Unknown Epidemic Causes Camel Deaths in Egypt

[sharon sanders]

Medical report: Purchase ?Jamal? sick behind the death of 22 sentences using smallpox and wounding 85 in St. Catherine

كتب شيماء عبدالهادي ٣/٨/٢٠٠٨​

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كشف تقرير حصلت ?المصري اليوم? علي نسخة منه أعده برنامج الرعاية الطبية في محمية سانت كاترين، حقيقة المرض الوبائي الذي تسبب في نفوق أعداد كبيرة من الجمال، في ظاهرة هي الأولي من نوعها في مدينة سانت كاترين.​

A report obtained ?Egyptian today? a copy of which was prepared by the medical care at St. Catherine protectorate, a disease epidemic that caused the deaths of large numbers of camels, the phenomenon is the first of its kind in the city of Saint Catherine.

أرجع التقرير بداية ظهور المرض إلي أوائل يونيو ٢٠٠٨، وبالتحديد في وادي الراحة، حيث طلب أحد البدو من برنامج الرعاية الطبية بالمحمية الكشف علي جمل يمتلكه يعاني طفحاً جلدياً في كل جسمه، وهو ما تزامن مع شراء ?جمال? من مناطق خارج المحمية، مدينة شرم الشيخ ومدينة العريش، من قبل سكان محليين، وتم إحضارها إلي سانت كاترين دون إجراء الحجر البيطري والفحص من جانب الوحدة البيطرية.​

The report attributed the onset of the disease to early June 2008, specifically in the valley of rest, as requested by one of Bedouins from the medical care protectorate inspecting the strings owned suffers rash Geldia in each of his body, which coincided with the purchase of ?Jamal? from areas outside the protected city of Sharm el - Sheikh and the city of Al-Arish, by local residents, was brought to St. Catherine without a veterinary quarantine and inspection by veterinary unit.

أضاف التقرير أنه بعد شهر من إحضار ?الجمال? للمنطقة ظهرت الأعراض المرضية علي أحد الجمال في منطقة وادي الراحة ثم بدأ المرض في الانتشار بين الجمال نظراً للاحتكاك بينها في العمل في السياحة والتجمعات السكنية في مدينة سانت كاترين وما حولها.​

The report added that after a month of bringing ?beauty? developed symptoms of the disease on one of beauty in the valley area amenities and then began to spread disease among the camels because of the friction between them in work in the tourism and residential areas in the city of St. Catherine and its environs.

وبدأ اكتشاف الجمَّالين لتلك الحالة بملاحظة ظهور تورم بالخصيتين وطفح جلدي وتقرحات بالفم وعدم القدرة علي الأكل.​

The discovery began aesthetic of that situation by noting the emergence of swelling of testicles, skin rash and mouth ulcers and the inability to eat.

وطبقاً للتقرير فقد تم الكشف علي ٥٢ حالة مرضية من قبل الأطباء بالمحمية، وحوالي ٣٣ حالة من قبل مديرية الطب البيطري، بحيث وصل مجموع الجمال المصابة ٨٥ جملاً والنافقة ٢٢، وتم تشخيص المرض علي أنه جدري الجمال وتليف جلدي متهيج وهو ما يحتاج من ٧ إلي ٢١ يوماً للشفاء بعد العلاج بالمضادات الحيوية طويلة المفعول وخافض الحرارة.​

According to the report, was disclosed on 52 satisfactory condition by doctors protectorate, and about 33 cases before the directorate of veterinary medicine, bringing the total infected beauty sentences 85 dead and 22, was diagnosed disease that camel pox and skin fibrosis Mthij which needs 7 to 21 Days recovering after treatment with antibiotics long Tabs force and heat.

