Viral infections in the craniofacial region.

1. KIMATHI DENIS
1

2. INTRODUCTION
Many of the systemic diseases are caused by a wide range of bacteria, viruses and
fungal organisms.
Some of these microbial diseases can exhibit oral manifestations, however some
are localized in the oral cavity.
Orofacial viral infections may be less common but appear in different clinical
forms and affect all age groups.
Infection from a virus follows a different aetiopathogenic pathway compared with
bacteria, fungi and other organisms, as a virus metabolism is dependent on host
cells.
In general, most of the viral infections of the orofacial region are self-limiting in
an otherwise healthy individual, whilst compromised individuals may present
with a myriad of local and systemic complications of viral infections.
2

3. CAUSATIVE ORGANISMS
o The common viral infections affecting the orofacial region include:
1. Herpes group of viruses
 Alpha herpes viruses – HSV-1, HSV-2 and VZV
 Beta herpes viruses – CMV, HHV-6 and HHV-7
 Gamma herpes viruses – EBV and HHV-8
2. Human Immunodeficiency Virus
3. Human Papilloma Virus
4. Coxsackle Virus.
5. Mumps Virus
3

4. 1. HERPES GROUP OF
VIRUSES
Herpes viruses are double stranded DNA viruses.
Herpes viruses are a leading cause of human viral disease, second only to
influenza and cold viruses
It is estimated that out of the 80 known herpes viruses at least 8 are known to
infect human beings.
They belong to the family Herpesviridae which is divided into three subfamilies –
alpha, beta and gamma viruses.
Orofacial viral infections are common among immunocompromised patients; the
most common being those caused by the herpes simplex virus (HSV)
4

5. Human herpes
type
Name Sub Family Target cell type Latency Transmission
1
Herpes simplex-1
(HSV-1)
Alphaherpesvirina
e
Mucoepithelia Neuron Close contact
2
Herpes simplex-2
(HSV-2)
Alphaherpesvirina
e
Mucoepithelia Neuron
Close contact
usually sexual
3
Varicella Zoster
virus (VZV)
Alphaherpesvirina
e
Mucoepithelia Neuron
Contact or
respiratory route
4
Epstein-Barr
Virus (EBV)
Gammaherpesviri
nae
B lymphocyte,
epithelia
B lymphocytes Saliva
5
Cytomegalovirus
(CMV)
Betaherpesvirina
e
Epithelia,
monocytes,
lymphocytes
Monocytes,
lymphocytes and
possibly others
Contact, blood
transfusions,
transplantation,
congenital
6
Herpes
lymphotropic
virus
Betaherpesvirina
e
T lymphocytes
and others
T lymphocytes
and others
Contact,
respiratory route
7
Human herpes
virus-7 (HHV-7)
Betaherpesvirina
e
T lymphocytes
and others
T lymphocytes
and others
Unknown 5

6. 8
Human herpes
virus-8 (HHV-8)
Kaposi's
sarcoma-
associated
herpes virus
(KSHV)
Gammaherpesvir
inae
Endothelial cells Unknown
Exchange of
body fluids?
6
Source - http://www.microbiologybook.org/

7. ALPHA HERPES VIRUS
INFECTIONS HERPES SIMPLEX VIRUSES INFECTIONS
 AETIOLOGY AND PATHOGENESIS
Caused by two types of DNA viruses namely; HSV-1 and HSV-2.
Characteristically HSV-1affects the areas above the waistline, and HSV-2
mainly causes genital lesions or lesions below the waistline, although HSV-1
and -2 can affect either area.
HSV needs physical contact for transfer of infection.
The incubation period ranges from 2days to 3 weeks.
Primary infection of HSV-1 occurs either during childhood as gingivostomatitis
or, if not exposed, then as pharyngotonsilitis in an adult. Latent reactivation of
HSV-1 most commonly manifests as herpes labialis (or the common cold sore)
or as atypical forms (intraoral herpes) in an immunocompromised individual.
7

8. After primary infection the virus hides within trigeminal ganglia and becomes
activated when the environment is conducive for viral replication.
Factors that may trigger recurrent infections include: immunosuppression, stress,
trauma, exposure to sunlight(UV light), changes in weather especially colder
months and menstruation.
8

