Veterinary discussion help and assistant info group

TRYPANOSOMIASIS:

An important disease of cattle and buffalo caused by protozoa. It is transmitted mechanically by biting flies. Death may occur in 2 weeks to 2 months.

What disease does Trypanosoma cause in Cattles?
The disease is caused principally by three species of trypanosome (Trypanosoma congolense, T. vivax and T. brucei) which are transmitted by several species of tsetse flies (Glossina). Trypanosomiasis in cattle results in poor productivity and mortality

💢Symptoms of trypanosomiasis :-

_ infect the blood of the vertebrate host, causing

🔷 fever
🔷 weakness
🔷 lethargy
🔷 weight loss
🔷 anemia
🔷 severe headaches
🔷 irritability
🔷 extreme fatigue
🔷 swollen lymph nodes
🔷 aching muscles sickness
🔷 some People develop a skin rash
🔷 Progressive confusion

What 3 types of diseases does Trypanosoma
cause?

brucei, which causes sleeping sickness in humans and nagana in cattle. T. cruzi, which causes Chagas disease in humans. Trypanosoma culicavium, which infects birds and mosquitoes.

How do you prevent trypanosomiasis in cattle?

Trypanosomiasis can be controlled by treating livestock with trypanocides or insecticide – killing parasites or vectors, respectively. Mathematical modeling of trypanosomiasis was used to compare the impact of drug- and insecticide-based interventions on R 0 with varying densities of cattle

How is trypanosomiasis treatment?
The acute phase of trypanosomiasis (Chagas disease) is treated with nifurtimox or benznidazole. Cases of congenital Chagas disease have been successfully treated with either drug. A single case of successful treatment of an adult with posaconazole

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Is your pet a little (or a lot) chonky? 🫢

Pet obesity can be caused by a range of factors. It might be obvious, but walking is a great addition to a weight loss plan. If that's not an option for you or your pet, try having regular playtime together 🙌

Dogs are family love them care for them and feed them

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diseases causing (sudden death) in cattle :-
ـــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
1-Anthrax
2-Black leg
3-Pulpy kidney
4-Malignant edema
5-bacillary hemoglobinurea
6-acute salmonellosis
7-babesiosis
8-hemorrhagic septicemia
9-pneumonic pasteurellosis
10-coliform mastitis
11-FMD (calves)
12-Acute leptospirosis (calves)
13-Rinderpest (peracute)

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COMMON CHICKEN DISEASES

1. Gumboro Disease (Infections Bursal Disease)
It's an acute highly contagious viral infection caused by Infectious Bursal Disease virus (IBDV).
It destroys the lymph cells within the cloacal bursa of Fabricus , tonsils and spleen.
Has an incubation period of 3 weeks with signs appearing at 3 - 6 weeks.
The virus is shed in droppings and spread by contaminated surfaces, equipments, clothes or footwears.

Signs/Symptoms
√. Stained feathers around the vent area with faecal substance containing a lot of urates.
√. Sleeping with beaks on the floor ( severe prostration).
√. Rapid drop in feed and water consumption.
√. Vent picking.
√. Ruffled feathers.
√. Trembling and huddling.

2. Newcastle Disease
Highly contagious viral infection that attacks birds and can also attack humans causing conjunctivitis and minor flu-like symptoms.
It's spread by direct physical contact with infected birds, contaminated surfaces, food, water, footwears and carcasses. It's also present in manure and can also be breathed out in air.
Some stains of the virus attacks the nervous system while others attack the respiratory or digestive system.

Signs/Symptoms
√. Coughing and sneezing.
√. Nasal discharge.
√. Greenish wattery diarrhea.
√. Drop in egg production/ shapeless/thin or rough shells/ Eggs with watery albumen.
√. Muscle tremors.
√. Drooping wings.
√. Swelling of eyes or neck.
√. Twisted neck and head.
√. Circling paralysis.
√. Sudden death.

3. Fowl pox
A slow - spreading viral infection that occurs through skin abrasions and bites or by the respiratory routes.
It's transmitted by birds, formites or mosquitoes.
Infected birds can carry it for 3 - 5 weeks before showing any signs.
Most common in cockerels due to their tendency of fighting and causing skin damage, and birds affected by external parasites that bites infected birds and transmit the virus.
Individual birds may take 2 - 4 weeks to recover but may take long to fully eradicate it from chicken coop because it affects birds at different times.

Treatment and Prevention
The three diseases (Gumboro, Newcastle and Fowl pox) have no treatment.
Ensure that your chickens are vaccinated in time to prevent the diseases.
Also, remember to;
Isolate sick birds from the rest.
Maintain high levels of hygiene.
Dispose carcasses immediately.
Avoid unnecessary visits to people's poultry farms.
Disinfect your hands, clothes footwears before and after attending to your chickens.

Please Fill in the gap by answered the question below

Anthrax is a _______disease caused by _____while
Newcastle disease is a ______ and the etiological agent is _________

Coryza is usually acute and sometimes chronic, highly infectious disease of chickens, occasionally pheasants and guinea-fowl.
It is a bacterial disease characterised by catarrhal inflammation of the upper respiratory tract, especially nasal and sinus mucosae.