وعن إجراءات السيطرة علي المرض أشار التقرير إلي أنه تم الاجتماع بشيخ الجمالين وبعض الجمَّالين والتنبيه عليهم بضرورة عزل الجمال المصابة بالمرض، ومنعها من العمل في السياحة مع إخراج جميع الحالات المصابة بالمرض من منطقة دير سانت كاترين وجبل موسي، والتنسيق مع شرطة السياحة لمنع دخول أي جمل مصاب إلي تلك المناطق التي يعمل بها ما يقرب من ٣٨٦ جملاً في السياحة.​

And procedures for controlling the disease report pointed out that the sheikh and some aesthetic beauty, and the warning they need to isolate infected camel disease, and prevent them from working in tourism with dismissing all cases infected with the disease from the Monastery of St. Catherine and Mount Moses, and coordination with the tourism police to prevent the entry of any strings Suffering to those areas which employ about 386 sentences in tourism.



http://translate.google.com/transla...m/Default.aspx?r=t&sl=ar&tl=en&hl=en&ie=UTF-8



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[Oracle]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

This little puzzle is quite interesting.

Location:
South Sinai Governate
http://st-katherine.net/en/
http://en.wikipedia.org/wiki/South_Sinai_Governorate

Probable agent: Camelpox.

Symptoms: Clinical symptoms started with fever, salivation and general exanthema. The main features were facial and legs oedema, pustules on the mucosa of the lips and a high rate of abortion. Lesions may also occur on the whole body including scrotum and udder. (mortality occurs primarily in young camels, at a rate of ~30%)

This is a recently emerging disease of the Middle East, India and Central Asia affecting domesticated and wild camelids.

The first outbreak of camelpox in Syria. J. Veterinary Med. Sci. 69:541-543 (2007). http://www.jstage.jst.go.jp/article/jvms/69/5/69_541/_article

Group: Group I (dsDNA)
Family: Poxviridae
Genus: Orthopoxvirus

Our clue to the plausible origin of this virus:

The Genome of Camelpox Virus. Virology Volume 295(1):1-9 (2002).

Camelpox virus (CMLV), a member of the Orthopoxvirus genus in the Poxviridae, is the etiologic agent of a disease of camels. Here we report the CMLV genomic sequence with analysis. The 205,719-bp CMLV genome contains 211 putative genes and consists of a central region bound by identical inverted terminal repeats of approximately 7 kb. <b>A high degree of similarity in gene order, gene content, and amino acid composition in the region located between CMLV017 and CMLV184 (average 96% amino acid identity to vaccinia virus (VACV))</b> indicates a close structural and functional relationship between CMLV and other known orthopoxviruses (OPVs). Notably, CMLV contains a unique region of approximately 3 kb, which encodes three ORFs (CMLV185, CMLV186, CMLV187) absent in other OPVs. These ORFs are most similar to B22R homologues found in other chordopoxvirus genera. <b>Among OPVs, CMLV is the most closely related to variola virus (VARV)</b>, sharing all genes involved in basic replicative functions and the majority of genes involved in other host-related functions. Differences between CMLV and VARV include deletion and disruption of a large number of genes. Twenty-seven CMLV ORFs are absent in VARV, including seven full-length homologues of NMDA-like receptor, phospholipase D, Schlafen, MT-4 virulence, kelch, VACV C8L, and cowpox (CPXV) B21R proteins. Thirty-eight CMLV ORFs, some of which are fragments of larger genes, differ in size from corresponding VARV ORFs by more than 10% (amino acids). Genome structure and phylogenetic analysis of DNA sequences for all ORFs indicate that CMLV is clearly distinct from VARV and VACV and, as it has been suggested for VARV, it may have originated from a CPXV virus-like ancestor.

So, it seems as though vaccinia/variola vaccine viruses are involved the evolution of this relatively recently emerged camel disease (the Saudis and UAE actually requested technical assistance from CDC/USDOD infectious disease labs, when this agent began to decimate their prized racing camel herds).

Sure enough...

When good vaccines go wild: Feral Orthopoxvirus in developing countries and beyond.

Nissin Moussatch?,1,2 Clarissa R. Damaso,2 and Grant McFadden. J. Infect. Dis. Developing Countries 2(3):93-? (June 2008). Full paper available online.
http://www.jidc.org

The presence of zoonotic poxviruses in nature represents a potential human health risk that has to be re-evaluated by health authorities not only in developing countries, but also in many developed countries. For example, buffalopox virus infection remains to be a threat to humans and cattle in India, and monkeypox virus infection persists in several inhabited places in Africa and, more recently, in the USA. There are also a great number of zoonotic transmissions of cowpox virus from cats to humans in Europe. For almost a decade in Brazil, vaccinia-like viruses have been isolated from human and cattle infections. This review examines the ability of potentially pathogenic orthopoxviruses, including feral versions of vaccinia virus vaccine, to persist in nature and re-emerge for reasons we do not yet understand.

