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Transcript
Research Updates in Medical Sciences (RUMeS)
2015, Volume 3; Issue 1 page 75 – 76.
Editorial
Feline Infectious Peritonitis: The Fatal Disease of the Feline.
Ahmad Naqib Shuid
Institut Biosains, University Putra Malaysia, Serdang, Selangor, Malaysia
Advanced Medical and Dental Institute (AMDI), Universiti Sains Malaysia, Kepala Batas, Pulau
Pinang, Malaysia
Correspondence should be addressed to Ahmad Naqib Shuid, [email protected]
Received 8-01-2015; Accepted 15-01-2015
Copyright © 2014 Naqib et al. This is an open access article distributed under the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
How to cite:
Naqib et al., 2015, Feline Infectious Peritonitis: The Fatal Disease of the Feline. 3(1) : 75– 76.
Feline coronavirus (FCoV) is a positive single stranded
RNA virus that is ubiquitous in cat populations. Depending on FCoV strains, the virus is able to cause different
types of diseases from asymptomatic mild enteritis to a
highly systemic immune-mediated fatal infection called
feline infectious peritonitis (FIP). FIP is caused by a virulent form of feline coronavirus known as feline infectious
peritonitis virus (FIPV) that arises from mutation of feline
enteric coronavirus (FECV). Meanwhile, FECV only
caused mild enteritis in cats. It is believed that FECVs
and FIPVs came from a common ancestry [1]. FIPV
strain WSU 79-1146 and FECV strain WSU 79-1683 and
several different strains of FIPV and FECV have been
studied, respectively [2].
FECV infect the cell of the intestinal mucosa of kittens and can cause from mild to moderate transient enteritis [3]. This is in contrast to FIPV which can cause
fatal systemic disease. FIP was first recognized in the
1950’s [4] and considered the leading cause of death
among pedigree cats and cats from shelters [1]. In addition, it has been suggested that the presence of cat antibodies might have accelerated FIP development [5]. Despite over 40 years of research, the mechanisms of FIPinduced disease and immunity in cats are still not clear.
FIPV utilize several immune evasion mechanisms to
avoid clearance of infected cells by the humoral immune
response [6]. As a result, FIPV may developed into two
types of infection namely dry or wet FIP. High humoral
response without cell mediated immunity (CMI) resulted
in the most common form of FIP referred to as wet FIP.
Wet FIP causes inflammation of the linings of the abdominal viscera, and less commonly of the thoracic organs. On the other hand, poor CMI response leads to dry
forms of FIPV, characterized by type IV hypersensitivity
[7]. Dry FIP is the more chronic form of the disease that
often ends up with jaundice, weight loss, diarrhea, ataxic
and fever.
Innate and adaptive immunity are two equally important component of the immune system. Innate immunity is rapid and nonspecific while adaptive immunity is
specific but requires time to produce response after infection. Helper T cells or CD4+ lymphocytes are mediators in adaptive immune response. There are two major
subtypes of effector CD4+ T helper cell known as the
Type 1 helper T cells (Th1) and Type 2 helper T cells
(Th2) [8]. Th1 dominates CD4+ T lymphocytes response
in virus infection, which is influenced by the presence of
interferon gamma (IFN-g) and interleukin 12 (IL-12). Th2
with the help of interleukin-10 (IL-10) promote humoral
immunity in response to viral infections. However, the
role of humoral immunity in protection against FIPV is
controversial and apart from that FIPV infection also impairs CMI responses. Antibody-dependent enhancement
(ADE) might play a role in FIPV infection which is likely to
be mediated by opsonisation of the virus facilitating viral
uptake by macrophages [9] that enables the virus to infect and replicates in the macrophages [3]. However, the
role of ADE in natural infection is not clear as in the
75
fields, cats were most likely to develop FIP on first exposure to FCoV [10].
2744.
FIP can be treated with cytotoxic drugs and steroids. These drugs merely improve the quality of life and
may prolong the cat’s life for a few months, but the prognosis is still poor.
References
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3.
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4.
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6.
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31;121(1–2):131–137
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