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The Mycobacteria

(Acid Fast Bacilli)

Obligate pathogens

Mycobacterium. tuberculosis - TB
Mycobacterium bovis - bovine TB
Mycobacterium. leprae - Hansen's disease (leprosy)
Emerging Diseases
Hansens Disease(1873) Leprosy
caused by Mycobacterium leprae
large amounts of mycolic acids on the cell
surface
multiplies very slowly
mostly infects skin, nerves and mucous
membranes
never cultivated in laboratory media or cell
culture, but has been cultivated in mouse
foot pads
Emerging Diseases
Leprosy
route of infection is not known, but probably via
respiratory droplets
most people are resistant and do not develop active
disease

Transmissions:
Long and close contract with lepromateous patients
Nasal secretion
Skin lesions
Inhalation
Emerging Diseases

Leprosy the disease process


patients develop discolored patches on skin
that do not itch or hurt

ringworm-like patches, may have raised edges

patients experience loss of feeling within the


patch of discolored skin
Leprosy
Emerging Diseases

Leprosy other symptoms


loss of eyebrows
thick or lumpy earlobes
loss of feeling (burns or scars)
painless ulcers on the feet
drop feet
deformities of hands and/or feet
Classical facial appearance of advanced leprosy
Leprosy diagnosis
in more advanced disease patient experiences
numbness or tingling in hands and feet

enlarged nerves appear in arms and neck

leprosy bacilli can be found in skin lesions

painless ulcers become infected

infected ulcers become necrotic

lack of pain allows infection to become deep and


attack bone
Diseases Production

Two main forms:


1. Tuberculoid leprosy (TT)

2. Lepromatous leprosy (LL)


Others forms: Borderline leprosy

Low TT BT BB BL LL High

Poor prognosis
Emerging Diseases
Tuberculoid Leprosy (TT)
usually in persons with relatively high
resistance

no bacilli in skin smear

person cannot pass leprosy on to others

skin patches are few, are variable in


appearance, but often have raised margins
and flat centers
Emerging Diseases
Tuberculoid Leprosy (TT)
usually only involves loss of feeling in skin
patches

when hands or feet involved it often happens


early and causes loss of feeling or strength in
only one hand or foot

usually responds quickly to treatment


Emerging Diseases

Borderline Leprosy
few to many bacilli in skin smears

many skin patches, some feeling loss, patches


about the same on both sides of the body

severe nerve damage, loss of feeling and


strength, deformities in both hands and both
feet
Emerging Diseases

Borderline Leprosy

Depending on where it falls along the line between


the two extremes, borderline leprosy is divided into:
borderline tuberculoid (BT)
borderline (BB)
borderline lepromatous (BL)
Emerging Diseases
Lepromatous Leprosy (LL)
in persons with very low resistance

large numbers of leprosy bacilli in skin


patches

patients are infectious until treated

numerous skin patches, often with raised


lumps or thickened areas
Emerging Diseases
Lepromatous Leprosy (LL)
facial skin becomes thick, lumpy, reddish,
especially over the eyebrows, cheeks, nose,
and ears.

bridge of the nose may gradually sink in

nerve damage and paralysis appear late if


not treated
Emerging Diseases
Lepromatous Leprosy (LL)
loss of feeling and strength affects both
hands and both feet equally

response to treatment is often slow

treatment must be continued for at least 2


years
Diagnosis
Acid fast, auramine-rhodamine stains
Skin lesions or nasal scraping
Anaestheic checks
Granulomatous formation

Lepromin skin test : not for Lepromatous leprosy


Treatment

Tuberculoid leprosy:
Dapsone combined with rifampin

Lepromatous leprosy:
Dapsone, rifampin and clofazimine

Borderline leprosy: with ENL


(erythema nodusum leprosum)
Thalidomine
HERPESVIRIDAE
Human Herpes Viruses
1. Herpes simpleks virus type 1.
2. Herpes simpleks virus type 2.
3. Variocella zoster virus.
4. Cytomegalovirus
5. Epstein Barr virus
6. Human Herpes Virus 6.
7. Human Herpes Virus 7.
8. Kaposis Sarcoma Herpesvirus (KSHV).
Sifat-sifat Virus Herpes
Virion: spheris, icosahedral capsid
Genom : linear, DNA untai ganda
Protein: > 35 jenis protein pada virion
Envelope: glikoprotein, reseptor Fc
Replikasi: nucleus bertunas dari membran nuclear.
Ciri khas infeksi virus herpes:
1.Menyebabkan infeksi laten
2. Menetap secara indefenitif pada penderita
3. Sering reaktif pada immunosuppressed host
Infeksi virus herpes pada manusia

1. Virus herpes simpleks tipe 1


- hanya pada manusia, tidak memiliki vektor/reservoir hewan
- Infeksi laten: Sacral ganglia
- Usia terinfeksi: anak balita
- Transmisi/ penularan: kontak langsung, saliva
- Gejala Klinis:
a. Inf. Primer:gingingostomatitis, pharyngotonsilitis,
keratoconjuctivitis, inf neonatal.
b. Recurent inf: fever, keratitis.
c. Inf primer/ recurrent: Herpes kulit di atas pinggang, pd tangan,
siku, herpatic withlow, eczema herpeticum, genital herpes,
herpes encephalitis, herpes meningitis.
2. Virus herpes simpleks tipe 2

Tidak memiliki vektor/ resevoir hewan.


