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Hepatitis of microbial origin Flashcards

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1
Q

Hepatitis caused by what organisms besides virus?(2)

A

Bacterial

Fungal

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2
Q

Hepatitis caused in what bacterial disease?(2)

A

Any systemic bacterial infection:

  1. Leptospirosis
  2. Q fever (Coxiella burnetii)
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3
Q

hepatitis caused by what fungal disease?(3)

A

Histoplasmosis

Disseminated candidiasis

Invasive aspergillosis

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4
Q

LEPTOSPIROSIS
Causal agent

Transmission

Route

excreted

High risk group

A

Leptospira interrogans

Zoonosis of rodents, cattle, pets

fecal-oral route

Leptospirae excreted in urine

Veterinarians, 
pet shop
owners
Sewage workers
 Farmers
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5
Q
  1. Pathogenesis of LEPTOSPIROSIS

2. Outcome /Clinical Presentation

A

1.Entry through mucous membranes or skin–>bacteraemia to
liver, kidneys, CNS, lungs

  1. Outcome /Clinical Presentation
    a) PHASE 1 type 1 Anicteric leptospirosis –fever, chills, headache, myalgias- “Influenza-like illness”

b)PHASE 2: type 2Weil’s sydrome
1.aseptic meningitis
2.hepatitis
3.uraemia
4.haemorrhages
Mortality : 5%-40%

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6
Q

Diagnosis-investigation for LEPTO

A

Microbiological

  • Isolation of leptospirae
  • blood : first 1 - 2 weeks of illness
  • urine : several weeks to months
  • Culture & identification
  • Microscopy
  • Detection of antibodies-ELISA
  • LEPTO dipstick assay

Liver Function tests

  • Serum bilirubin : marked increase
  • Alkaline phosphatase : marked increase
  • Aminotransferases : moderate increase

Urine examination

  • Microscopic changes
  • Proteinuria
Blood tests
* Leucocytosis :  marked
* Thrombocytopaenia
\: mild
* ESR : elevated
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7
Q

LEPTO Prevention

A 
Avoid contact : Skin / Mucous membrane
* Occupational hazard
* Pre or Post exposure prophylaxis
\: Doxycycline 200 mg per week
\: Period of potential exposure
* Vaccination: Human - Killed whole cell leptospiral vaccine
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8
Q

1.Viral Hepatitis

A,B,C,D,E,F,G?

2.What are hepatitis other than A & B called?

A 
1. Infectious-A
 Serum-B, D
Parentally-C
Enterically-E
Others- F,G
  1. non-A non-B (NANB
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9
Q

State for HEP A B C D E F G:

virus name

virus family

dna/rna

envelope

A

HAV : Hepatovirus : Picornaviridae : RNA : Env (-)

HBV : Orthohepadnavirus : Hepadnaviridae : DNA: Env (+)

HCV : Hepacivirus : Flaviviridae : RNA: Env (+)

HDV : Deltavirus : Deltaviridae : RNA: Env (+)

HEV : Hepevirus : Hepeviridae : RNA: Env (-)

HFV : Uncertain : :DNA:

HGV : Flaviviridae : RNA: Env (+)

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10
Q

A

1.Source of
virus

2.Route of
transmission

3.Chronic
infection

4.Prevention

A
  1. feces
  2. fecal- oral
  3. not chronic
  4. pre/post exposure/ immunization
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11
Q

B

1.Source of
virus

2.Route of
transmission

3.Chronic
infection

4.Prevention

A
  1. blood/ Blood derived body fluids
  2. Body contact
  3. yes
  4. pre/post exposure/ immunization
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12
Q

C

1.Source of
virus

2.Route of
transmission

3.Chronic
infection?

4.Prevention

A
  1. blood/ Blood derived body fluids
  2. Body contact
  3. yes
  4. blood donor Screening, risk behavior modification
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13
Q

D

1.Source of
virus

2.Route of
transmission

3.Chronic
infection?

4.Prevention

A
  1. blood/ Blood derived body fluids
  2. Body contact
  3. yes

4.pre/post exposure
/ immunization, risk behavior modification

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14
Q

E

1.Source of
virus

2.Route of
transmission

3.Chronic
infection?

4.Prevention

A
  1. feces
  2. fecal- oral
  3. no
  4. Drink safe water
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15
Q

F

1.Source of
virus

2.Route of
transmission

3.Chronic
infection?

4.Prevention

A
  1. feces
  2. fecal- oral
  3. UNKNOWN
  4. Drink safe water
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16
Q

G

1.Source of
virus

2.Route of
transmission

3.Chronic
infection?

