1. Infectious Diseases

2. Viral Infections:
TRANSIENT VIRAL INFECTIONS:
 are structurally heterogeneous.
 elicits an immune response that eliminates the
virus and may or may not confer lifelong
protection.
 The mumps virus, for example, has only one
serotype and infects people only once.
 influenza viruses, can repeatedly infect the same
individual owing to antigenic variation.
 The immune response to respiratory syncytial
virus wanes with time, allowing even the same
serotype of virus to infect repeatedly

3. Measles:
 single-stranded RNA virus of paramyxovirus family
 spread by respiratory droplets, initially multiplies within
upper respiratory epithelial cells.
 then spreads to lymphoid tissues, where it can replicate
in mononuclear cells, including T lymphocytes,
macrophages, and dendritic cells.
 then spreads by blood throughout the body.
 Measles may cause croup, pneumonia, diarrhea, keratitis
with scarring and blindness, encephalitis(SSPE), and
hemorrhagic rashes ("black measles") in malnourished
children .

4. Morphology:
 blotchy, reddish-brown rash on face, trunk, and
proximal extremities produced by dilated skin vessels,
edema, and a moderate nonspecific mononuclear
perivascular infiltrate.
 Ulcerated mucosal lesions in oral cavity (the
pathognomonic Koplik spots) are marked by necrosis,
neutrophilic exudate, and neovascularization.
 The lymphoid organs: marked follicular hyperplasia,
large germinal centers, and randomly distributed
multinucleate giant cells (Warthin-Finkeldey cells)
which have eosinophilic nuclear and cytoplasmic
inclusion bodies are pathognomonic of measles and
are also found in lung and sputum

6. Mumps:
 member of paramyxovirus family.
 enter upper respiratory tract through inhalation
of respiratory droplets.
 spread to draining lymph nodes where they
replicate in lymphocytes (preferentially in
activated T cells).
 then spread through blood to salivary glands.
 Mumps virus also can spread to central nervous
system, testis, ovary, and pancreas.
 Aseptic meningitis is most common extra salivary
gland complication of mumps infection, occurring
in about 10% of cases.

7. Morphology:
 mumps parotitis: bilateral in 70% of cases,
affected glands are enlarged, have a doughy
consistency, and are moist, glistening, and reddish
brown on cross-section.
 On microscopic examination, the gland
interstitium is edematous and diffusely infiltrated
by macrophages, lymphocytes, and plasma cells,
which compress acini and ducts.

9.  mumps orchitis: testicular swelling caused by
edema, mononuclear cell infiltration, and focal
hemorrhages. swelling may compromise blood
supply and cause areas of infarction.
 Pancreas: lesions may be destructive, causing
parenchymal and fat necrosis and neutrophil-rich
inflammation.
 Mumps encephalitis.

10. Poliovirus Infection:
 spherical, unencapsulated RNA virus of enterovirus
genus.
 like other enteroviruses, is transmitted by fecal-oral
route.
 It first infects tissues in oropharynx, is secreted into
saliva and swallowed, and then multiplies in intestinal
mucosa and lymph nodes, causing a transient viremia
and fever.
 Although most polio infections are asymptomatic,
in about 1 of 100 infected persons poliovirus invades
central nervous system and replicates in
motor neurons of spinal cord (spinal poliomyelitis),
or brain stem (bulbar poliomyelitis).

11. Viral Hemorrhagic Fevers:
 VHFs are systemic infections characterized by fever
and hemorrhage.
 Caused by enveloped RNA viruses in four different
families: arena viruses, filo viruses, bunya viruses,
and flavi viruses.
 All depend on an animal or insect host for survival
and transmission. Humans are infected when they
come into contact with infected hosts or insect
vectors.
 human-to-human transmission can occur.
 There are no cures or effective drug therapy.
 VHF viruses are potential biologic weapons.

12.  The pathogenesis of hemorrhagic manifestations
are due to thrombocytopenia, or severe platelet
or endothelial dysfunction.
 there is increased vascular permeability.
 There may be necrosis and hemorrhage in many
organs, and often there is widespread
hepatocellular necrosis.

13. CHRONIC LATENT VIRAL INFECTIONS (HERPES
VIRUS INFECTIONS):
 Herpes viruses are large encapsulated viruses
that have a double-stranded DNA genome that
encodes approximately 70 proteins.
 Herpes viruses cause acute infection followed by
latent infection in which the viruses persist in
a noninfectious form with periodic reactivation
and shedding of infectious virus.
 There are nine types of human herpes viruses,
belonging to three subgroups :

14. α-group viruses: including herpes simplex virus-1
(HSV-1), HSV-2, and varicella zoster virus (VZV),
which infect epithelial cells and produce latent
infection in neurons.
β-group viruses: including CMV, human
herpesvirus 6 ( causes exanthem subitum which is
a benign rash of infants),and human herpesvirus7
(not yet associated with a specific disease).
γ-group viruses: KSHV/HHV-8 ( cause Kaposi
sarcoma).