Usia terinfeksi: dewasa muda
Transmisi: sexual
Gejala klinis:
1. Inf primer: Inf neonatal
2. Inf primer/ recurent: herpes kulit di bawah pinggang, pd
tangan, siku, herpetic withlow, genital hwerpes, herpes
meningitis.
3. Virus Varicella-Zoster
A. Varicella (chickenpox)=cacar air
Sangat menular, terutama pada anak
m.i : 10-21 hr, transmisi: sal nafas, conjuctiva
GK: malaise, demam, diawali rash pada badan kemudian pada
wajah, kaki & tangan, 2-4 hr kemudian muncul makula,
papul;a dan erupsi vesicular pada kulit dan mukosa.
Komplikasi: encephalitis, pneumonia.

B. Zoster:
Infeksi akut pada syaraf & dorsal root ganglion
Inflamasi& nyeri hebat pd ganglia unilateral pada badan,
kepala & leher.
Human herpes virus 6
T- lymphtropic HHV 6: 1986.
GK: exanthema subitum pd infant (roseola infantum)
demam, skin rash.

Human Herpes Virus 7


T-lyphotropic HHV 7: 1990
Inf pada anak. Dekat dg sifat cytomegalovirus.

Human Herpes Virus 8


Disebut juga KSHV (Kaposis Sarcoma asscociated Herpes
Virus), sxually transmitted.
Virus dijumpai pada 90% penderita Sarcoma Kaposi (tumor
vascular) pd penderita AIDS.
POXVIRIDAE
Largest & most complex of viruses
Three pox viruses of medical important:
Smallpox virus, vaccinia virus, and molluscum
contagiosum.
POXVIRIDAE
Structure & composition:
- Oval or brick shaped, 400nm (length) x 230nm ()
external surface shows ridges, contains core & lateral
bodies
- Composition: DNA (3%),protein (90%), lipid(5%)
- Genome: linear double stranded DNA, MW 85-150x106
rich in adenine & thymine bases, low
guanine-plus-cytosine
- Contain >100 polypeptides many enzimes in core
- Envelope (+)
Structure & composition:
- Very resistant to inactivation
- Parapoxvirus: * 260x160nm, smaller than
orthopoxvirus
* genomes: MW 85X106, have a
higher guanine-plus-cytosine
content (63%)
- Unique among DNA viruses :
the entire multiplication cycle takes place in
cytoplasm of infected cells
VACCINIA & VARIOLA
(Poxvirus infection in humans)

1798 : Jenner introduced vaccination with live


virus
1967 : WHO worldwide campaign to
eradicate smallpox
1980 : smallpox was officially declared
eliminated
Composition of vaccinia & variola viruses:

# Host :
- variola : only humans & monkeys
- vaccinia : broad host range, including
rabbits & mice
# Grow on chorioallantoic membrane of 10-12 days
old chick embryo, but variola produces much
smaller pocks
# Grow in several types of chick & primate cell
lines
Pathogenesis of smallpox:

- Portal of entry : mucous membranes of upper


respiratory tract
- After viral entry :
1. primary multiplication in the lymphoid tissue
draining the site of entry
2. transient viremia and infection of reticulo-
endothelial cells throughout the body
3. secondary phase of multiplication in those cells
4. secondary, more intense viremia
5. clinical disease
Clinical findings :

Incubation period of variola (smallpox) = 12 days


1. Fever & malaise : 1-5 days
2. Exanthems appear : - papular (1-4 days)
- vesicular (1-4 days)
- pustular (2-6 days)

3. Crusts formed (2-4 weeks after 1st sign of lesion)


and leaving pink that faded slowly
Laboratory diagnosis:

a. Isolation & identification :


- skin lesions specimen (choice for viral isolation)
- direct exam (electron microscope) :
rapid identification of viral particles ( 1 hr)
differentiate poxvirus infection from
chickenpox
- viral isolation is carried out by inoculation of
vesicular fluid onto the chorioallantoic
membrane of chick embryos
Laboratory diagnosis:
- in 2-3 days vaccinia pocks are large with
necrotic centers, whereas variola pocks are
much smaller
- cell cultures also be used for viral isolation
(orthopox, parapoxviruses)
- agar gel precipitation detect viral antigen,
identifies orthopoxviruses as a group
b. Serology : HI, Nt, ELISA, RIA or
immunofluorescence tests
- antibodies appear after 1st week infection
- cannot distinguish among orthopoxviruses
Molluscum contagiosum (MCV)
MCV: transmitted by close personal
contact, including sexually.
The disease is quite common in children,
and the lesions can be wide spread in
patients with reduced cellurar immunity.
In immunocompetent patients, the lesions
are self-limited but may last for month.
Clinical Findings:
Causes small, pink, papular, wartlike
benign tumors of the skin or mucous
membranes. The lesions have a
characteristic cup-shaped crater with a
white core.
Papovaviridae
Important properties of Papovaviruses
Virion: Icosahedral
Composition: DNA (10%), protein (90)%
Genome: ds DNA, circular, MW 3-5 million
Envelope: none
Replication: nucleus
Outstanding characteristic:
- Stimulate cell DNA synthesis
- Polyomaviruses are significant causes of human disease
- Viral oncoprotein interact with cellular tumor supressor proteins
Important properties of Papovaviruses

Oncogenic potential tumor in natural host


Result of natural infection: Benign tumor (wart)
Target tissue: Surface epithelia
Most significant human illness: Skin warts,
laryngeal papillomas, cervical carcinoma
Important animal isolates: Papillomaviruses from
cows and rabbits
Papillomavirus
Cause: skin warts, plantar warts, flat warts,
genital condylonmas, laryngeal papillomas in
human.
HPV :
- sexually transmitted genital lesions,
- premalignant and malignant disease of
vulva, cervix, penis and anus.
- genital condylomas, dysplasia to
invasive cervical cancer (HPV type 16, 18,
and 11, 31, 33, 35).
- Laryngeal papilloma in children: HPV 6, 11
Thank You

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