- The disease may be complicated due to secondary infections.
Morbidity is high but mortality low if uncomplicated, although it may be up to 20%.

- The route of infection is conjunctival or nasal with an incubation period of 1-3 days followed by rapid onset of the disease over a 2-3 day period with the whole flock affected within 10 days. The carrier transmission is via exudates and by direct contact. It is not egg-transmitted.

/SYMPTOMS
- Facial swelling.- Purulent ocular and nasal discharge.- Swollen wattles.-Sneezing.
- Dyspnoea.- Loss in condition. - Drop in egg production of 10-40%. - Lack of appetite.


- Gently squeeze the swollen eyes to remove the white substance then apply Propeta drops or any other antibiotic eye drops in the eyes or wash with salt water solution.

- Administer antibiotics like Tylodoxy 200, Tylosin and preferably ESB3 30% in water for five to seven days.


The best prevention method is by vaccination at the age of 5 to 6 weeks.

MUST READ FOR POULTRY FARMERS!

HOW TO IDENTIFY DIFFERENT DISEASES IN POULTRY FROM THEIR DROPPINGS AND HOW TO PREVENT AND TREAT THEM.

First, let us talk about the easiest approach to disease outbreak in poultry farming. Yes, you guessed right, the easiest and cheapest way to deal with diseases in poultry is by PROPER HYGIENE!

Many poultry farmers have lost a lot of money, even got discouraged and gave up on poultry farming because of disease outbreak, farmers losing birds in tens, hundreds every day is a poultry farmer's worse nightmare, trust me. However, you can prevent this through simple management practices. More of this will be discussed in our subsequent posts. Like, share and follow our page if you will like to see more tips.

Now to today's tips.

Different types of droppings in poultry birds and what they are trying to tell you:

1. YELLOW AND FOAMY DROPPINGS: Early stage of Coccidiosis. Embazim fort can be used for preventative and curative measures.

2. DROPPINGS WITH BLOOD: Coccidiosis. You didn't have to wait this long! You need Embazim fort or Amprolium and changing of litter more often than you normally do to prevent it! (For deep litter system)

3. GEENISH DROPPINGS: Late stage of worms, New Castle Disease, fowl cholera/typhoid, eaten not well dried feed or eaten a lot of green vegetables if free ranged. Action should be taken depending on other signs shown.

4. WHITE MILKY RUNNING DROPPING: Worms, Gumboro disease (Infectious Bursal Disease-IBD).

5. BROWN RUNNING DROPPING: E.coli Infection. You can treat with floxinor or gentylo and vitaflash

6. BLACK DROPPING: Possibility of internal bleeding or too much of proteins. To avoid internal bleeding and enteritis, you should use water acidifiers that's LIPTOBAC L PLUS

7. CLEAR OR WATERING RUNNING DROPPINGS: Infectious Bronchitis or Stress. This can also be caused by Mycotoxins. Also overdose of antibiotics.


STRESS!

Stress can be caused by any reason like transferring from one place to another. It could be too much heat or lack of water and/or feeds. It could also be unbalanced, unstable or insufficient feed and water. Figure out the actual cause by paying close attention and make amends, then place them on vitaflash to reduce stress.

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Identify the organ

Bloat in cattle:

Bloat is simply the build up of gas in the rumen.
This gas is produced as part of the normal process of digestion, and is normally lost by belching (eructation).
Bloat occurs when this loss of gas is prevented.

There are two sorts of bloat:

The least common type is gassy bloat, which occurs when the gullet is obstructed (often by foreign objects such as potatoes) or when the animal can’t burp (such as with milk fever or tetanus).

The second type of bloat is frothy bloat, which happens as the result of a stable foam developing on top of the rumen liquid, which blocks the release of the gas.
This is by far the most common form of bloat, and unlike gassy bloat, it is highly seasonal with peaks in the spring and autumn.
This is because the foam is formed by breakdown products from rapidly growing forages (particularly legumes such as clover and alfalfa).
These increase the viscosity (stickiness) of the rumen fluid and prevent the small bubbles of gas formed by rumen fermentation from coming together to form free gas that can be belched off

𝘾𝙡𝙞𝙣𝙞𝙘𝙖𝙡 𝙎𝙞𝙜𝙣𝙨

Distended left abdomen is the most obvious sign
Usually associated with pain, discomfort, and bellowing.

Death can occur within 15 minutes after the development of bloat.
Gaseous bloat is usually seen in one or two animals.
Frothy bloat can affect up to 25% of cases.
In some cases sudden death may be the first sign seen by the stockman, although in such cases it is likely that there will be other cattle with bloat that are still alive.

𝘿𝙄𝘼𝙂𝙉𝙊𝙎𝙄𝙎

History of what ruminants have fed on is key
Auscultation and Palpation
The use of a stomach tube help to distinguish between Gassy and Frothy Bloat. If is Gassy Bloat, the gas will escape through the tube.
However in Frothy Bloat, no gas will escape.

