULOMA VENEREUM LVG. women with infection with serotype G are increases risk of developing cervical cancer.
LVG biovar are characterised in the lab by some abilities: what are they?
1) grow fast and vigorously in cell cultures 2) grow unassisted without centrifuge infection and pre treatment with polycations.
LVG BIOVAR is remarkable for its tropism (ability to infet diff cells) which include?
Lymphoid cells and cause systemic disease. it primarily occurs in homosexuals as genital infections and Must be considered in differential diagnosis of genital ulcers.
In the secondary stage, where most patient appear in the clinic, the characteristic features include
Marked Lymphadenopathy (unilateral). Retroperitoneal in women and inguinal in men. in the bubonic form, both the inguinal and femoral lymph nodes are involved giving rise to the 'characteristic 'grooves sign'.
Rectal infection with LVG biovar of C. trachomatis is relatively common in homosexual men. when compared to other chlamydial proctitis, LVG biovar of C. trachomatis is accompanied by?
Signs of systemic Cachexic(loss of body weight and muscle mass and weakness) illness: fever, chills, weight loss and constipation.
LVG biovar of C. Trachomatis involves primary, secondary and tertiary complications which include?
Primary: PROCTOCOLITIS secondary: RECTAL STRICTURE, ACUTE MENINGEOENCEPHALITIS, FOLLICULAR CONJUNCTIVITIS tertiary: GENITAL ELEPHANTIASIS, FISTULAE, RECTAL STRICTURE
Complications of secondary LVG
RECTAL STRICTURE, ACUTE MENINGEOENCEPHALITIS, FOLLICULAR CONJUNCTIVITIS
Complication of tertiary LVG
GENITAL ELEPHANTIASIS, FISTULAE, RECTAL STRICTURE
In lab diagnosis, the gold standard in chlamydial diagnosis is via
Culturing(incubation 40-72 hrs). Geimsa stain is used for staining smear/ scrapping from urethra, cervix vagina, lymph nodes and ulcer.
Serological diagnosis(not recommended in diagnosis of genital tract disease) of chlamydia is inadequate in chronic infection, however in acute infection they may be useful. what immuoglobulins are measured.
Four fold rise in IgA/IgG titres measure over several weeks apart. Pos IgM is marker for current infection. diagnosis is made via Micro-immunoflorescence(MIF) which uses EBs as antigen.
Sensitivity, specificity and predictive values of serologic studies for chlamydia are not high enough to make any of them clinically useful in the diagnosis of active disease, the antibodies measured include?
IgA,IgG and IgM antibodies that can distinguish recent infection (IgM) from past infections(IgG) as well as primary infections. ELISA can also measure the three antibodies.
Complimet fixation test can also be used in detection of antibodies in chlamydial infections although it lacks specificity, it is beneficial because?
1) much less demanding the MIF 2)LP antibodies are produced very early in primary infection. (60% sensiitivity)
Other lab techiniques for chlamydia infections
1)DFA method of choice for confirming other assays: sensitivity 50-80, specificity: 99% 2)ELISA used in A&E: sensitvity:40-60, specificity 99%.
Newer probes used in nucleic acid detection of chlamydia trachomatis and N. gonorrhoeae use MSU may obviate the need of direct sampling in uncomplicated cases and in evaluation of sexual abuse. some methods of NAD include
1) pcr (can deteect 10-100 EBs) 99/99. rapid and relaible diagnosis. 2)lcr 3) strand displacemnt amplification (SDA) 4) HYbrid capture system(HCS) 5) transcription mediated amplification (TMA) or RNA 6) specific probes for DNA
Other tests and biopsy for chlamydia
Biopy: genital tract or material aspirated for lymph nodes CT: identify Fitz-hugh- curtis syndrome (perihepatitis) and free perotoneal fluid Ultrasound: tubo-ovarian abscess radiography: infants suspected of pneumonia.
Treatment of chlamydia infections
1)doxycycline is the drug of choice. 2)tet/ macrolides: erythromycin and azithromycin. flouroquinolones can also be used.
