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Dairy Cattle Rotation

There are so many rectal palpations and I did not enjoy that

My arm is sometimes briefly warm, but it’s not worth it.

Cows may still try to alligator roll on you even if they are ‘down’

Never forget the 5 M’s of a down dairy cow (mastitis, metritis, metabolic (hypocalcemia, fatty liver), musculoskeletal, and massive infection)

Would you put that milk in your cereal? If not, culture it!

Lameness happens. 90% of lameness is in the hind limb, 90% of that is in the lateral claw!

Palpation to determine pregnancy is an art form and I suck at it so far. Sorry, cows.

Double glove/sleeve to go in a cow. For palpation or surgery!

There’s an effective vaccine for Johne’s disease (map) that is not commonly used in states with high prevalence of TB, which is why I had never heard of it before!

Actively dying cows may exhibit rotary nystagmus.

It’s really hard to collect blood samples from calves when they are group housed because they all come over to try to suckle your coat, pants, elbow, whatever they can reach

Epidurals are pretty awesome because you can hear a vacuum when you get the needle in! Time for lidocaine!

Rumen is love, rumen is life

Administering a slurry to a cow to help keep their rumen full is a wild ride, but very easy once you get the hang of it!

Meconium staining on a neonatal calf is a sign of fetal distress.

BIOSECURITY is essential. Anything that has been around cows needs to be kept separate. Boots should be cleaned any time they go to their holding area. Always wear gloves, always wash your hands

Barns are still cold. Put on as many layers as you can fit. You can always ditch layers, but you’ll miss the ones you did not bring! Bring gloves to put under your exam gloves!

Cows make so much milk. The avg on this farm was 82 lb. milk/day/cow

Prevention is the answer to most problems on the farm. Training staff is the hard part.

Sand is a very hygienic bedding for cows and comfy too

Pasteurization machines can cost upwards of $30,000 US.

Cows actually want to be milked! They get excited to come to the parlor and this is even more evident where robotic milking systems are in place. They choose to show up and get milked.

Cows are so insanely curious and it’s adorable

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[4amstudythoughts]

Might have been a slow few days, but the days of productivity haven't been broken yet. Yesterday I ended up having to complete a compensation PowerPoint on DNA hybridisation for my epizoo class. I'm at Q13/160 done and today we're flying to the UK before flying back to Slovakia tomorrow.

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Day 5/? Wouldn't be a vet student blog without a cat. Pepé and studying Q8-11/160.

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Day 4/? Q5-7/160 not quite willing to let go of those Christmas vibes, so studying with a Julebrus (Christmas pop) 🌲😁🇳🇴

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Today was a slow day on the studying front but every little helps? Day 3/?

Q4/160 and I learnt that colliquative (liquefactive) necrosis is common in the central nervous system, as encephalomalacia and myelomalacia, due to a high content of lysosomal enzymes (repsonsible for liquefaction) and small amounts of albumin (needed for coagulative necrosis).

Continued learning a little about adrenal tumours but finding it a bit above my level of knowledge!

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The One Where my textbook reached peak tumblr. Q2-3/160 on necrosis and a little more extracurricular focus on adrenal tumours. Day 2/?

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New year, new attempt at productivity. Last exam of the exam season Q1/160 and some extracurricular oncology reading. 1/?

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BIOCHEMISTRY BLOOD TESTING

Biochemistry blood test measures the levels of chemical substances carried in the blood. This type of test allows us to evaluate the how well the liver and kidneys are working and how much fat and sugar is circulating in the bloodstream.

Blood Glucose 

When carbohydrates are eaten they are broken down and stored in the Liver as Glycogen until the animal needs energy where it is then converted to glucose and transported around the body. We use blood glucose as a monitor of metabolism and physiology.

Normal BG (Canine) - 5.6 to 13.9mmol/L

Normal BG (Feline) - 5.6 to 16.7mmol/L

INCREASED BG - Diabetes Mellitus is indicated however it is recommended that the urine is also checked for Glucose as if present this means the kidneys have reached their threshold and Diabetes is very likely. Note that cats can have stress induced hyperglycemia and so a diagnosis of diabetes should not be made on a single BG reading.