9. CLINICAL FEATURES
Primary infection is common among children and young adults, either
asymptomatic or in the form of gingivostomatitis, following a usual course of fever,
headache, irritability, loss of appetite, lethargy, hypersalivation and regional
lymphadenopathy (especially submandibular and superficial cervical group of
nodes are involved).
Most of the individuals who suffer from recurrent herpes labialis will experience a
prodromal phase of tingling, burning sensation, itching, mild pain and/or fever.
Upper respiratory tract infection may precede the onset of the disease
Clinically, single or multiple small erythematous papules develop and form
vesicles that appear on either upper or lower lip, which may or may not coalesce.
They will either rupture or may heal by crusting, leaving no noticeable scar in
most circumstances.
9

10. An atypical clinical presentation may occur in immunocompromised patients.
The healing may be prolonged with pain in the immunocompromised patient.
There may be widespread vesicles with ulcerations involving large areas of the
lip mucosa and adjacent cutaneous surfaces of the peri-oral region.
Herpetic Whitlow and Herpes gladitorium are herpes simplex lesions affecting
the fingers/ toes and in the bodies of wrestlers or sportsmen(contact sports)
respectively.
10

11. DIAGNOSIS
 Diagnosis is clinical but laboratory confirmations may be needed in atypical
cases and immunocompromised patients.
 Laboratory confirmations include:
1. Cytological smears
o Requires deroofing a fresh vesicle, followed by scraping of the base of the lesion and
the smear stained with Papanicolaou’s, Wright’s or Giemsa’s stain.
o Characteristic findings include presence of multinucleated giant cells and
intranuclear viral inclusion bodies eg Lipschutz bodies or Cowdry Type A.
The cells exhibit ballooning degeneration.
2. Serological tests – detect antibodies in the pt suffering from primary HSV.
3. Viral isolation – one of the most definitive methods of identifying HSV.
4. Biopsy – microscopy reveals ulcerated epithelium with large keratinocytes showing
glassy giant marginated nuclei (Tzanck cells)
11

12. TREATMENT
Both primary and secondary or recrudescent infections are self-limiting.
Antiviral treatment is often recommended for the immunocompromised and in
moderate to severe infection in otherwise healthy individuals.
Systemic acyclovir, 200 mg, 5 times daily for 7 days or topical application of 5%
acyclovir cream every four hours for 5 days is the recommended dose.
Valacyclovir 1−2 milligrams twice daily may be used as a prophylactic treatment,
which is most effective when initiated early during the prodrome phase.

12

13. VARICELLA ZOSTER
INFECTIONS
Chickenpox is the primary infection in childhood due to VZV as a droplet infection
from the nasopharynx.
If a child is not exposed during childhood, an overt infection may occur during
adulthood.
Chickenpox can have orofacial lesions such as vesicles, especially over the facial
skin and the oral mucosa, in addition to the cutaneous lesions of the trunk. If not
secondarily infected, usually the lesions on the facial skin will heal without
scarring.
13

14. After chickenpox, VZV remains latent in sensory ganglia until reactivation and
replication, resulting in herpes zoster (shingles).
Herpes zoster affects those above the age of 50 years or the
immunocompromised and is characterized by a unilateral, distinctive painful
vesicular rash over a dermatome, corresponding to the sensory ganglion where
the VZV was latent.
 Orofacial manifestations are within the ophthalmic, maxillary and mandibular
nerve distribution of the trigeminal nerve, with maxillary and mandibular
causing intra-oral vesicles and painful ulcerations.
Clinical appearance of these lesions is very similar to herpes simplex except for
the unilateral location.
14

15. 15

16. COMPLICATIONS ASSOS.
WITH HERPES ZOSTER
1. Post – herpetic neuralgia
 The most common complication.
 The pain continues to persist even when the herpetic lesions have resolved.
 Pain typically presented as sharp or burning pain.
 Usually seen in individuals over 5th decade of life.
2. Generalized involvement of herpes zoster
 Herpes zoster is generally unilateral. However in immunocompromised individuals or an
associated malignancy, herpes zoster can exhibit a generalized involvement.
3. Zoster ophthalmicus
 Seen when herpes zoster involves the ophthalmic ganglion of the trigeminal nerve.
 Pts present with painful inflammatory condition of the eye along with impaired vision or
transient blindness.
16