Benefit of azithromycin in chlamydia infection
It is long actin and concentrated within cells, allowing for single dose in genital infections and is a short course therapy (3 dasy) for pneumonia.
Reommended regimens for LVG
1a)AZITHROMYCIN: 1G orally in a single dose/ or 1b)DOXYCYCLINE 100mg p/o 2x/7days alternative regimens) 2a) ERYTHROMYCIN ETHYLSUCCINATE 800mg P/O 4x /7d or 2b)ERTHROMYCIN base 500mg p/o 4x/7days OR 2c)LEVOFLOXACIN 500mg p/o1x/7days or 2d)OFLOXACIN 300mg p/o 2x/7 days.
The overall sequence homology between HSV I and II is about 50% the tropism for each virus is?
HSV I has tropism for oral epithelium and HSVII has tropism for genital epithelium, although in some unique populations, HSV I is associated with genital infection than HSV II
The mediator for HSV infection
Attachment via ubiquitous(surface glycoproteins) receptors to cell: sensory neurons, leading to establishment of latency.
The HSV family comprises of large, DNA containing enviloped viruses and have identical morphology which cannot be distinguised from each other on the EM. the viridae structure include?
1) core: contains linear DNA 2)capsid: 162 capsomers that form icosadeltahedron 3) tegument: contains protiens including Virion Host Shutoff (VHS) 4)envelope: proteins and lipids 5) surface protein: glycosylated protein spikes: gB-gJ( no gF gK &gN)
Distributed world wide, it is the most common cause of genital ulcers in the USA. how is HSV transmitted?
Close contact via inoculation of virus into susceptible mucosal surfaces through small cracks in the skin: oropharynx, cervix, conjunctiva.
Increased age after onset of sexual activity and numbers of partners are independent factors associated with increased seroprevelance of HSV II antibodies. what is the distribution in men vs women?
Seropositivity to HSVII is more common in women 25% than in men 10%. HSV II genital infection in women can be an indication of sexual abuse.
The overall mortality rate associated with HSV infection is related to 3 situations?
1) perinatal infection 2) encephalitis 3) infection in immunocompromised.
HSV I and II are characerised by unique biological properties:
1) Neurovirulence: invade and replicate in nervous tissue 2) Latency: latent infection in nerve ganglion prox to site of infection 3)Reactiviation: in area supplied by ganglia where latency was established. may be induced via: fever, trauma, emotional stress, sunlingh and menstruation.
In HSV neurovirulence, the site of oral and genital infection are most commonly?
Oral :trigeminal ganglia genital: sacral nerve root ganglia (s2-s5)
Clinical HSV infections
1) acute herpetic gingivostomatitis(subclinical genital herpes; can also ne caused by HSV I) and pharyngotonsilitis( recurrent mucocutaneous HSV infection) 2) herpes labilis 3) herpetic whitlow 4) herpes gladiatorum 5) eczema herpeticum 6) genital herpes( primary and recurrent)
Differential diagnosis of HSV
1)candidiasis 2) chancroid 3) herpes zoster 4) syphilis 5) Bechet syndrome 6) HFMD
Primary genital herpes with incubation period of 3-7 days, can be caused by both HSV I and II which can be asymptomatic. more severe and complicated in women, primary genital herpes is characterised by?
Severe and prolonged systemic and local symptoms: fever, head aches, malaise and myalgia( prominent in first3-4 days). local symptoms include : itching, pain, dysuria, vaginal and urethral discharge and tender lymphadenopathy. primary HSV I protects or lessen the severity of HSV II or genital HSV I infection.
Clinical features in women
Herpetic vesicles appear: external genitalia, labia major/minor, vaginal vestibule and introitus. vesicles may rupture and tender ulcers. cervix may be involved in 70-90% of cases
Clinical features in men
Herpetic vesicles : glans penis, prepuce, shaft and sometimes scrotum, thighs, buttocks. herpetic Urethritis occur in 30-40% of men.