DECREASED BG - Patients that are sick and deliberated often have hypoglycemia. but puppies who have been starved for procedures can also suffer from a low BG. In addition to this hunting breeds that have been working hard for a prolonged time can also suffer from a low BG.

Bun Urea Nitrogen (BUN)

BUN is the by product produced when Proteins are broken down and used within the body. This by-product is excreted by the Kidneys in the urine. 

INCREASED BUN - This would mean the kidneys are not working sufficiently and could be an indicator of kidney disease or kidney obstruction that is preventing urine reaching the bladder and therefore build up in the Kidney. Heart disease causing poor circulation to the kidneys could also be a cause of increased BUN.

DECREASED BUN - As the liver breaks down Protein a lower level of BUN could indicate that the liver is not working as well as it should and isn’t breaking down protein as well as it should.

Creatinine (CREA)

Creatinine is solely filtered out of the blood by the kidneys.

INCREASED CREA - Impaired Kidney function

Calcium (CAL)

Calcium is a mineral that is found at a consistent level within the blood. It’s needed for muscle and nerve function and without it death can occur.

INCREASED CAL - Some types of cancers and medications can cause an increase in Calcium.

DECREASED CAL - Some animals can experience low calcium levels during pregnancy, post partum and during lactation. This condition is called Eclampsia.

Total Protein (TP) 

The measurement of two blood protein molecules: Albumin and Globulins. Albumin is produced by the Liver and levels are often decreased when the animal is going through a period of poor nutrition. Chronic infectious disease will also cause low Albumin levels.

Globulins include immunoglobulins which are used by the body to fight infection. Certain diseases such as FIP can cause an increase in this.

Bilirubin (BIL)

Haemoglobin is found inside red blood cells, it carries oxygen to tissues around the body. When RBC’s die or are destroyed and the haemoglobin is broken down, bilirubin is a by product of this process which is then excreted by the Liver. 

INCREASED BIL -  An increase can be seen when the Liver is diseased and is can’t clear the bilirubin efficiently. A liver or bile duct obstruction can cause bilirubin to build up thus resulting in high levels in the blood so this should also be considered.

Alkaline Phophatese (ALKP)

This is an enzyme used to assist with various chemical reactions within the body. The normal levels vary from animal to animal but in dogs, an increase could indicate some forms of cancer or Liver disease.

Atanine Amino Transferase (ALT)

This is an important enzyme for adequate Liver function. An increase in this enzyme would indicate that Liver cells are breaking down, this could be because of cancer, cirrhosis, or liver congestion due to heart failure.

Cholesterol (CHOL)

INCREASE CHOL - Inadequate Thyroid function

DECREASE CHOL - The animal has been through a period of starvation or is not having their nutritional requirements met.

SODIUM: POTASSIUM RATIO

These levels are almost always interpreted together. Their levels can be affected if there is a disease of the adrenal glands, heart, or kidneys. 

INCREASED RATIO - Not clinically significant

DECREASED RATIO - Primary Hypoadrenocorticism

When evaluated on their own: 

INCREASED K+ -  Acute kidney failure, Chronic kidney disease or Addisons disease.

DECREASED K+ - Chronic kidney disease, or lost through vomiting and diarrhoea.

INCREASED SODIUM - Dehydration through vomiting and diarrhoea

DECREASED SODIUM - caused by severe vomiting and diarrhoea or can be seen if the patient has been on diuretics. 

I’m sorry this has taken so long to do and that it’s so rushed :( 

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Duck virus enteritis (DVE)

.INTRODUCTION

Duck virus enteritis (DVE) OR Duck plauge is an acute, sometimes chronic, contagious virus infection that occurs naturally only in ducks, geese and swans, all members of the family Anatidae of the order Anseriformes. The disease is a potential threat to commercially reared, domestic and wild waterfow.

CAUSES :

The aetiological agent, anatid herpesvirus-1 or DVE virus (DEV), is a member of the Alphaherpesvirinae subfamily of the Herpesviridae. DVE may also be referred to as duck plague, anatid herpes, eendenpest, entenpest and peste du canard. The infection has not been reported in other avian species, mammals or humans.

incubation period :

The time between infection and the development of signs varies from 3 to 7 days.