𝙏𝙍𝙀𝘼𝙏𝙈𝙀𝙉𝙏

The passage of a stomach tube is the best treatment for a Gassy Bloat.
Should a stomach tube fail, a Trochar and Cannula can be used to punch the side

Please if you have vet job vacancy in your area you DM me
I will advertise it so that some graduate can get something doing

𝐕𝐞𝐭𝐞𝐫𝐢𝐧𝐚𝐫𝐲____________________𝐃𝐕𝐌 𝐆𝐄𝐄𝐋𝐋𝐄
____________________________________________
𝐄𝐲𝐞 𝐝𝐢𝐬𝐞𝐚𝐬𝐞 (𝟐)

( 𝐄𝐲𝐞 𝐖𝐨𝐫𝐦 )
___________________________________________

These worms live in the conjunctival sac (eyelid) of the eye in many species of livestock, in many countries.
Cattle, sheep, horses, camels, goats, pigs, dogs, cats, birds, and humans can be affected.

The most common species is ✔Thelazia rhodesii, which parasitizes cattle and sheep. The worms are up to 2cm long and are thin and white.
One or both eyes may be affected.

___________________________________________
𝐌𝐨𝐝𝐞 𝐨𝐟 𝐬𝐩𝐫𝐞𝐚𝐝
___________________________________________
Various species of fly, in which the worm has part of its life cycle, are responsible for the spread of the worm from one animal to another.

The fly has a preference for eye secretions which are ideal for transmission. The fly ingests the larvae which become infective in 2-4 weeks.

These larvae are mechanically deposited in teh host's eye by the fly during feeding. Development of sexually mature worms takes about 1-4 weeks in cattle.

The worm lives under the eyelids, in the conjunctival sac and under the third eyelid. The worm has a rough cuticle (skin) which causes irritation and inflammation to the cornea.
___________________________________________

𝐒𝐢𝐠𝐧𝐬 𝐨𝐟 𝐞𝐲𝐞 𝐰𝐨𝐫𝐦𝐬
___________________________________________
1.Excessive production of tears which may contain pus.

2.Avoiding sunlight.

3.Inflammation of the thin membrane covering the white of teh eye and the inner surface of the eyelid (Conjunctivitis).

4.Cloudiness of the cornea and sometimes ulceration and piercing of the cornea.

5.Lack of response to treatment with antibiotics.
___________________________________________

𝐃𝐢𝐚𝐠𝐧𝐨𝐬𝐢𝐬
___________________________________________
1.Close inspection of the eyes will reveal small white worms swimming in the conjunctival fluid. Several animals should be examined as it will not be possible to see worms in every animal. Even if the worms can be seen with the naked eye, a veterinarian should be consulted to confirm their presence.
___________________________________________

𝐏𝐫𝐞𝐯𝐞𝐧𝐭𝐢𝐨𝐧 𝐨𝐟 𝐄𝐲𝐞 𝐖𝐨𝐫𝐦𝐬 𝐈𝐧𝐟𝐞𝐬𝐭𝐚𝐭𝐢𝐨𝐧
___________________________________________
The condition is less severe than Pink Eye. Control of the fly is not practical.
___________________________________________

𝐑𝐞𝐜𝐨𝐦𝐦𝐞𝐧𝐝𝐞𝐝 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐚𝐧𝐝 𝐂𝐨𝐧𝐭𝐫𝐨𝐥
___________________________________________
1. Using an eye wash containing a local anaesthetic and wash the worms out of the eye. A mixture of 10 ml of 2% local anaesthetic solution with 40-50ml of clean water makes the eye wash. 5-10 ml is put onto the eye and after waiting for about 2 minutes, the worms are washed out of the eye using clean cold water.

2. Certain systemic dewormers such as Levamisole at 5 mg/kg under the skin and Ivermectin and Doramectin both at 0.2 mg/kg SC or in the muscle are effective treatments.

3. Pour-on forumlations of Ivermectin and Doramectin, delivered on the back of the animal to achieve a dosage of 0.5 mg/kg are also highly effective.

4. Treatment is also possible with topical application of Levamisole or topical Ivermectin. Bother are given as a 1% aqueous solution directly into the eye. If the eye discharge is cloudy or white it may be advisable to put an antibiotic ointment into the eye following removal of the worm or following the administration of dewormers.
___________________________________________