Lab diagnosis
1)tzank smear: multinucleated giant cells and epithelial cells with eosiniphilic intranuclear inclusion bodies distinguish herpesviruses 2)DFA rapid test 3)Molecular: pcr rapid for confirmatory test 4) cell line culture:
In genital herpes, diagnosis include
Viral culture pcr serology tzank prep
Treatment of genital HSV
1) nucleoside(guanosine) analog: antiviral triphosphate activity leads to DNA chain termination 2)acyclovir, valcyclovir, peniclovir, famciclovir: phosyphyrilation of parent compound by viral TK and cellular enzymes
With multiple serotypes of close to 140, where infected persons are asymptomatic, although mild symptoms presents as genital warts, the commonest STD in human is?
HUMAN PAPILLOMA VIRUS. persistent anogenital infection is strongly associated with invasive carcinoma of cervix, vulva, penis and anus
HPV produce epithelial tumors of the skin and mucous membranes. current classification correlates with 3 clinical categories which are:
1) anogenital or mucosal (latent, subclinical, clinical) 2) nongenital cutaneous 3) epidermodysplasia verruciformis
The etiology of HPV is such that?
Definitive cuase of anogenital warts. capsid lacks envelope making it resistant to treatment. no serotype of HPV due to lack of vitro culture methods. typing is based on genotype via melecular hybridization.
None enveloped virus of icosahedral symmetry with 72 capsomers that surround a genome containing doouble stranded DNA of apprx 8000 base pairs. these genome are divided into 3 functional regions:
1) (E) region: codes for 6 non structural genes associated with cellular transformation 2) (L) region: 2 structural protiens: L1 and L2 that form the capsid 3) (C) noncoding long control region: regulates replication and gene function
Production of viral particles CAN ONLY OCCUR IN HIGHLY DIFFERENTIATED KARATINOCYTES. The process of virus replication alters the character of the epidermis resulting in cutaneous or mucosal warts, it penetrates the basal layer and eventually is released at the surface; the modes of replication are?
STABLE replication of episomal genomes in BASAL CELLs RUNAWAY/VEGITATIVE replication in DIFFERENTIATED CELLS to generate progeny virus. note: viral genes are not activated until infected karatinocyte leaves basal layer.
An individual with plantar warts can spread the virus walking barefoot.this is because?
HPV virus can survive for many months and at low temperature without host.
HPV alone does not cause malignant transformation of infected tissues, co factors include:
Tobacco use, UV radiation, pregnancy, folate deficiency and immune suppression. people on immunosuppressive drugs and HIV infection are susceptible to HPV.
Risk factors of HPV
1) sexual activity 2) tobacooc smoking 3) oral contraceptive 4) chewing indian betel quid 5) UV and X-ray
Virtually all cases of cervical cancer are caused by
HPV, which also causes Anal cancer 90%, vulvar cancer 40%, vaginal cancer 40%, oropharyngeal cancer 12%, oral cancer 3%
Clinical presentation of HPV is associated with cauliflower like warts (anogenital warts) others include
Non anogenital mucous disease: oral wars nongenital cutanous HPV: common cutaneous warts epidermodysplasia verruciformis: autosomal recesssive familial trait
Lab diagnosis of HPV
DNA: hybrid cpature II and PCR acetic acid test tissue biopsy histologic findings
Hpv screening
Pap smear: high risk, sexualy active 1/yr, low risk 1/3 yrs
HPV treatment options
1)immune repsonse modifiers: Imiquimod and interferon alfa : used for external anogenital warts and condylomate acuminate 2)cytotoxic agents: podofilox, podophyllin, 5-fu. or chempdestructive/karatolytic agents: salicylic acid, trichloroacetic acid(TCA) bichloroacetic acid(BCA) are the only agents recommended for nongenital cutaneous warts.
HPV complications include
Meningitis, encephalitis and meningeoenciphalitis, cervical ca. STD complications in pregnancy.