  Death typically occurs around 1 to 5 days after the first clinical signs.

Distribution

DVE, also known as duck plague, was first diagnosed in the western hemisphere in 1967 from a concentrated commercial duck producing area in Suffolk County, N.Y. DVE had been frequently recorded in the Netherlands where it first appeared in 1923. It has been suspected in France and China, and known to occur in Belgium and India.

The first epizootic of DVE in wild waterfowl in the U.S. occurred in January and February 1973, in the vicinity of Lake Andes National Wildlife Refuge, South Dakota. The Lake Andes epidemic struck with devastating swiftness and severity. Approximately 40% of 100,000 wintering waterfowl, mostly mallards, were lost. During the peak of the die-off, daily losses exceeded 1,000 birds.

All species of waterfowl present at Lake Andes suffered some mortality. Included were Canada geese, mallards, black ducks, pintail-mallard hybrids, American widgeon, wood ducks, American goldeneyes, redheads, common mergansers, a Muscovy duck and a Pekin duck. Birds that survived the Lake Andes epidemic have dispersed widely over North America. Blood samples taken from survivors at Lake Andes indicated that about 30% of the population were exposed to the virus. These birds are potential carriers of DVE, capable of triggering future outbreaks.

In Michigan, DVE has been reported in 1979 in Muscovy and mallard ducks.

pathoginicty :

After infection, the virus replicates in the lining cells of the gastro-intestinal tract, predominantly in the oesophagus before spreading to other parts of the body including the tissues of the immune system (bursa of fabricius, spleen and thymus) and the liver.

The virus induces vascular damage, especially in smaller blood vessels, venules, and capillaries. This results in the development of generalized hemorrhages and progressive degenerative changes of parenchymatous organs. Recently, it has been proposed that apoptosis and necrosis of lymphocytes induced by this virus may result in lymphoid depletion and possibly immunosuppression. An immunosuppressive state induced by DVE may also explain the presence of secondary infections by Pasteurella multocida, Riemerella anatipestifer, and Escherichia coli, which are frequently seen in natural outbreaks of DVE in ducklings.

Susceptible species

This virus can infect members of the Anatidae, i.e. ducks, swans and geese. Muscovy ducks are particularly sensitive to this disease.

Transmission and Development

Some scientists think DVE is usually spread by infected waterfowl that shed the virus in their droppings. It survives in water and may persist in polluted, stagnant and slow-moving pools, ponds and waterways. Waterfowl pick up the disease by drinking or swimming in polluted water or by eating contaminated food. The virus may enter susceptible birds through the mouth, nose, cloaca or breaks in the skin.

vertical transmission (i.e. from female bird to egg) has been reported to occur in Muscovy, Peking Ducks and Mallard ducks.

Birds that are exposed but survive the disease may become carriers, which maintain the infection between outbreaks and release the virus at some future time and location.

Field Signs There is no prolonged illness associated with duck plague; therefore, sick birds are seldom seen in the field, and birds that are healthy one day may be found dead the next. The incubation period between virus exposure and death is generally 3–7 days in domestic ducks, and experimental studies have found that it is as long as 14 days in wild waterfowl. Wing-clipped mallards released to monitor the Lake Andes duck plague outbreak died 4–11 days after their release. Sick birds may be hypersensitive to light, causing them to seek dense cover or other darkened areas. They may exhibit extreme thirst, droopiness, and bloody discharge from the vent or bill . The ground may be blood-stained where sick birds have rested. Therefore, duck plague should be suspected when bloodsoiled areas are seen following the flushing of birds, where blood splotches that do not appear to be related to predation or other plausible explanations are seen in the environment, or where bloody discharges are seen where dead birds are lying .