(Ha! The authors may not know why they persist and re-emerge, but I believe I do. The causal mechanics are <i>drop dead gorgeous.</i>)

See Figs 2 and 3.

The sequence of camelpox virus shows it is most closely related to variola virus, the cause of smallpox. Journal of General Virology (2002), 83, 855-872.

Camelpox virus (CMPV) and variola virus (VAR) are orthopoxviruses (OPVs) that share several biological features and cause high mortality and morbidity in their single host species. The sequence of a virulent CMPV strain was determined; it is 202182 bp long, with inverted terminal repeats (ITRs) of 6045 bp and has 206 predicted open reading frames (ORFs). As for other poxviruses, the genes are tightly packed with little non-coding sequence. Most genes within 25 kb of each terminus are transcribed outwards towards the terminus, whereas genes within the centre of the genome are transcribed from either DNA strand. The central region of the genome contains genes that are highly conserved in other OPVs and 87 of these are conserved in all sequenced chordopoxviruses. In contrast, genes towards either terminus are more variable and encode proteins involved in host range, virulence or immunomodulation. In some cases, these are broken versions of genes found in other OPVs. The relationship of CMPV to other OPVs was analysed by comparisons of DNA and predicted protein sequences, repeats within the ITRs and arrangement of ORFs within the terminal regions. Each comparison gave the same conclusion: CMPV is the closest known virus to variola virus, the cause of smallpox.

http://vir.sgmjournals.org/cgi/content/abstract/83/4/855

Pretty darned cool, if it is indeed camelpox. For those of you keeping up with the technical joneses, the NMDA receptor is enriched in epidermeral keratinocytes, suggesting a possible association with CMLV pathogenesis.

Camelpox virus encodes a schlafen-like protein that affects orthopoxvirus virulence. J Gen Virol 88 (2007), 1667-1676.

http://vir.sgmjournals.org/cgi/content/full/88/6/1667

Camelpox virus (CMLV) gene 176R encodes a protein with sequence similarity to murine schlafen (m-slfn) proteins. In vivo, short and long members of the m-slfn family inhibited T-cell development, whereas in vitro, only short m-slfns caused arrest of fibroblast growth. CMLV 176 protein (v-slfn) is most closely related to short m-slfns; however, when expressed stably in mammalian cells, v-slfn did not inhibit cell growth. v-slfn is a predominantly cytoplasmic 57 kDa protein that is expressed throughout infection. Several other orthopoxviruses encode v-slfn proteins, but the v-slfn gene is fragmented in all sequenced variola virus and vaccinia virus (VACV) strains. Consistent with this, all 16 VACV strains tested do not express a v-slfn detected by polyclonal serum raised against the CMLV protein. In the absence of a small animal model to study CMLV pathogenesis, the contribution of CMLV v-slfn to orthopoxvirus virulence was studied via its expression in an attenuated strain of VACV. Recombinant viruses expressing wild-type v-slfn or v-slfn tagged at its C terminus with a haemagglutinin (HA) epitope were less virulent than control viruses. However, a virus expressing v-slfn tagged with the HA epitope at its N terminus had similar virulence to controls, implying that the N terminus has an important function. A greater recruitment of lymphocytes into infected lung tissue was observed in the presence of wild-type v-slfn but, interestingly, these cells were less activated. Thus, v-slfn is an orthopoxvirus virulence factor that affects the host immune response to infection.

 

[AlaskaDenise]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

...the NMDA receptor is enriched in epidermeral keratinocytes, suggesting a possible association with CMLV pathogenesis....

Is there an english translation available for the above?

...potentially pathogenic orthopoxviruses, including feral versions of vaccinia virus vaccine, to persist in nature and re-emerge for reasons we do not yet understand.

A feral vaccine?

.

 

[Giuseppe]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

Is there an english translation available for the above?



A feral vaccine?

.

Perhpas, the live vaccinia virus that transmits to immunological naive animals through viral particles dispersion...