4.Prevention

A
  1. blood/ Blood derived body fluids
  2. Body contact
  3. UNKNOWN
  4. risk behavior modification
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17
Q

Hepatitis A Virus

  1. Virus family
  2. virus shape
  3. presence of envelope
  4. DNA/RNA (SS OR DS?)
  5. Incubation period

6.Jaundice by
age group

  1. Complications
A

Picornaviridae

Icosahedral symmetry

Envelope (-)

ssRNA

Average 30 days
Range 15-50 days

> 14 yrs

Fulminant hepatitis
(acute liver failure)  Cholestatic hepatitis  Relapsing hepatitis
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18
Q

PATHOGENESIS OF HEPATITIS A

A

Virus replicates in GI tract —>blood stream—>liver

Infected hepatocytes damaged by cytotoxic T cells

Infection cleared, no chronic infection, no carrier

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19
Q

Clinical Course of hepatitis A

symptoms of most infections

incubation period length

presence of chronic hepatitis

liver cancer presence

A

Most infections are asymptomatic

Fever, anorexia, nausea, vomiting and jaundice
Incubation Period : short (2 - 5 week)

No chronic hepatitis

No predisposition to liver cancer

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20
Q

Typical Serological Course of Hep A

A

SLIDE

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21
Q

Laboratory Diagnosis

HEP A

A

Acute infection is diagnosed by the detection of HAV-IgM in serum by EIA.
Past Infection i.e. immunity is determined by the detection of
HAV-IgG by EIA.

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22
Q
  1. Hepatitis A Virus Transmission
  2. Who are reservoirs?
  3. Who are commonly infected?
A

Close personal contact
(e.g., household contact, sex contact, child day care centers)
Contaminated food, water
(e.g., infected food handlers, raw shellfish)
Blood exposure (rare)
(e.g., injecting drug use, transfusion)

Humans are the only reservoirs
Children are more commonly infected

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23
Q

Specific Measures HEP A

A

Inactivated HAV vaccine (ACTIVE IMMUNITY)
Immune serum globulin (PASSIVE IMMUNITY)
Combined active & passive immunity

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24
Q

Hep B morphology

  1. what particles present?
  2. describe these particle:
    - shape

infectious?