DRUGS OF CHOICE FOR VETERINARY USES...
----------------------------------------------------------
1. Paracetamol poisoning- :- - acetyl cysteine
2. acute bronchial- asthma :- salbutamol
3. acute gout :- NSAIDS
4. acute hyperkalemia:- calcium gluconate
5. severe DIGITALIS toxicity :-DIGIBIND
6. acute migraine :- sumatriptan
7. cheese reaction :- phentolamine
8. atropine poisoning :- physostigmine
9. cyanide poisoning :- amyl nitrite
10. benzodiazepine poisoning:- flumazenil
11. cholera :- tetracycline
12. KALA-AZAR :- lipozomal amphotericin- B
13. iron poisoning :- desferrioxamine­
14. MRSA :- vancomycin
15. VRSA :- LINEZOLID
16. warfarin overdose :- vitamin-K (NIPER- 2009)
17. OCD :- fluoxetine
18. alcohol poisoning :- fomepizole
19. epilepsy in pregnency :- phenobarbitone
20. anaphylactic shock :- Adrenaline
21. MRSA Infection-Vancomycin
22. Malaria in Pregnancy-Chloroquine
23. Whooping Cough or Perteusis- Erythromycin
24. Kawasaki disease-IV Ig
25. Warferin Overdose-Vit-K
26. Heparin Overdose-Protamine
27. Hairy Cell Leukemia-Cladirabine
28. Multiple Myeloma- Melphalan
29. CML-Imatinib
30. Wegner's granulomatosis-
Cyclophosphamide
31. HOCM- Propranolol
32. Delirium Tremens-Diazepam
33. Drug Induced Parkinsonism-Be
nzhexol
34. Diacumarol Poisoning-Vit-K
35. Type-1 Lepra Reaction-Steroids
36. Type- 2 Lepra Reaction-Thalidomide
37. Allergic Contect Dermatitis-Steroids
38. PSVT- 1st-Adenosine, 2nd-Verapamil, 3rd-Digoxin
39. Z-E Syndrome- Proton Pump Inhibitor
40. Chancroid-Cotrimoxazole
41. Dermatitis Herpetiformis-Dapsone
42. Spastic Type of Cerebral Palsy-Diazepam
43. Herpis Simplex Keratitis-Trifluridine
44. Herpes Simplex Orolabialis-Pan
cyclovir
45. Neonatal Herpes Simplex-Acyclovir
46. Pneumocystis carinii Pneumonia-Cotri
moxazole For Nodulo
47. 47. Cystic Acne-Retinoic acid
48. Trigeminal Neuralgia-Carbamezapine
49. Actinomycosis-Penicillin
50. Plague- Streptomycin
51. Opioid Withdrawal- Methadone 2nd-Clonidine
52. Alcohol Withdrawal- Chlordiazepoxide 2nd-Diazepam
53. Post Herpetic Neuralgia- Fluphenazine
54. WEST Syndrome-ACTH
55. Diabetic Diarrhoea- Clonidine
56. Lithium Induced Neuropathy-Amil
orideCommunicable Disease:
57. Tetanus: PEN G Na; TETRACYCLINE; (DIAZEPAM
58. Diphteria: PEN G K; ERYTHROMYCIN
59. Pertusis: ERYTHROMYCIN; AMPICILLIN
60. Meningitis: MANNITOL (osmotic diuretic);DEXAMETHASONE (anti-inflammatory); DILANTIN/PHENYTOIN (anti-convulsive); PYRETINOL/
ENCEPHABO L (CNS stimulant)
61. Cholera: TETRACYCLINE
62. Amoebic Dysentery: METRONIDAZOLE
63. Shigellosis: CO-TRIMOXAZOLE
64. Typhoid: CHORAMPHENICOL
65. Rabies: LYSSAVAC, VERORAB
66. Immunoglobulins: ERIG or HRIg
67. Malaria: CHLOROQUINE
68. Schistosomiasis: PRAZIQUANTEL
69. Felariasis: DIETHYLCARBAMAZINE CITRATE
70. Scabies: EURAX/ CROTAMITON
71. Chicken pox: ACYCLOVIR/ZOVIRAX
72. Leptospirosis: PENICILLIN; TETRACYCLINE;ERYTHROMYCIN
73. Leprosy: DAPSONE, RIFAMPICIN
74. Anthrax: PENICILLIN
75. Tuberculosis: R.I.P.E.S.
76. Pneumonia: COTRIMOXAZOLE; ProcainePenicillin
77. Helminths: MEBENDAZOLE; PYRANTELPAMOATE
78. Meningitis: MANNITOL (dec. ICP) ;DEXAMETHASONE ( relieve cerebral edema) ;DIAZEPAM ( anticonvulsant); PENICILLIN
79. Syphilis: PENICILLIN
80. Gonorrhea: PENICILLIN...

Dear Poultry Farmers,

CAUSES OF EARLY CHICKS MORTALITY IN POULTRY (Broiler farming)

Chicks are very fragile during the first few weeks of their life, so sound management is very vital to keep flock healthy. It should be noted that no matter the quality of the chicks supplied/procured and the soundness of management, mortality cannot be totally avoided in a flock. A mortality of between 1-5% is considered normal but anything higher than this should alarm the farmer.

Early chick mortality can be caused by many factors ranging from genetic, to management, nutritional and disease causes

🐣. GENETIC CAUSES
There are many lethal gene mutations in birds, most of which cause death during the incubation period and first few days of life because such chicks find it difficult to survive.

🐣. MANAGEMENT CAUSES
Poor management is often one of the most important causes of early chick mortality. Sound management is very vital to the survival and performance of any flock. With bad management, chicks sourced from reliable sources will perform poorly might never manifest their full genetic potentials.