Human vaccinia virus is known to cause secondary infection in individuals in contact with skin lesions of a vaccinate relative that (the lesions) were broken or unprotected. An example was cited by US CDC about an infant developed severe human vaccinia virus infection after his/her father (a soldier) received vaccination and subsequently went home and perhaps removed band protecting his variola.

 

[AlaskaDenise]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

Ah yes, my smallpox vaccination - gotta keep that bandaid on.
below from: http://en.wikipedia.org/wiki/Vaccinia_virus

...the boy who acquired it from his father:

The child acquired the infection due to eczema, which is a known risk factor for vaccinia infection.

also regarding a "feral vaccine":

A Vaccinia virus infection is very mild and is typically asymptomatic in healthy individuals, but it may cause a mild rash and fever. Immune responses generated from a Vaccinia virus infection protects the person against a lethal smallpox infection. For this reason, Vaccinia virus was, and is still being used as a live-virus vaccine against smallpox.

While some physicians have said that a smallpox vaccination can protect people against shingles, I know of plenty of cases among the generation that reglarly received smallpox vaccnation who still get shingles.

I wonder how any cross-protection works among the animal with various "pox" family virus infections.

.

 

[Oracle]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

Yes Ma'am. Eczema would be one of several predisposing factors for increased risk of acquiring live vaccine shed virus from a recently inoculated source.

Live attenuated vaccine shedding has been documented in lab animals and in human patients, but the indication has always (happily) been that the shed rate is low and of short duration. In healthy hosts.

What if you had a host that had ongoing infection, such that viral replication was 'ramped-up' beyond that expected for a given suboptimal infective dose of attenuated virus? Or perhaps shedding occurred for a prolonged period and the new host was highly susceptible to infection?

Maybe you get escapees that find refuge in a new host (like camelids or crocodilans), undergoing successive adaptation cycles under specific conditions that promote low grade infective viral maintenance.

Answer to your previous question:
Carrying NMDA receptor genes that can be inserted in the host may provide a virus with an internal route of host transport to distant target tissues, via enhanced signaling of cellular inflammation cascade and immune attack/cell clearance.

This is a mechanism employed by a number of pathogens (bacterial, protozoal and viral).

D*mn clever.

Smallpox virus (variola virus) is significantly different than varicella virus (chickenpox). Both spread by viral particle packed blisters in the mouth and throat, but one is shed before the skin rash forms (chickenpox) and the other only after the rash develops. Chickenpox lesions are much more superficial than smallpox, and there are specific differences in the viruses themselves, beyond host symptoms.

Chickenpox vaccine's protection fades: Study.
Mar 14, 2007.
http://www.thestar.com/News/article/191903

 

[tropical]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

#1:
"the purchase of ?Jamal? from areas outside the protected city of Sharm el - Sheikh and the city of Al-Arish, by local residents, was brought to St. Catherine without a veterinary quarantine and inspection by veterinary unit."

That means that the areas outside the protected city of Sharm el - Sheikh and the city of Al-Arish are endemic camelpox harboring zones, or that's an novel episode in that region?

 

[Giuseppe]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

Yes Ma'am. Eczema would be one of several predisposing factors for increased risk of acquiring live vaccine shed virus from a recently inoculated source.

Live attenuated vaccine shedding has been documented in lab animals and in human patients, but the indication has always (happily) been that the shed rate is low and of short duration. In healthy hosts.

What if you had a host that had ongoing infection, such that viral replication was 'ramped-up' beyond that expected for a given suboptimal infective dose of attenuated virus? Or perhaps shedding occurred for a prolonged period and the new host was highly susceptible to infection?

Maybe you get escapees that find refuge in a new host (like camelids or crocodilans), undergoing successive adaptation cycles under specific conditions that promote low grade infective viral maintenance.

Answer to your previous question:
Carrying NMDA receptor genes that can be inserted in the host may provide a virus with an internal route of host transport to distant target tissues, via enhanced signaling of cellular inflammation cascade and immune attack/cell clearance.

This is a mechanism employed by a number of pathogens (bacterial, protozoal and viral).

D*mn clever.