17. 4. Ramsay Hunt Syndrome
 It’s one of the rare manifestations of HZV infection where geniculate ganglion is
involved.
 The facial and auditory nerves can be involved.
 The condition is characterized by facial paralysis, pain and vesicles in the external
auditory canal and pinna of the ear and the oral cavity.
 Associated findings are tinnitus, vertigo and ipsilateral hearing loss.
5. Zoster Sine Herpete
 A phenomenon where some individuals exhibit only prodromal symptoms of pain and
paresthesia without the development of a visible cutaneous rash.
6. Other relatively uncommon complications involve
 Encephalitis
 Peripheral nerve palsies
 Myelitis.
17

18.  INVESTIGATIONS
Cytological smears derived from vesicles reveal multinucleated giant cells
along with intranuclear inclusion bodies.
PCR and Immunofluorescence assay are more effective in diagnosing HZV
infections.
 DIFFERENCIAL DIAGNOSIS
Recurrent herpetic lesions and aphthous ulcers should be considered in the
differential diagnosis of intraoral lesions.
 TREATMENT
In healthy pts, if diagnosis occurs within 72hrs of initiation of the disease
course of acyclovir or valacyclovir can be administered.
If the pt is seen later during the course of the dx, symptomatic relief in the
form of magic mouthwash can be prescribed.
In immunosuppressed patients a prescription of acyclovir or valacyclovir can be
administered
18

19. BETA HERPES VIRUS
INFECTIONS
 1. CYTOMEGALOVIRUS (CMV)
Primary infection can be transmitted via exposure to saliva, genital secretions,
blood or tissue, and perinatally.
After primary infection, it establishes latency in the host after the acute infection
in monocytes, lymphocytes and possibly others.
 Reactivation from latent infection can occur with immunosuppression, such as
HIV infection, transplantation, or acute illness.
19

20. CLINICAL
MANIFESTATIONS
Clinically, primary infection with CMV in immunocompetent individuals may
manifest as asymptomatic illness or benign CMV mononucleosis.
CMV mononucleosis is characterized by fever, malaise, lymphadenopathy.
In contrast with EBV, CMV mononucleosis is not typically associated with
exudative tonsillopharyngitis.
CMV esophagitis can present as odynophagia and dysphagia.
CMV retinitis is more commonly seen in patients with advanced
immunosuppression, such as with HIV/AIDS.
HIV-infected patients with CD4 fewer than 50 cells/mm3 are at risk for CMV
retinitis.
20

21. 21

22. DIAGNOSIS
Lab findings of lymphocytosis and atypical lymphocytes in CMV IM.
The heterophil agglutinin test is negative in CMV mononucleosis and positive in
EBV mononucleosis.
The diagnosis is established by detection of intranuclear inclusion body in tissue.
CMV detected by PCR supports the diagnosis.
CMV retinitis diagnosis is made by clinical appearance. White fluffy retinal
infiltrate with hemorrhage that can be appreciated on funduscopic examination
22

23. MANAGEMENT
CMV mononucleosis is self-limited and is managed by supportive care.
On the other hand, CMV disease, such as CMV esophagitis and CMV retinitis,
requires antiviral treatment with either intravenous ganciclovir or oral
valganciclovir.
 In patients with HIV/AIDS, initiation of anti-retroviral treatment will allow
recovery of CMV-specific, T cell–mediated immunity.
23

24. 2. HUMAN HERPESVIRUS-6
 Human herpesvirus-6 is one of the first, so called ‘ancient’ human herpes
viruses identified by molecular characterization.
 The main mode of viral transmission is through contaminated saliva.
 The primary infection is usually asymptomatic and commonly occurs during
childhood by age 2 years.
 The clinical form is called exanthema subitum or roseala infantum or ‘sixth
disease’. This biphasic disorder usually runs a benign course, causing fever,
then a maculopapular rash on subsidence of fever at the end of the fourth
febrile day.
 Uvulo-palatoglossal junction ulcers are useful early signs
 The condition requires no antiviral treatment.
 Role of HHV-6 in the etiology of human oral squamous cell carcinoma??
24

25. 3. HUMAN HERPESVIRUS-7
 The spectrum of diseases caused by primary HHV-7 infection is similar to HHV-6,
with milder clinical presentation.
 Severe complications due to HHV-6 and 7 are treated with ganciclovir and its
derivatives or foscarnet and cidofovir
25