Some of these management blunders are;
* High brooding temperature
* Low brooding temperature
* High relative humidity
* High stocking density
* Litter contamination
* Operational injuries
* Wrong or inadequate feeders and drinkers
* Predators

🐣. NUTRITIONAL CAUSES
Good nutrition means giving a balanced diet to a flock in the right quantity evenly distributed among the flock. Good nutrition goes beyond providing good feed alone, it also entails providing adequate clean and disease free water to flock.

🐣. DISEASE CAUSES
If biosecurity measures are not maintained then there is a great chance of disease out-break, because the young chick lack immunity .

a) Omphalitis
b) Pullorum
c) Salmonellosis
d) Colibacillosis

Please share to let s

𝗺𝗼𝗻𝗸𝗲𝘆 𝗽𝗼𝘅

Monkeypox is a viral zoonosis (a virus transmitted to humans from animals) with symptoms similar to those seen in the past in smallpox patients, although it is clinically less severe. With the eradication of smallpox in 1980 and subsequent cessation of smallpox vaccination, monkeypox has emerged as the most important orthopoxvirus for public health. Monkeypox primarily occurs in central and west Africa, often in proximity to tropical rainforests, and has been increasingly appearing in urban areas. Animal hosts include a range of rodents and non-human primates

The pathogen

Monkeypox virus is an enveloped double-stranded DNA virus that belongs to the Orthopoxvirus genus of the Poxviridae family. There are two distinct genetic clades of the monkeypox virus: the central African (Congo Basin) clade and the west African clade. The Congo Basin clade has historically caused more severe disease and was thought to be more transmissible. The geographical division between the two clades has so far been in Cameroon, the only country where both virus clades have been found

Natural host of monkeypox virus

Various animal species have been identified as susceptible to monkeypox virus. This includes rope squirrels, tree squirrels, Gambian pouched rats, dormice, non-human primates and other species. Uncertainty remains on the natural history of monkeypox virus and further studies are needed to identify the exact reservoir(s) and how virus circulation is maintained in nature.

Outbreaks

Human monkeypox was first identified in humans in 1970 in the Democratic Republic of the Congo in a 9-month-old boy in a region where smallpox had been eliminated in 1968. Since then, most cases have been reported from rural, rainforest regions of the Congo Basin, particularly in the Democratic Republic of the Congo and human cases have increasingly been reported from across central and west Africa.

Since 1970, human cases of monkeypox have been reported in 11 African countries: Benin, Cameroon, the Central African Republic, the Democratic Republic of the Congo, Gabon, Cote d’Ivoire, Liberia, Nigeria, the Republic of the Congo, Sierra Leone and South Sudan. The true burden of monkeypox is not known. For example, in 1996–97, an outbreak was reported in the Democratic Republic of the Congo with a lower case fatality ratio and a higher attack rate than usual. A concurrent outbreak of chickenpox (caused by the varicella virus, which is not an orthopoxvirus) and monkeypox was found, which could explain real or apparent changes in transmission dynamics in this case. Since 2017, Nigeria has experienced a large outbreak, with over 500 suspected cases and over 200 confirmed cases and a case fatality ratio of approximately 3%. Cases continue to be reported until today.

Monkeypox is a disease of global public health importance as it not only affects countries in west and central Africa, but the rest of the world. In 2003, the first monkeypox outbreak outside of Africa was in the United States of America and was linked to contact with infected pet prairie dogs. These pets had been housed with Gambian pouched rats and dormice that had been imported into the country from Ghana. This outbreak led to over 70 cases of monkeypox in the U.S. Monkeypox has also been reported in travelers from Nigeria to Israel in September 2018, to the United Kingdom in September 2018, December 2019, May 2021 and May 2022, to Singapore in May 2019, and to the United States of America in July and November 2021. In May 2022, multiple cases of monkeypox were identified in several non-endemic countries. Studies are currently underway to further understand the epidemiology, sources of infection, and transmission patterns.

Transmission

Animal-to-human (zoonotic) transmission can occur from direct contact with the blood, bodily fluids, or cutaneous or mucosal lesions of infected animals. In Africa, evidence of monkeypox virus infection has been found in many animals including rope squirrels, tree squirrels, Gambian poached rats, dormice, different species of monkeys and others. The natural reservoir of monkeypox has not yet been identified, though rodents are the most likely. Eating inadequately cooked meat and other animal products of infected animals is a possible risk factor. People living in or near forested areas may have indirect or low-level exposure to infected animals.

Human-to-human transmission can result from close contact with respiratory secretions, skin lesions of an infected person or recently contaminated objects. Transmission via droplet respiratory particles usually requires prolonged face-to-face contact, which puts health workers, household members and other close contacts of active cases at greater risk. However, the longest documented chain of transmission in a community has risen in recent years from 6 to 9 successive person-to-person infections. This may reflect declining immunity in all communities due to cessation of smallpox vaccination. Transmission can also occur via the placenta from mother to fetus (which can lead to congenital monkeypox) or during close contact during and after birth. While close physical contact is a well-known risk factor for transmission, it is unclear at this time if monkeypox can be transmitted specifically through sexual transmission routes. Studies are needed to better understand this risk.