Smallpox virus (variola virus) is significantly different than varicella virus (chickenpox). Both spread by viral particle packed blisters in the mouth and throat, but one is shed before the skin rash forms (chickenpox) and the other only after the rash develops. Chickenpox lesions are much more superficial than smallpox, and there are specific differences in the viruses themselves, beyond host symptoms.

Chickenpox vaccine's protection fades: Study.
Mar 14, 2007.
http://www.thestar.com/News/article/191903

Further, smallpox skin lesions are all at the same evolution status, rather than chickenpox where the blisters are in different status: macula, papula, vescicula, pustola...

 

[Oracle]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

First report of camelpox in Western zoonotic literature, is 1953 in Sudan (described with an Arabic term, Al Geddari). Outbreaks in Egypt, Kenya, Somolia, Saudi Arabia, Iraq, Iran, USSR followed (the most recent in Syria reported in 2006).

Epizootiology of Camel Pox, Camel Contagious Ecthyma and Camel Papillomatosis in the Sudan. Proceed. 3rd Annual Meet. Animal Prod. Under Arid Conditions, Vol. 2: 115-131 (1998).
www.isocard.org/Documents/Proceedings_1998_Camel%20Conference/vol_02_11.pdf

That the Sudanese had a name for camelpox suggests that it may have been known for some period before the mid-20th century. Camelpox position on VARV phylogeny trees that have been published, with respect to a molecular clock discussion of smallpox ancestor evolution. Camelpox diverged from the smallpox VARV primary ancestor sometime after humans spread out of Africa and into Asia (~16,000 YrsBeforePresent), but before radiation of modern strains (< 2000 yrs ago).

http://www.pnas.org/content/104/40/15787/F3.large.jpg

On the origin of smallpox: Correlating variola phylogenics with historical smallpox records. PNAS 2007 104(40):15787-15792.
http://www.pnas.org/content/104/40/15787.full

Camelpox occurs in two distinct forms, causing, respectively, mild and severe disease in young animals (Khalafalla, 1998).

I strongly suspect that virulence factors not found in VARV prime ORV (mentioned in recent VARV phylogeny genome comparisons mentioned in citations), were acquired in the last 2000 years.

Genome Sequence Diversity and Clues to the Evolution of Variola (Smallpox) Virus. Science (2006) 313(5788): 807 - 812.
http://www.sciencemag.org/cgi/content/abstract/313/5788/807

Further, I suggest that the modern form that causes serious disease emerged as the predominate type in the last 60 years.

Camels were used in battle for thousands of years in Asia and North Africa. They are considered to be quite valuable for their many and varied uses for transport, food, and as trade animal; they served nomadic merchants for at least 3-4000 years on the Silk Road route linking Mediterranean ports with the Far East and are the only animal to successfully compete and displace the wheel as transport. Domestication of the Arabian camel has been dated to the second millennium BC.

While camel disease literature is sparse (and historical accounts of camelid infectious agents even more spare), if there had been a camel-killer wiping out herds in North Africa and Asia, we would have heard about it before the twentieth century, because they were used by Western armies for at least several hundred years.

http://upload.wikimedia.org/wikipedia/commons/6/62/800px-2003camel.PNG

Global camel density map shows a significant population in the Western Egyptian deserts (Alexandria and westward), nothing in the Sinai desert or its mountains. There may have been small numbers of camels used for tourism and by a few nomadic tribes for transport and milk, but your report seems to indicate that the outbreak originated in camels brought into the area.

Nightmare fodder: Poxviruses as possible vectors for horizontal transfer of retroposons from reptiles to mammals. PNAS 2007; 104(29): 12046?12051.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1924541

 

[AlaskaDenise]

Re: Unknown Epidemic Causes Camel Deaths in Egypt

re Oracle's:

What if you had a host that had ongoing infection, such that viral replication was 'ramped-up' beyond that expected for a given suboptimal infective dose of attenuated virus? Or perhaps shedding occurred for a prolonged period and the new host was highly susceptible to infection?

This sounds like something that could happen with HIV infected people. (remember, I'm not a scientist, so I'm just speculating)
Wasn't it Robert Webster who proposed that HIV patients could become H5N1 super-spreaders (or dead) due to a prolonged shedding period?

Oracle - reading your posts is like reading plots for Sci-Fi movies.

.