Infectious Diseases

HEPATITIS

HAV
-acute infection: <6 months
-transmission: fecal + oral route
-structures: no envelope + single stranded RNA

HBV
-acute + chronic
-transmission: sex + blood + perinatal  detected in:
saliva + tears + sweat + semen + breastmilk
-structure: envelope + double stranded DNA
-incubation period 2-6 months

HCV
-acute + chronic
-transmission: sex + blood + perinatal
-structure: envelope + single stranded DNA
-no vaccine for that until now

HDV
-chronic
-transmission: sex + blood + perinatal
-need HBV requires HBsAg to enter the hepatocytes:
 Co-infection: HBV and HDV
 Super-infection: HBV infect the cell than comes later HDV
-structure: envelope + single stranded RNA
-vaccine for HBV protects against HDV
-someone who has HDV that means he has also HBV !!!

HEV
-acute
-transmission: fecal + oral
-structure: no envelope + single stranded RNA
- no vaccine for it until now
- Pregnant women with hepatitis E are at increased risk of acute liver failure, fetal loss and
mortality  Fulminant hepatitis !!

Stages + Symptoms & Signs

1. Prodromal Phase (uncharakteristisches Anfangsstadium einer Erkrankung): fever +

malaise + vomiting + nausea + dehydration + electrolyte changes + weight loss +
diarrhea:
o liver damage  produce cytokines: IL1 + IL6 + TNF-alpha  blood
circulation  CNS  trigger prostaglandin: PGE2 + PGF2  fever + malaise
 o hepatotoxins  blood stream  CNS  chemo trigger zone  activate:
emetic center  GIT  vomiting + nausea  dehydration  electrolyte
changes  weight loss also diarrhea
2. Icteric Phase: icterus + dark urine + pale stool + hepatomegaly + increase PTT +
decreased INR/PT
 more damage of liver cells  high uncunj. Bilirubin + high conjucated
bilirubin

-normally: Hb  hem  uncunj. Bilirubin UCB  lever  cunjo. Bilirubin CB)

-in case of lever damage  in biliary system  biliary salts to blood  high bile
acids in blood
-UCB + CB + bile acids they accumulate in sclera  yellow  icterus
-also UCB + CB deposits in skin  hands: palms + soles
-also in kidney: more CB will filtrate  CB in urine  dark urine appearance
-low lever activity  reduce bile production  decrease bilirubin  in gut: less
urobilinogen  less stercobilin  clay colored stool (pale)
-liver damage  inflammation  lot of immune cells + more blood flow 
hepatomegaly  right upper quadrant pain

 liver damage  liver enzymes to blood:

o increase of: AST + ALT + ALP + GGT:
 viral hepatitis + drug induced liver injury + ischemic hepatitis
 ALT > AST
 alcoholic hepatitis: AST > ALT
o decrease of clotting proteins: intrinsic: increase PTT + extrinsic: low
INR/PT

-virus  immune system reaction  plasma cells produce AB against virus  AB + Virus
bind together and form: immune complex  deposits in:
 synovial joints  arthritis
 in vessels  vasculitis  polyarthritis nodosa (HBV)
 in pericardium & myocardium  myocarditis + pericarditis
 in glomerulo BM  GN
 platelets + erythrocytes + neutrophiles  thrombocytopenia + hemolytic
anemia + neutropenia
 in viral infection  high lymphocytes

3. Convalescence phase = resolving phase

-in chronic infection in HBV + HCV + HDV  infect the cell  cell death:
1. increase fibrosis formation  increase cirrhosis
2. increase mitosis  high risk for mistake in replication  increase dysplasia 
increase hepatic cancer
Serology:

HAV & HEV:

-IgM antibody  active infection
-IgG antibody  recovery

HBV (s=surface + e=envelope + c=core)

-HBsAg if positive  infection

-HBeAg if positive  increase replication + increase infection poor prognosis + high
transmissibility
-HBcAg: not measured (not in blood only after biopsy)  we measure AB against it
-HBV DNA if positive  increase replication + increase infection

-Anti-HBs if positive  pat. is cured or vaccinated

- Anti-HBe if positive  decrease replication + decrease infection  low transmissibility
-Anti-HBc if positive  IgM: acute infection + IgG: chronic
-in the beginning we will have Ag and then AB !!

-The “window period” refers to that period in infection when neither hepatitis B surface
antigen (HBsAg) nor its antibody (HBsAb) can be detected in the serum of the patient. It is an
immunologically mediated phenomenon caused by the precipitation of antigen-antibody
complexes in their zone of equivalent concentrations and, thereby, their removal from the
circulation BUT positive for HBcAb and HBeAb.
-window period:
 Negative: HBsAg + HBsAb
 Positive: HBcAb + HBeAb

HCV

1. Check blood for HCV-AB (IgG) if positive  PCR (HCV-RNA) if positive  infection 
acute: positive <6 months & chronic: positive >6 months
-if negative PCR (HCV-RNA)  cleared virus

-if pat. has chronic HCV  3 options:

1. liver biopsy: invasive
2. fibrosure test: expensive
3. APRI score = AST to Platelet Ratio Index score  determines the likelihood of
hepatic fibrosis and cirrhosis in patients with
Hepatitis C
((AST pat. [IU/L] ÷ AST standard [IU/L]) ÷ platelet count × 10 9/L) x 100
Result: APRI >1.5  high risk for fibrosis

Differential Diagnosis:
1. With other forms of hepatitis: alcoholic + drug-induced + acute biliary obstruction +
autoimmune + idiopathic + fatty liver
2. Cytomegalovirus
3. Epstein-Barr virus
4. Herpes simplex virus

Management:

1. HAV: no specific treatment, hygiene

2. HBV:
 Acute: symptomatic + entecavir or tenofovir for persistent HbeAg beyond 12
weeks
 Chronic:
o Interferons
o Antiviral drugs: entecavir + tenofovir  first line

3. HCV:
 Acute: monitoring HCV RNA for few weeks  if viral load is falling  not
treatment required
 Chronic: sofosbuvir/velpatasvir or sofosbuvir/ledipasvir

4. HEV: ribavirin
MENINGITIS

Signs & Symptoms:

 Fever
 Headache
 Stiff neck
 Change in mental status  GCS <14
 Photosensitivity
 Seizures

Signs:
 Nuchal rigidity
 Kernigs sign
 Brudzinski sign

 Fundoscopic findings: papilledema + absent

venous pulsations

 Focal neurologic deficits: hemiparesis + aphasia

+ CN palsies + visual field cuts

 Sinus tenderness + clear rhinorrhea

 Skin findings: petechial rash  in case of Neisseria

meningitis  gram positive bacilli !!

Causes:
1. Strep pneumoniae: most common cause beyond
neonatal period
-osler triad: meningitis + pneumonia + endocarditis  Austrian syndrome

2. Neisseria meningitidis: most common cause of meningitis in adolescents

-petechiae + purpura
-especially affect pat. With c5-c9 deficient +splenectomy + immunosuppressed
-transmitted through: contaminated dairy + raw vegetables

3. Staph. Aureus: neurosurgical intervention

4. Haemophilus influenzae
5. Cryptococcus  in HIV pat. With CD4 <100
6. Viruses  aseptic menintigitis