Signs and symptoms

The incubation period (interval from infection to onset of symptoms) of monkeypox is usually from 6 to 13 days but can range from 5 to 21 days.

The infection can be divided into two periods:

the invasion period (lasts between 0–5 days) characterized by fever, intense headache, lymphadenopathy (swelling of the lymph nodes), back pain, myalgia (muscle aches) and intense asthenia (lack of energy). Lymphadenopathy is a distinctive feature of monkeypox compared to other diseases that may initially appear similar (chickenpox, measles, smallpox)

the skin eruption usually begins within 1–3 days of appearance of fever. The rash tends to be more concentrated on the face and extremities rather than on the trunk. It affects the face (in 95% of cases), and palms of the hands and soles of the feet (in 75% of cases). Also affected are oral mucous membranes (in 70% of cases), genitalia (30%), and conjunctivae (20%), as well as the cornea. The rash evolves sequentially from macules (lesions with a flat base) to papules (slightly raised firm lesions), vesicles (lesions filled with clear fluid), pustules (lesions filled with yellowish fluid), and crusts which dry up and fall off. The number of lesions varies from a few to several thousand. In severe cases, lesions can coalesce until large sections of skin slough off.

Monkeypox is usually a self-limited disease with the symptoms lasting from 2 to 4 weeks. Severe cases occur more commonly among children and are related to the extent of virus exposure, patient health status and nature of complications. Underlying immune deficiencies may lead to worse outcomes. Although vaccination against smallpox was protective in the past, today persons younger than 40 to 50 years of age (depending on the country) may be more susceptible to monkeypox due to cessation of smallpox vaccination campaigns globally after eradication of the disease. Complications of monkeypox can include secondary infections, bronchopneumonia, sepsis, encephalitis, and infection of the cornea with ensuing loss of vision. The extent to which asymptomatic infection may occur is unknown.

The case fatality ratio of monkeypox has historically ranged from 0 to 11 % in the general population and has been higher among young children. In recent times, the case fatality ratio has been around 3–6%.



Diagnosis

The clinical differential diagnosis that must be considered includes other rash illnesses, such as chickenpox, measles, bacterial skin infections, scabies, syphilis, and medication-associated allergies. Lymphadenopathy during the prodromal stage of illness can be a clinical feature to distinguish monkeypox from chickenpox or smallpox.

If monkeypox is suspected, health workers should collect an appropriate sample and have it transported safely to a laboratory with appropriate capability. Confirmation of monkeypox depends on the type and quality of the specimen and the type of laboratory test. Thus, specimens should be packaged and shipped in accordance with national and international requirements. Polymerase chain reaction (PCR) is the preferred laboratory test given its accuracy and sensitivity. For this, optimal diagnostic samples for monkeypox are from skin lesions – the roof or fluid from vesicles and pustules, and dry crusts. Where feasible, biopsy is an option. Lesion samples must be stored in a dry, sterile tube (no viral transport media) and kept cold. PCR blood tests are usually inconclusive because of the short duration of viremia relative to the timing of specimen collection after symptoms begin and should not be routinely collected from patients.

As orthopoxviruses are serologically cross-reactive, antigen and antibody detection methods do not provide monkeypox-specific confirmation. Serology and antigen detection methods are therefore not recommended for diagnosis or case investigation where resources are limited. Additionally, recent or remote vaccination with a vaccinia-based vaccine (e.g. anyone vaccinated before smallpox eradication, or more recently vaccinated due to higher risk such as orthopoxvirus laboratory personnel) might lead to false positive results.

Therapeutics

Clinical care for monkeypox should be fully optimized to alleviate symptoms, manage complications and prevent long-term sequelae. Patients should be offered fluids and food to maintain adequate nutritional status. Secondary bacterial infections should be treated as indicated. An antiviral agent known as tecovirimat that was developed for smallpox was licensed by the European Medicines Agency (EMA) for monkeypox in 2022 based on data in animal and human studies. It is not yet widely available.

If used for patient care, tecovirimat should ideally be monitored in a clinical research context with prospective data collection.

Vaccination

Vaccination against smallpox was demonstrated through several observational studies to be about 85% effective in preventing monkeypox. Thus, prior smallpox vaccination may result in milder illness. Evidence of prior vaccination against smallpox can usually be found as a scar on the upper arm. At the present time, the original (first-generation) smallpox vaccines are no longer available to the general public. Some laboratory personnel or health workers may have received a more recent smallpox vaccine to protect them in the event of exposure to orthopoxviruses in the workplace. A still newer vaccine based on a modified attenuated vaccinia virus (Ankara strain) was approved for the prevention of monkeypox in 2019. This is a two-dose vaccine for which availability remains limited. Smallpox and monkeypox vaccines are developed in formulations based on the vaccinia virus due to cross-protection afforded for the immune response to orthopoxviruses.