26. GAMMA HERPES VIRUSES
 1. EPSTEIN – BARR VIRUS-4 (HUMAN HERPES VIRUS-4)
EBV replicates primarily in B lymphocytes but may also replicate in the
epithelial cells of the pharynx and parotid duct.
Transmission is by direct contact with salivary secretion because oral viral
shedding persists for a prolonged period.
EBV has been known to cause both local and systemic infections and benign
and malignant diseases of the orofacial region.
They include :
i. Infectious mononucleosis or monoglandular fever.
ii. Oral Hairy Leukoplakia (OHL).
iii. Malignancies such as lymphomas (Burkitt’s).
iv. Nasopharyngeal carcinoma.
26

27. INFECTIOUS
MONONUCLEOSIS (IM)
Also known as Monoglandular fever or Kissing Disease.
IM is a clinical syndrome caused by EBV-4.
Children and young adults are usually affected.
The virus is transmitted via intimate contact.
 Children may acquire the virus through sharing of saliva contaminated fingers, toys and
serving spoons.
 Direct transfer of contaminated saliva may occur in adults following kissing or sharing of
straws.
Incubation period is 4-8weeks.
27

28. CLINICAL FEATURES - IM
Clinical features of IM include; fatigue, tonsillopharyngitis and lymphadenopathy.
These are followed by a high fever which lasts for almost 2 weeks.
Most striking feature – presence of bilateral and symmetrical lymphadenopathy.
Others include; - tonsillar enlargement, jaundice, rhinitis and pharyngitis.
Oral manifestations include
Hard and soft tissue petechiae, necrotizing ulcerative mucositis, NUG &
pericoronitis.
Occasionally the parotid gland may be affected along with facial nerve palsy.
Complications of IM include – myocarditis and cardiac conduction abnormalities,
neurologic abnormalities, meningitis, encephalitis, cranial nerve palsies,
hemolytic anemia, thrombocytopenia and upper airway obstruction.
28

29. DIAGNOSIS
i. Mononuclear spot test or monospot test
Detects heterophile antibodies due IM due EBV infection.
Its an improvement of Paul-Bunnel test.
ii. VCA-IgG and VCA-IgM tests
Useful for diagnosing pts with highly suggestive clinical features but negative heterophile
antibody test results.
iii. Antibody to Epstein Barr nuclear antigen (EBNA)
Typically not detectable until 6-8 weeks after onset of symptoms can help distinguish acute
and previous infections.
iv. Elevated hepatic transaminase may be seen in about 50& of the IM patients
29

30. MANAGEMENT
IM usually resolves in about 6 weeks.
Best managed with extensive palliative and supportive healthcare.
Pts should be adequately hydrated.
Fever and malaise may be managed with acetaminophen and NSAIDs.
Steroids are best used in emergencies to relieve the pt of resp compromise
secondary to pharyngeal edema.
 SYNDROME ASSOCIATION
 Chronic fatigue syndrome and Lemierre’s Syndrome.
30

31. ORAL HAIRY
LEUKOPLAKIA (OHL)
OHL is a result of EBV infection of oral squamous epithelial cells and can be seen
in immunosuppressed patients, including those with HIV infection.
It appears as white, shaggy, plaque and painless lesions commonly seen on the
lateral border of the tongue, but can also involve the buccal mucosa and gingiva.
It cannot be scraped, in contrast to candida. The surface is corrugated, but might
not be corrugated if it is seen on the inferior surface of the tongue and buccal
mucosa.
The diagnosis is made clinically, but occasionally a biopsy is performed to rule out
other causes of leukoplakia
On biopsy - hair-like projections, hyperkeratosis, koilocytic like cells and no
inflammation is seen.
31

32. 32

33. BURKITT’S LYMPHOMA
It’s a B cell neoplasm endemic in some parts of Africa and sporadic in other areas.
The tumor is the human cancer most closely linked with EBV.
The tumor is considered the fastest growing human tumor as it doubles in 1-3
days.
Both endemic and sporadic forms mostly affect children and young adults.
In both forms the dx rarely arises in lymph nodes.
Treatment involves aggressive chemotherapy.
33

34. 2. HUMAN HERPESVIRUS-8
Human herpesvirus-8 is associated with Kaposi’s sarcoma (KS), especially in
patients with HIV disease or acquired immune deficiency syndrome (AIDS).
The virus was formerly known as Kaposi's sarcoma associated herpes virus and is
found in the saliva of many AIDS patients.
It infects peripheral blood lymphocytes.
The distribution of the virus may explain why some populations of HIV-infected
people go down with Kaposi's sarcoma while others do not.
34

