VIRUS PADA SISTEM

MUSKULOSKELETAL

DR. RAHMIATI
SISTEM MUSKULOSKELETAL
 INFEKSI DAN INFLAMASI PADA SISTEM
MUSKULOSKELETAL

Osteomyelitis
Myositis/Polymyositis
/Pyomyositis/
Muscular dystrophy

Bursitis/Tendinitis/ Arthritis/Polyarthritis
Tunnel syndrom
ETIOLOGI INFEKSI DAN INFLAMASI PADA SISTEM
MUSKULOSKELETAL
VIRUSES THAT CAN GIVE RISE TO VIRAL ARTHRITIS

• Parvovirus B19
• Hepatitis viruses ( hepatitis A virus [HAV], hepatitis B virus [HBV], and HCV)
• Rubella virus
• Alphaviruses and flaviviruses
• Retroviruses
PARVOVIRUS B19 (B19V)

• A single-stranded DNA virus of the family Parvoviridae and genus Erythrovirus

• Clinical features of arthritis associated with parvovirus B19 infection in children
include the following:
As many as 70% of patients are asymptomatic
A few may have flulike symptoms (eg, fever, headache, sore throat, cough, anorexia,
vomiting, diarrhea, or arthralgia)
A bright red rash is typically noted, often characterized as having a “slapped-cheek”
appearance (see the images below)
Joint symptoms are rare (5-10%)
ALPHAVIRUSES (CHIKUNGUNYA)
WHAT IS THIS TONGUE TWISTER ?
• It is CHIKUNGUNYA
• To be pronounced as [chick’-en-GUN-yah]
• It is not written as CHICKEN GUINEA
• Nothing to do with chicken or mutton eating
• Derived from the Makonde verb - Kun gunyala
• In Swahili it means ‘to become contorted’ or
• More specifically as ‘that which bends up’
8 • Refers to the stooped posture of the patient www.drsarma.in
SYNONYMS

• CHIKV Fever
• Buggy Creek virus infection
• Knuckle fever
• Me Tri virus infection
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• Semliki Forest virus infection www.drsarma.in
SHOULD WE BE PANICKY ?

• A common viral fever

• Self limiting – non fatal illness
• Fever, myalgia, arthralgia, lasting 2 - 7 days
• Should give big name for it and be panicky ?
• Should create such media hype and chaos ?
• Above all, should we politicize to this extent?
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ALPHAVIRUSES (CHIKUNGUNYA)
ALPHAVIRUSES

Geographic distributions are as follows:

• Chikungunya virus – Historically,, East Africa, India, Southeast Asia, and Philippines [4] ; however, in
2013 the virus spread to the Caribbean and in 2014 it reached the United States [5]
• O’nyong-nyong virus – East Africa
• Ross River virus – Australia, New Zealand, and South Pacific islands
• Mayaro virus – South America
• Sindbis virus – Europe, Asia, Africa, Australia, and Philippines
• Barmah Forest virus – Australia
A DISEASE OF AFRICA AND ASIA

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WHAT IS THIS VIRUS ?

• Causative agent is an RNA – VIRUS

• Class – Arbor Virus (Arthropod Borne)
• Family – Togaviridae
• Genus – Alpha Virus
• Species – Chikungunya Virus
• Similar to Semliki Forest Viruses (SFV) in Africa and Asia.
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CHIKUNGUNYA VIRUS - EM

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TRANSMISSION

• Reservoir – Non-human primates in Africa

• No animal reservoir is found in India
• Maintained in nature by man – mosquito – man cycle
• Vector – Aedes aegypti, Ae. albapticus mosquito
• Same vector as for Dengue and Yellow fevers
• Vehicle of transmission – None
• No known mode - other than mosquito bite
16 • Incubation Period – 2 days to 12 days www.drsarma.in
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THE VECTOR