Prevention

Raising awareness of risk factors and educating people about the measures they can take to reduce exposure to the virus is the main prevention strategy for monkeypox. Scientific studies are now underway to assess the feasibility and appropriateness of vaccination for the prevention and control of monkeypox. Some countries have, or are developing, policies to offer vaccine to persons who may be at risk such as laboratory personnel, rapid response teams and health workers𝗺𝗼𝗻𝗸𝗲𝘆 𝗽𝗼𝘅

Monkeypox is a viral zoonosis (a virus transmitted to humans from animals) with symptoms similar to those seen in the past in smallpox patients, although it is clinically less severe. With the eradication of smallpox in 1980 and subsequent cessation of smallpox vaccination, monkeypox has emerged as the most important orthopoxvirus for public health. Monkeypox primarily occurs in central and west Africa, often in proximity to tropical rainforests, and has been increasingly appearing in urban areas. Animal hosts include a range of rodents and non-human primates

The pathogen

Monkeypox virus is an enveloped double-stranded DNA virus that belongs to the Orthopoxvirus genus of the Poxviridae family. There are two distinct genetic clades of the monkeypox virus: the central African (Congo Basin) clade and the west African clade. The Congo Basin clade has historically caused more severe disease and was thought to be more transmissible. The geographical division between the two clades has so far been in Cameroon, the only country where both virus clades have been found

Natural host of monkeypox virus

Various animal species have been identified as susceptible to monkeypox virus. This includes rope squirrels, tree squirrels, Gambian pouched rats, dormice, non-human primates and other species. Uncertainty remains on the natural history of monkeypox virus and further studies are needed to identify the exact reservoir(s) and how virus circulation is maintained in nature.

Outbreaks

Human monkeypox was first identified in humans in 1970 in the Democratic Republic of the Congo in a 9-month-old boy in a region where smallpox had been eliminated in 1968. Since then, most cases have been reported from rural, rainforest regions of the Congo Basin, particularly in the Democratic Republic of the Congo and human cases have increasingly been reported from across central and west Africa.

Since 1970, human cases of monkeypox have been reported in 11 African countries: Benin, Cameroon, the Central African Republic, the Democratic Republic of the Congo, Gabon, Cote d’Ivoire, Liberia, Nigeria, the Republic of the Congo, Sierra Leone and South Sudan. The true burden of monkeypox is not known. For example, in 1996–97, an outbreak was reported in the Democratic Republic of the Congo with a lower case fatality ratio and a higher attack rate than usual. A concurrent outbreak of chickenpox (caused by the varicella virus, which is not an orthopoxvirus) and monkeypox was found, which could explain real or apparent changes in transmission dynamics in this case. Since 2017, Nigeria has experienced a large outbreak, with over 500 suspected cases and over 200 confirmed cases and a case fatality ratio of approximately 3%. Cases continue to be reported until today.

Monkeypox is a disease of global public health importance as it not only affects countries in west and central Africa, but the rest of the world. In 2003, the first monkeypox outbreak outside of Africa was in the United States of America and was linked to contact with infected pet prairie dogs. These pets had been housed with Gambian pouched rats and dormice that had been imported into the country from Ghana. This outbreak led to over 70 cases of monkeypox in the U.S. Monkeypox has also been reported in travelers from Nigeria to Israel in September 2018, to the United Kingdom in September 2018, December 2019, May 2021 and May 2022, to Singapore in May 2019, and to the United States of America in July and November 2021. In May 2022, multiple cases of monkeypox were identified in several non-endemic countries. Studies are currently underway to further understand the epidemiology, sources of infection, and transmission patterns.

Transmission

Animal-to-human (zoonotic) transmission can occur from direct contact with the blood, bodily fluids, or cutaneous or mucosal lesions of infected animals. In Africa, evidence of monkeypox virus infection has been found in many animals including rope squirrels, tree squirrels, Gambian poached rats, dormice, different species of monkeys and others. The natural reservoir of monkeypox has not yet been identified, though rodents are the most likely. Eating inadequately cooked meat and other animal products of infected animals is a possible risk factor. People living in or near forested areas may have indirect or low-level exposure to infected animals.

Human-to-human transmission can result from close contact with respiratory secretions, skin lesions of an infected person or recently contaminated objects. Transmission via droplet respiratory particles usually requires prolonged face-to-face contact, which puts health workers, household members and other close contacts of active cases at greater risk. However, the longest documented chain of transmission in a community has risen in recent years from 6 to 9 successive person-to-person infections. This may reflect declining immunity in all communities due to cessation of smallpox vaccination. Transmission can also occur via the placenta from mother to fetus (which can lead to congenital monkeypox) or during close contact during and after birth. While close physical contact is a well-known risk factor for transmission, it is unclear at this time if monkeypox can be transmitted specifically through sexual transmission routes. Studies are needed to better understand this risk.


Signs and symptoms

The incubation period (interval from infection to onset of symptoms) of monkeypox is usually from 6 to 13 days but can range from 5 to 21 days.