A
  1. non infectious spherical particle HBsAg
  2. non infectious tubular filaments of various lengths
  3. infectious dane particle with outer envelope and
    nucleocapsid containing protein, DNA genome and DNA polymerase
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25
Structural components of HBV
Hepatitis B Surface Antigen Hepatitis B Core Antigen Hepatitis B "e " Antigen Viral DNA
26
Clinical Course HEP B 1. incubation period 2. symptoms of infection 3. what levels are elevated/ decreased? 4. spectrum of disease
1.Incubation Period : long (6 - 24 weeks) 2. Many infections are asymptomatic Fever, anorexia, nausea, vomiting, jaundice 3. Elevated transaminase levels 4. Wide range of disease spectrum
27
Incubation period of hep B
60-90 days
28
Flow of Acute HBV infection
slide
29
Spectrum of Chronic Hepatitis B Diseases
1Chronic Persistent Hepatitis - asymptomatic Chronic Active Hepatitis - symptomatic exacerbations of hepatitis Cirrhosis of Liver Hepatocellular Carcinoma
30
PATHOGENESIS of HEP B 1. how it enters body and what happens in body 2. can predispose to?
1.Virus enters via skin/mucosa blood stream liver Infected hepatocytes damaged by cytotoxic T cells Chronic infection/ carrier state in 5 – 10 % of patients 2. Chronicity predisposes to hepatocellular carcinoma
31
Typical Serologic Course of Acute Hepatitis B Virus Infection with Recovery
Three antigen-antibody system 1) HBsAg-- anti-HBs system: HBsAg appears 1-2 weeks (late to 11-12 weeks) after exposure, persists for 1-6 weeks( even 5 months) in acute hepatitis B. In chronic patients or carrier, HBsAg persist many years HBsAg antigencity but no infectivity HBsAg is the marker of infectivity HBsAg can be found in humors and secretions: salive, urine, semina, tears, sweat and breast milk Anti-HBs appear after HBsAg disappear several weeks (or months) anti-HBs is protective antibody, can persist for many years 2 . HBcAg—anti-HBc system HBcAg can be found in the nuclei of liver cells, no free HBcAg in serum HBcAg is the marker of replication of HBV The stage called window phase Anti-HBc IgM is a marker of acute infection and acute attack of chronic infection of HBV. Anti-HBc IgG is the marker of past infection, high titer means low level replication of HBV 3. HBeAg—anti-HBe system HBeAg is a soliable antigen HBeAg is a reliable indicator of active replication of HBV Anti-HBe is a marker of reduced infectivity. If exist long may be a marker of integration of HBV into liver cell
32
Progression to Chronic Hepatitis B Virus Infection
slide
33
Concentration of Hepatitis B Virus in Various Body Fluids 1. high in ? 2. moderate in ? 3. Low/ not detectable in?
1. blood, serum, wound exudate 2. semen, vaginal fluid, saliva 3. urine, feces, sweat, tears breastmilk
34
Hepatitis B Virus | Modes of Transmission
Sexual - sex workers and homosexuals are particular at risk. Parenteral - IVDA, Health Workers are at increased risk. Perinatal - Mothers who are HBeAg positive are much more likely to transmit to their offspring than those who are not. Perinatal transmission is the main means of transmission in high prevalence populations.
35
Treatment of hep b
Chronic HB treatment goals-Suppression of virus, Prevention of drug-resistant strains and Remission of liver disease Interferon - for HBeAg +ve carriers with chronic active hepatitis. Response rate is 30 to 40%. Lamivudine - a nucleoside analogue reverse transcriptase inhibitor. Well tolerated, most patients will respond favorably. However, tendency to relapse on cessation of treatment. Another problem is the rapid emergence of drug resistance. Successful response to treatment will result in the disappearance of HBsAg, HBV-DNA, and seroconversion to HBeAg.
36
3 Prevention hep b
1.Vaccination - highly effective recombinant vaccines are now available. Vaccine can be given to those who are at increased risk of HBV infection such as health care workers. It is also given routinely to neonates as universal vaccination in many countries. 2. Hepatitis B Immunoglobulin - HBIG may be used to protect persons who are exposed to hepatitis B. It is particular efficacious within 48 hours of the incident. It may also be given to neonates who are at increased risk of contracting hepatitis B i. e. whose mothers are HBsAg and HBeAg positive. 3. Other measures - screening of blood donors, blood and body fluid precautions.
37
``` HCV Family Genus Morphology RNA STRAND , ENVELOPE Genotypes ```
Family :Flaviviridae Genus : Hepacivirus Morphology: ``` 55-65 nm : Icosahedral symmetry : Enveloped : Single-strand RNA ``` Six : Determine potential response to therapy
38
Hepatitis C - Clinical Features 1. Incubation period 2. Clinical illness (jaundice): 3. Chronic hepatitis: 4. Persistent infection: 5. Immunity:
1.Average 6-7 wks Range 2-26 wks 2. 30-40% (20-30%) 3. 70% 4. 85-100% 5.No protective antibody response identified
39
Clinical Manifestations HEP C
Fever, anorexia, nausea, vomiting Jaundice * Milder than hepatitis B
40
NATURAL HISTORY OF HEP C INFECTION
SLIDE
41
DESCRIBE Chronic Hepatitis C Infection
The spectrum of chronic hepatitis C infection is essentially the same as chronic hepatitis B infection. All the manifestations of chronic hepatitis B infection may be seen, albeit with a lower frequency i.e. chronic persistent hepatitis, chronic active hepatitis, cirrhosis, and hepatocellular carcinoma.