35. KAPOSI’S SARCOMA (KS)
Kaposi sarcoma (KS) is a cancer that develops from the cells that line lymph or
blood vessels (endothelial cells) when they are infected with HHV8.
The virus brings genes into the cells that can cause the cells to divide too much
and to live longer than they should. These types of changes may eventually turn
them into cancer cells.
Infection with HHV8 seems to be needed to cause KS, but in most cases infection
with HHV8 alone does not lead to KS.
Most people who develop KS also have a weakened immune system, due to HIV
infection, organ transplant, older age, or some other factor.
35

36. TYPES OF KAPOSI
SARCOMA
 The different types of KS are defined by the different populations it develops in,
but the histological changes within the KS cells are very similar.
 1. Epidemic (AIDS-related) Kaposi sarcoma
This type of KS is the most common and develops in people who are infected with
HIV, the virus that causes AIDS.
When HIV damages the immune system, people who also are infected with a
certain virus (HHV8) are more likely to develop KS.
KS is considered an “AIDS defining” illness.
Treating HIV infection with HAART has resulted in fewer cases of epidemic KS.
36

37. 2. CLASSIC (MEDITERRANEAN) KAPOSI
SARCOMA
Classic KS occurs mainly in older people of Mediterranean, Eastern European,
and Middle Eastern heritage.
Classic KS is more common in men than in women.
Getting older can naturally weaken the immune system a little. When this occurs,
people who already have HHV8 infection are more likely to develop KS.
Patients typically have one or more lesions on the legs, ankles, or the soles of the
feet. Compared to other types of KS, the lesions in this type do not grow as
quickly, and new lesions do not develop as often.
37

38. 3. ENDEMIC (AFRICAN) KAPOSI
SARCOMA
Endemic KS occurs in people living in Equatorial Africa.
HHV8 infection is much more common in Africa than in other parts of the world,
so the risk of KS is higher.
Other factors in Africa that weaken the immune system (such as malaria, other
chronic infections, and malnutrition) also probably contribute to the development
of KS, since the disease affects a broader group of people that includes children
and women.
Endemic KS tends to occur in younger people (usually under age 40).
Endemic KS used to be the most common type of KS in Africa. Then, as AIDS
became more common in Africa, the epidemic type became more common.
38

39. 4. IATROGENIC (TRANSPLANT-RELATED)
KAPOSI SARCOMA
Develops in people whose immune systems have been suppressed after an organ
transplant.
Immunosuppressive therapy during organ transplant increase the chance that
someone infected with HHV8 will develop KS.
Stopping the immune-suppressing drugs or lowering their dose often makes KS
lesions go away or get smaller.
 5. Kaposi's sarcoma can also occur in young gay men who are not HIV-infected.
39

40. CLINICAL PRESENTATION
KS usually appears first as spots (called lesions) on the skin.
The lesions can be purple, red, or brown. KS lesions can patches, plaques, or
bumps (called nodules).
The skin lesions of KS most often develop on the legs or face.
KS lesions can also develop on mucous membranes such as inside the mouth and
throat and on the outside of the eye and inner part of the eyelids. The lesions are
usually not painful or itchy.
KS lesions can also sometimes appear in other parts of the body such the lungs,
stomach and intestines.
Sometimes KS lesions bleed and over time could lead to anemia.
40

41. 41

42. DIAGNOSIS
Kaposi sarcoma (KS) is often found when a person goes to the doctor because of
signs and symptoms they are having.
Sometimes KS may be found during a routine physical exam.
If KS is suspected, further tests will be needed to confirm the diagnosis.
i. Medical history and physical exam
History - illnesses, operations, sexual activity, possible exposures to HHV8 and HIV.
Exam - skin and oral mucosa, sometimes the rectum to look for KS lesions.
check the stool for occult (unseen) blood, since KS in the intestines can cause
bleeding.
ii. Biopsy
To confirm the lesion is caused by KS. Either punch biopsy or excisional biopsy.
iii. Chest x-ray
iv. Bronchospy
v. GIT endoscopy
42