The infection can be divided into two periods:

the invasion period (lasts between 0–5 days) characterized by fever, intense headache, lymphadenopathy (swelling of the lymph nodes), back pain, myalgia (muscle aches) and intense asthenia (lack of energy). Lymphadenopathy is a distinctive feature of monkeypox compared to other diseases that may initially appear similar (chickenpox, measles, smallpox)

the skin eruption usually begins within 1–3 days of appearance of fever. The rash tends to be more concentrated on the face and extremities rather than on the trunk. It affects the face (in 95% of cases), and palms of the hands and soles of the feet (in 75% of cases). Also affected are oral mucous membranes (in 70% of cases), genitalia (30%), and conjunctivae (20%), as well as the cornea. The rash evolves sequentially from macules (lesions with a flat base) to papules (slightly raised firm lesions), vesicles (lesions filled with clear fluid), pustules (lesions filled with yellowish fluid), and crusts which dry up and fall off. The number of lesions varies from a few to several thousand. In severe cases, lesions can coalesce until large sections of skin slough off.

Monkeypox is usually a self-limited disease with the symptoms lasting from 2 to 4 weeks. Severe cases occur more commonly among children and are related to the extent of virus exposure, patient health status and nature of complications. Underlying immune deficiencies may lead to worse outcomes. Although vaccination against smallpox was protective in the past, today persons younger than 40 to 50 years of age (depending on the country) may be more susceptible to monkeypox due to cessation of smallpox vaccination campaigns globally after eradication of the disease. Complications of monkeypox can include secondary infections, bronchopneumonia, sepsis, encephalitis, and infection of the cornea with ensuing loss of vision. The extent to which asymptomatic infection may occur is unknown.

The case fatality ratio of monkeypox has historically ranged from 0 to 11 % in the general population and has been higher among young children. In recent times, the case fatality ratio has been around 3–6%.



Diagnosis

The clinical differential diagnosis that must be considered includes other rash illnesses, such as chickenpox, measles, bacterial skin infections, scabies, syphilis, and medication-associated allergies. Lymphadenopathy during the prodromal stage of illness can be a clinical feature to distinguish monkeypox from chickenpox or smallpox.

If monkeypox is suspected, health workers should collect an appropriate sample and have it transported safely to a laboratory with appropriate capability. Confirmation of monkeypox depends on the type and quality of the specimen and the type of laboratory test. Thus, specimens should be packaged and shipped in accordance with national and international requirements. Polymerase chain reaction (PCR) is the preferred laboratory test given its accuracy and sensitivity. For this, optimal diagnostic samples for monkeypox are from skin lesions – the roof or fluid from vesicles and pustules, and dry crusts. Where feasible, biopsy is an option. Lesion samples must be stored in a dry, sterile tube (no viral transport media) and kept cold. PCR blood tests are usually inconclusive because of the short duration of viremia relative to the timing of specimen collection after symptoms begin and should not be routinely collected from patients.

As orthopoxviruses are serologically cross-reactive, antigen and antibody detection methods do not provide monkeypox-specific confirmation. Serology and antigen detection methods are therefore not recommended for diagnosis or case investigation where resources are limited. Additionally, recent or remote vaccination with a vaccinia-based vaccine (e.g. anyone vaccinated before smallpox eradication, or more recently vaccinated due to higher risk such as orthopoxvirus laboratory personnel) might lead to false positive results.

Therapeutics

Clinical care for monkeypox should be fully optimized to alleviate symptoms, manage complications and prevent long-term sequelae. Patients should be offered fluids and food to maintain adequate nutritional status. Secondary bacterial infections should be treated as indicated. An antiviral agent known as tecovirimat that was developed for smallpox was licensed by the European Medicines Agency (EMA) for monkeypox in 2022 based on data in animal and human studies. It is not yet widely available.

If used for patient care, tecovirimat should ideally be monitored in a clinical research context with prospective data collection.

Vaccination

Vaccination against smallpox was demonstrated through several observational studies to be about 85% effective in preventing monkeypox. Thus, prior smallpox vaccination may result in milder illness. Evidence of prior vaccination against smallpox can usually be found as a scar on the upper arm. At the present time, the original (first-generation) smallpox vaccines are no longer available to the general public. Some laboratory personnel or health workers may have received a more recent smallpox vaccine to protect them in the event of exposure to orthopoxviruses in the workplace. A still newer vaccine based on a modified attenuated vaccinia virus (Ankara strain) was approved for the prevention of monkeypox in 2019. This is a two-dose vaccine for which availability remains limited. Smallpox and monkeypox vaccines are developed in formulations based on the vaccinia virus due to cross-protection afforded for the immune response to orthopoxviruses.

Prevention

Raising awareness of risk factors and educating people about the measures they can take to reduce exposure to the virus is the main prevention strategy for monkeypox. Scientific studies are now underway to assess the feasibility and appropriateness of vaccination for the prevention and control of monkeypox. Some countries have, or are developing, policies to offer vaccine to persons who may be at risk such as laboratory personnel, rapid response teams and health workers