42
DESCRIBE SEROLOGICAL OF HCV ACUTE INFECTION TITRE: SYMPTOMS HCV RNA ANTI HCV ALT
SLIDE
43
7 Risk Factors Associated | with Transmission of HCV
1. Transfusion or transplant from infected donor 2. Injecting drug use 3. Hemodialysis (yrs on treatment) 4. Accidental injuries with needles/sharps 5.Sexual/household exposure to anti-HCV-positive contact 6. Multiple sex partners 7. Birth to HCV-infected mother
44
3. Laboratory Diagnosis HCV
HCV antibody - generally used to diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears. HCV-RNA - various techniques are available e.g. PCR and branched DNA. May be used to diagnose HCV infection in the acute phase. However, its main use is in monitoring the response to antiviral therapy. HCV-antigen - an EIA for HCV antigen is available. It is used in the same capacity as HCV-RNA tests but is much easier to carry out.
45
2 Treatment OF HCV
Interferon - may be considered for patients with chronic active hepatitis. The response rate is around 50% but 50% of responders will relapse upon withdrawal of treatment. Ribavirin - there is less experience with ribavirin than interferon. However, recent studies suggest that a combination of interferon and ribavirin is more effective than interferon alone.
46
3 Prevention of Hepatitis C
1. Screening of blood, organ, tissue donors 2. High-risk behavior modification 3. Blood and body fluid precautions
47
Hepatitis D (Delta) Virus 1. DESCRIBE STRUCTURE 2. Genus : 3. REPLICATION 4. CO-INFECTION
SLIDE 1. -Spherical virion - Envelope (HBsAg) 2. DELTA VIRUS 3. In vivo replication 4. coinfection with HBV
48
1. PATHOGENESIS OF HEP D 2. CLINICAL COURSE SEVERITY 3. MORTALITY
1. Virus enters via skin/mucosa blood stream liver 2. Defective virus : Replicates only in presence of HBV 3. Infected hepatocytes damaged by cytotoxic T cells 4. Coinfection with HBV & HDV 5. Clinical course : more severe 6. Mortality : higher
49
Hepatitis D - Clinical Features 2 TYPES PF CLINICAL FEATURES
1. Coinfection severe acute disease. low risk of chronic infection. 2. Superinfection usually develop chronic HDV infection. high risk of severe chronic liver disease. may present as an acute hepatitis
50
4. Hepatitis D Virus Modes | of Transmission
Percutanous exposures injecting drug use Permucosal exposures sex contact
51
HBV-HDV Typical COINFECTION Serologic Course TITRE : Symptoms ALT
SLIDE ALT ELEVATED
52
HBV - HDV SUPERINFECTION Typical Serologic Course
SLIDE
53
LABORATORY DIAGNOSIS 1. FOR HDV 2. HBV
1. HDV 2.Total anti-HDV / IGM antibodies 3.Detection of delta antigen in serum 4. HBV * Serologial markers for HBV infection Monitor ongoing HDV infection : HDV-RNA: Reverse transcriptase-PCR (RT-PCR)
54
Hepatitis D - Prevention
1.HBV-HDV Coinfection Pre or postexposure prophylaxis to prevent HBV infection. 2.HBV-HDV Superinfection Education to reduce risk behaviors among persons with chronic HBV infection
55
Hepatitis E Virus GENUS: SHAPE ENVELOPE RNA SS OF DS
Hepevirus Icosahedral : Non-enveloped : Diameter 34 nm : Single strand of RNA
56
1. Pathogenesis OF HEP E 2. Clinical course 3. Most infections are 4. CLEARANCE OF INFECTION 5. chronic infection, carrier
1. Virus replicates in GI tract -->blood stream--> liver 2. 2-4 weeks 3. asymptomatic/mild 4. Infection cleared completely No chronic infection, no carrier
57
CLINICAL FEATURES HEP E: Incubation period: Case-fatality rate: Illness severity: Chronic sequelae
1. Average 40 days Range 15-60 days 2 .Overall, 1%-3% 3. Pregnant women, 15%-25% 4. Increased with age 5. None identified
58
TYPICAL SEROLOGICAL COURSE OF HEP E
SLIDE
59
LABORATORY DIAGNOSIS HEP E
Serum : anti-HEV IgM anti-HEV IgG HEV RNA Stool : HEV-RNA
60
TRANSMISSION OF HEP E
Ingestion : Faecal - oral route Associated with large water – borne outbreaks
61
2 Prevention and Control Measures for Travelers to HEV-Endemic Regions
Avoid drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveler. Recombinant hep. E vaccine-HEV 239
62
VIRAL HEPATITIS F AKA? TRANSMISSION IDENTIFIED IN? USING?
Non A – E hepatitis Transmitted through fecal - oral route Can be identified in stool samples- Electron microscopy
63
1. HEP G AKA? 2. ASSOC WITH 3. FAMILY OF VIRUS 4. TRANSMISSION 5. MOST INFECTIONS ARE ? (SYMPTOMS)
Hepatitis G Virus HGV, now known as GBV-C Associated with post-transfusion hepatitis Member of Flaviviridae Parenteral, sexual, vertical transmission Most infections are asymptomatic / mild
64
PATHOGENESIS OF HEP G 1. REPLICATION PRIMARILY IN ? POORLY IN? 2. SURVIVAL... WHY?
Replicates primarily in lymphocytes Replicates poorly in hepatocytes HIV patients with GBV-C : survive longer- Slows progression of HIV infection
65
DIAGNOSIS HEP G
Anti-HGV antibody | HGV RNA- RT-PCR
66
1.WHICH VIRUS REPLICATE IN LIVER? 2. Which viruses cause elevated liver Enzyme level? 3. Viral haemorrhagic fever By what viruses ? 4. Hepatitis is major feature of ?
1. Herpesviruses- HSV, CMV, EBV- 2. AdV, coxsackieviruses, measles- 3. YFV, Marburg, Ebola virus, Lassa virus, Crimean- Congo hemorrhagic fever 4. Hepatitis is major feature of most disseminated viral infection in neonates and immunocompromised patient

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