43. MANAGEMENT
Choices about the best treatment options for each patient are based on; the
function of the immune system as well as the number, location, and size of the KS
lesions.
For patients with immune system problems, the most important treatment is
keeping the immune system healthy and any related infections under control.
Some of the other treatments used for KS are:
i. Local therapy – intra-lesional injection of vinchristine and vinblastine.
ii. Radiation therapy
iii. Chemotherapy
iv. Biologic therapy (immunotherapy)
 PREVENTION ?
43

44. 2. HUMAN
PAPPILOMAVIRUS (HPV)
HPV is a double-stranded DNA virus that infects squamous stratified epithelia of
the body and can cause benign or malignant tumors.
At least 184 types have been identified to date. Certain HPV types have a
predilection for skin or mucosa.
Orofacial manifestations of HPV are:
i. Verruca vulgaris or the common wart on the peri-oral skin
ii. Oral papilloma (squamous cell papilloma) of the oral mucosa
iii. Focal epithelial hyperplasia
iv. Condyloma accuminatum, a sexually transmitted disease.
44

45. CLINICAL
MANIFESTATIONS, DDX
AND TXCutaneous HPV infection, or more commonly known as warts, is the most common
manifestation.
Close personal contact is likely the mode of transmission in cutaneous warts.
Verrucae plana is the type most commonly found in distribution of face, neck, and
hands. It can appear as multiple, slightly elevated papules with irregular contours
and smooth surfaces.
The diagnosis of warts is essentially based on physical examination.
Treatment includes the use of keratolytic agents (e.g., salicylic acid), cryotherapy,
or laser surgery.
45

46. 46

47. Mucosal HPV can cause oral lesions of several types.
HPV type 6, 11, and 16 infections cause squamous papilloma;
HPV types 2, 4, and 57 cause verrucae vulgaris;
HPV types 3 and 13 cause focal epithelial hyperplasia.
Recurrent respiratory papillomatosis is an HPV infection of the upper
aerodigestive tract, but more commonly has laryngeal involvement during early
childhood or early adult life. In young children, acquisition is likely via the
passage through an infected birth canal, because HPV types are similar to
those of anogenital warts.
Among adults, the risk of recurrent respiratory papillomatosis is associated
with an increased number of sexual partners and oral-genital contact.
HPV virus has been strongly associated with malignancy.
HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 66 are considered
high risk for oncogenesis.
Oropharyngeal cancer has been associated with HPV among the younger
population and those with high-risk sexual behavior.
47

48. 3. HUMAN
IMMUNODEFICIENCY
VIRUS (HIV)HIV is a retrovirus that infects T helper cells (CD4+), macrophages, and dendritic
cells.
CD4+ count declines because of direct viral killing and by cytotoxic-mediated cell
(CD8+) killing of infected cells.
HIV can be transmitted by sexual contact, blood exposure, needle-stick injuries,
and maternal to fetal transmission.
 Acute HIV infection can manifest with fever, malaise, cervical lymphadenopathy,
and pharyngitis similar to infectious mononucleosis.
Patients with these symptoms should be screened for HIV.
48

49. CLINICAL
MANIFESTATIONS
Because of CD4+ T cell count decline, infected patients are susceptible to
opportunistic infections.
Oral manifestations of HIV/AIDS can be classified into three groups, based on the
clinical features and intensity:
i. Lesions that are ‘strongly associated’ with HIV infection such as candidiasis,
hairy leukoplakia, Kaposi’s sarcoma and Non-Hodgkin’s lymphoma.
ii. Lesions that are ‘less commonly associated’, such as HSV, HPV and VZV.
iii. CMV and molluscum contagiosum, which are classified as ‘lesions that are
seen’ in HIV infection.
49

50. DIAGNOSIS
i. Serological tests – Antibody and Antigen Tests
 Rapid HIV testing – Initial screening.
 ELISA test – confirmatory test.
 Western Blot Analysis – confirmatory test (rarely used).
 P24 antigen – detection of recent infection.
ii. Nucleic acid tests
 HIV-PCR – Viral detection in the blood (recent infection)
 HIV Viral load – For monitoring treatment.
iii. Immune Marker
 CD4 test – staging the disease and monitoring treatment efficacy.
50

51. MANAGEMENT
Combination therapy of ARV drugs is known as Highly Active Antiretroviral
Therapy (HAART).
Either combine 2 nucleoside RT inhibitors with a non-nucleoside RT inhibitor or
with a protease inhibitor.
Other classes of drugs include integrase inhibitors and fusion inhibitors.
51