15. Herpes Simplex Virus:
 HSV-1 and HSV-2 differ serologically but are genetically
similar and produce acute and latent infections.
 Both viruses replicate in skin and mucous membranes at
site of entrance of virus (usually oropharynx or genitals),
and cause vesicular lesions of epidermis.
 The viruses then spread to sensory neurons that
innervate these primary sites of replication, where
viruses establish latent infection.
Morphology:
 All HSV lesions are marked by formation of large pink to
purple intranuclear inclusions (Cowdry type A) that
contain intact and disrupted virions and push darkly
stained host cell chromatin to edges of nucleus.

17.  Gingivostomatitis: caused by HSV-1.
 Genital herpes: usually by HSV-2, but also HSV-1.
 Herpesvirus (usually HSV-2) can be transmitted to
neonates through birth canal of infected
mothers.
 HSV-1 is the major infectious cause of corneal
blindness.
 Herpes simplex encephalitis: by HSV-1 and HSV-2
 KSHV/HHV8 : Kaposi sarcoma.

18. Cytomegalovirus:
 β-group herpesvirus, can produce a variety of diseases
depending on age of host, and more important on host's
immune status.
 CMV causes a symptomatic or mononucleosis-like
infection in healthy individuals ,but devastating systemic
infections in neonates and in immunocompromised
patients.
 As its name implies, cytomegalovirus produces
enlargement of infected cells.
Infected cells exhibit gigantism of both entire cell and
its nucleus.
Within the nucleus is a large inclusion surrounded by
a clear halo (owl's eye).

20.  Transmission of CMV can occur by several
mechanisms :
• Transplacental transmission ("congenital CMV")
• Transmission of virus through cervical or vaginal
secretions at birth ("perinatal CMV")
• Transmission through saliva.
• Transmission by venereal route .
• Iatrogenic transmission through organ transplants
or by blood transfusions.

21. Varicella-Zoster Virus :
 Acute infection with VZV causes chickenpox( Varicella );
reactivation of latent VZV causes shingles ( zoster).
 In contrast to HSV, VZV is transmitted in epidemic
fashion by aerosols, disseminates hematogenously, and
causes widespread vesicular skin lesions.
 VZV infects neurons in dorsal root ganglia and may recur
many years after the primary infection, causing shingles.
 In contrast to numerous recurrences of HSV, VZV usually
recurs only once, most frequently in immunosuppressed
or elderly persons.

22. Morphology:
 The chickenpox rash occurs approximately 2 weeks
after respiratory infection and travels in multiple
waves centrifugally from the torso to head and
extremities.
 On histologic examination, chickenpox vesicles
contain intranuclear inclusions in epithelial cells like
those of HSV-1 .
 Shingles occurs when VZVs that have long remained
latent in dorsal root ganglia after a previous
chickenpox infection are reactivated and infect
sensory nerves

24. CHRONIC PRODUCTIVE VIRAL INFECTIONS:
 The immune system is unable to eliminate the
virus, and viral replication leads to persistent
viremia.
 The high mutation rate of viruses such as
HIV and hepatitis B may allow them to escape
control by immune system.

25. Hepatitis B Virus:
 significant cause of acute and chronic liver disease
worldwide.
 HBV is a DNA virus that can be transmitted
percutaneously (e.g., intravenous drug use or blood
transfusion), perinatally, and sexually.
 in chronic hepatitis: lymphocytic inflammation,
apoptotic hepatocytes and progressive destruction
of liver parenchyma.
 Long-term viral replication can lead to cirrhosis of
liver and an increased risk for hepatocellular
carcinoma.
 In some patients, immune response resulting in
establishment of a "carrier" state without progressive
liver damage.

27. TRANSFORMING VIRAL INFECTIONS:
includes viruses that causing human cancer:
Epstein-Barr virus (EBV), human papilloma virus (HPV),
HBV, and human T-cell leukemia virus-1 (HTLV-1).
Epstein-Barr Virus (EBV):
 causes infectious mononucleosis ( a benign self-limited
lympho proliferative disorder).
 Also hairy leukoplakia , certain lymphomas , and
nasopharyngeal carcinoma.
 Infectious mononucleosis is characterized by fever,
generalized lymphadenopathy, splenomegaly, sore
throat, and atypical T - lymphocytes (mononucleosis
cells) in blood .
 EBV is transmitted by close human contact( saliva ).

28. Morphology:
 peripheral blood : absolute lymphocytosis .
Many of these are large atypical lymphocytes
with an oval indented or folded nucleus, and
scattered cytoplasmic azurophilic granules .
 lymph nodes: discrete and enlarged throughout
the body principally in posterior cervical, axillary,
and groin regions.
On histologic examination expansion of
paracortical area ( T-cell area ).

30. Human Papillomaviruses (HPVs):
 Non- enveloped DNA viruses that are members
of papova virus family.
 Based on DNA sequence, papillomaviruses are
classified into over 100 types.
 Some HPVs cause warts, benign tumors of
squamous cells on skin ( papillomas ).
 Other HPVs are associated with warts that can
progress to malignancy, particularly squamous
cell carcinoma of cervix and anogenital area.

31.  Papillomaviruses are mainly transmitted by
skin or genital contact.
 HPVs infect squamous epithelial cells, but their
life cycle is not well understood since these
viruses cannot be cultured in vitro.
 In upper layers of stratified epithelium, HPV
leads to a characteristic perinuclear
vacuolization in epithelial cells (koilocytosis).

33. THANK YOU