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THE VECTOR
• Aedes aegypti mosquito, flight range < 100 meters
• Aggressive daytime biter – under lights – bites ankles
• Once infected – it has the virus until death (30 days)
• It is a man made mosquito – prefers its owner
• Breeds in man made household containers
• Indoor, peridomestic, fresh water mosquito
• Metallic, plastic, rubber, cement and earthen containers -
open, left or unused - get filled with water
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• Air coolers, ACs, Old oil drums, Over head tanks www.drsarma.in
AEDES AEGYPTI

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AEDES ALBAPTYCUS

Tiger Mosquito
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MADAM AEDES - AT HER LUNCH

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PATHOGENESIS

• Atthe early stage of the disease, the organs targeted for

CHIKV replication were lymphoid tissues, liver, CNS, joints, and
muscle, and

• The persistence of CHIKV could be found later in the lymphoid

organs, liver, joints, and muscle, macrophages being the main
reservoir.
PATHOGENESIS CONTINUED….

• In humans, acute CHIKV infection is characterized by a

very early viremia at fever onset that can increase up
to 109 to 1012 RNA copies/ml and lasts up to 12 days
.

• Invitro studies have shown that human epithelial and

endothelial cells, primary fibroblasts, and monocyte-
derived macrophages are susceptible to CHIKV
infection, whereas activated B and T CD4+
lymphocytes, monocytes, and monocyte-derived
dendritic cells were refractory to CHIKV infection .
ALPHAVIRUS-
INDUCED
ARTHRITIS
ROSS RIVER VIRUS

• Characterization of the inflammatory infiltrate within the skeletal muscle

tissue identified inflammatory macrophages, NK cells, and CD4+ and
CD8+ T lymphocytes
RETROVIRUSES
HIV infection is associated with several rheumatic manifestations:
• Psoriatic arthritis
• Painful articular syndrome (10%)
• Undifferentiated spondyloarthropathy
• Inflammatory myopathy
• Systemic vasculitis
• Diffuse infiltrative lymphocytosis syndrome (5%)
• Fibromyalgia (30%)
• Avascular necrosis
• Gout
 OTHER VIRUSES
• Epstein-Barr virus – This infection is usually associated with polyarthralgia, but monoarthritis of the
knee and ruptured Baker cysts may occur
• Varicella-zoster virus (VZV) – This infection in children rarely develops into pauciarticular arthritis [8]
• Mumps virus – In infected adults, this infection is associated with small or large joint synovitis that
lasts for several weeks; arthritis may precede or follow parotitis by up to 4 weeks
• Adenovirus or coxsackieviruses A9, B2, B3, B4, and B6 – These infections have been associated with
recurrent episodes of polyarthritis, pleuritis, myalgia, rash, pharyngitis, myocarditis, and leukocytosis
• Echovirus - This infection can be associated with polyarthritis, fever, and myalgias
• Herpes simplex virus (HSV) or cytomegalovirus (CMV) – Arthritis with these infections is rare; CMV
arthritis has been reported in patients after bone marrow transplantation; vaccinia virus has been
associated with postvaccination knee arthritis in only 2 reported cases
PATOPHYSIOLOGY

• Viruses can cause infection or act as cofactors in the development of rheumatic diseases. Viral
infection depends on both host and viral factors. Key host factors include age, sex, genetic
background, infection history, and immune response. Key viral factors include mode of host entry,
tissue tropism, replication, effects of cytokines, ability to establish persistent or latent viral
infections, and alterations of host antigens. Infected cells can undergo apoptosis (programmed cell
death).
• The immune complexes from an antibody response can be deposited at sites of viral infection or in
the synovium. Virus-induced autoimmunity, polyclonal B-cell activation, and immunodeficiency may
result in opportunistic infection, largely because of an inability of the immune system to eliminate
the virus (eg, HIV, human T-lymphotropic virus [HTLV]-1, or hepatitis C virus [HCV]). Molecular
mimicry may cause abnormal self-reactivity by altering immune tolerance