52. COXSACKLE VIRUS
Coxsackie viruses belong to the Enterovirus genus, and they are further divided
into Coxsackie A and Coxsackie B.
These viruses can be transmitted easily by direct contact or the oral route.
Coxsackie A virus is an important head and neck pathogen because it is a common
cause of herpangina and hand, foot, and mouth disease (HFMD).
52

53. CLINICAL MANIFESTATION
 I. HERPANGINA
Herpangina is a clinical syndrome characterized by fever, sore throat, painful
swallowing, and a papulovesicular enanthem with surrounding erythema
involving the fauces and soft palate.
The lesions can progress to ulcerations.
Enanthems persist 5 to 7 days and resolve spontaneously.
Herpangina is commonly caused by Coxsackie A serotypes 1 to 10, 16, and 22,
and Coxsackie B serotypes 1 to 5.13,14
53

54. 2.HAND, FOOT AND MOUTH
DISEASE (HFMD)
HFMD is a clinical syndrome characterized by fever, enanthem (mucosal
membrane lesion), and exanthem.
Exanthem appears 1 or 2 days after the enanthem.
Exanthem involving the hands, feet, buttocks, upper thighs and arms, or feet is
characterized by nonpainful, nonpruritic and macular, maculopapular, or vesicular
rash.
The enanthem has a vesiculoulcerative appearance with surrounding erythema
involving the tongue, palate, and buccal and gingival mucosa, but sparing the
oropharynx.
Spontaneous resolution can occur within 7 to 10 days. Several enteroviruses are
associated with HFMD, but Coxsackie A serotype 16 has been more frequently
associated with large outbreaks.
54

55. 55

56. DIAGNOSIS
The diagnosis for herpangina and HFMD is made clinically based on the typical
appearance of the lesions.
Confirmation by cell culture or nucleic acid amplification (e.g., PCR) may be
warranted if diagnosis is uncertain or in patients with complications that can
include rhombencephalitis, acute flaccid paralysis, aseptic meningitis, or
myocarditis.
Samples from the throat, stool, or vesicular fluid of an exanthema or enanthem
are appropriate for testing
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57. MANAGEMENT
HFMD and herpangina are self-limiting diseases, and therapeutic options are
limited to symptomatic relief and supportive care.
Children who are unable to tolerate solid food and liquids by mouth because of
painful oral lesions will require hospitalization for intravenous fluids to maintain
hydration.
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58. MUMPS VIRUS
Mumps virus is a single-stranded RNA virus that belongs to the genus
Paramyxovirus.
Only one serotype exists, but there are 13 genotypes.
Humans are the natural host of this virus.
Mumps is highly infectious; it is transmitted by direct contact, respiratory
droplets and fomites, and inoculates through nose or mouth.
Incubation period is 16 to 18 days from exposure to onset of symptoms.
An infected patient is typically contagious 1 to 2 days before the onset of
symptoms, which continue for a few more days.
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59. CLINICAL MANIFESTATION
Prodromal symptoms include low-grade fever, malaise, anorexia, and headache.
Within 48 to 72 hours, parotid gland enlargement and tenderness could be
appreciated.
Occasional earache can precede the parotid enlargement.
On examination, the enlarged parotid gland obscures the angle of the
mandible.
Contralateral parotid gland enlargement occurs in 90% of patients, but this
may be delayed by several days.
Patients may experience trismus and difficulty with mastication.
The parotid gland returns to normal size within 7 days.
Complications are rare, but meningitis, encephalitis, orchitis, and pancreatitis
can occur.
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60. 60

61. DIAGNOSIS
 Clinical diagnosis is made by history of exposure and physical findings.
 Diagnosis is confirmed by detection of one of the following:
i. mumps-specific IgM antibodies.
ii. a fourfold rise in IgG mumps-specific antibody in serum.
iii. detection of mumps virus, or viral nucleic acid in clinical specimen (saliva, urine,
seminal fluid, or cerebrospinal fluid).
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62. MANAGEMENT AND
PREVENTION
The disease is self-limiting, and therapy is mainly symptomatic and supportive.
Mumps can be prevented by administering a vaccine, which is often given in
combination with other vaccines, such as the measles-mumps-rubella (MMR)
combination.
The first dose of the MMR vaccine is recommended at 12 to 15 months old, and a
second dose is given at 4 to 6 years old.
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63. QUESTIONS?
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64. THANK YOU.
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