 In males, the penis may be prolapsed An ulcerative “cold sore” lesion under the tongue from which virus can be shed has been seen in some infected waterfowl  Routine examination of apparently healthy waterfowl for this lesion during banding operations may be helpful in identifying inapparent carriers. Birds with these lesions should be euthanized  and submitted to a qualified disease diagnostic laboratory for examination. Death may be preceded by loss of wariness, inability to fly, and finally by a series of convulsions that could be misinterpreted as pesticide poisoning or other diseases such as avian cholera.

POST MORTUM FINDING

A light-yellow, transparent liquid was observed when the swollen skin of the head and neck of a sick duck was incised.

Light edema and hyperemia were detected in the meninges.

light-yellow pseudomembrane covered the oral mucosa and the esophageal mucosa.

Sometimes there were “cheesy,” raised plaques along the longitudinal folds of the esophagus and proventriculus  and on the mucosal surface of the lower intestine.

Hemorrhagic ulcers between the glandular and muscular stomachs were found, and several circular hemorrhagic necrotic sites within the duodenum were observed . Severe hemorrhagic and pseudomembranous ulcers were apparent throughout the rectal and cloacal mucosa.

The spleen was swollen. 

Grey-yellow or gray-white necrotic areas of various sizes were observed on the liver surface. The follicles were hyperemic, hemorrhagic, and liquefied .

The endocardium and epicardium showed spotted and striated hemorrhages.

Of all the lesions illustrated, those of greatest value in diagnosing duck plague are hemorrhagic or necrotic bands or disks within the intestine, large amounts of free blood in the digestive tract,and cheesy plaques in the esophagus and cloaca. Liver and heart lesions of duck plague are grossly similar to those of avian cholera, and they cannot be used to distinguish between these two diseases.

Gross pathological lesions of DVE - Petichal haemorrhages in the intestine

Haemorrhage of the cloaca in a Muscovy duck infected with duck plague virus.

Gross pathological lesions of DVEhepatomegaly, haemorrhages with foci of necrosis.

Caseous material and haemorrhage along the longitudinal folds of the oesophagus of a Muscovy duck with duck plague.

1. Clinical and atopic symptoms: (A) edema of the head and neck; (B) diarrhea with white-green dejecta; © longitudinal pseudomembrane covering the esophageal mucosa; (D) circular hemorrhagic necropsy of duodenum; (E) hemorrhaging and ulceration of the rectum and cloaca; (F) follicular hyperemia and hemorrhaging, and necroscopic finding; (G) spotted hyperemia of the epicardium; and (H) petechial hemorrhaging of the endocardium.

(A) Swollen head and neck; (B) Greenish diarrhea; (C) A light-yellow and transparent liquid of the head; (E) Diffuse hemorrhage of the esophageal mucosa; (G) Hemorrhage of the annulus trachealis; (I) Spotted hemorrhage of the endocardium; (K) Petechial hemorrhaging of the epicardium; (M) Liver is enlarged with blood spots; (O) Splenomegaly and hemorrhage. D, F, H, J, L, N, and P represent the head, esophagus mucosa, trachea, endocardium, epicardium, liver, and spleen of ducks from the control group, respectively.

Histopathological analysis

Pathological changes were detected in various tissues in the infected ducks and the lesions increased with time. Slight granular degeneration of myocardial fibers (arrow on Fig. 2A) was observed in the infected ducks at 1 dpi, and erythrocytes infiltration (arrow on Fig. 2B) at 3 dpi. At 5 dpi, significant hemorrhage (arrow on Fig. 2C) was observed. In the liver, liver cells displayed diffuse fatty degeneration (vacuolus of the same size in the liver, arrow on Fig. 2E) at 1 dpi, fatty degeneration and focal necrosis of hepatocytes (arrow on Fig. 2F) at 3 dpi, and hepatocyte necrosis with hemorrhage (arrow on Fig. 2G) at 5 dpi. A small amount of erythrocyte infiltration (arrow on Fig. 2I) in the white pulp of the spleen at 1 dpi, coagulated necrotic foci of lymphocyte (arrow on Fig. 2J) was found at 3 dpi, and obvious lymphocytic necrosis (nuclei became pyknotic and underwent rupture and karyolysis) with diffuse hemorrhage (arrow on Fig. 2K) at 5 dpi. Coincidently, serious histopathological changes were also observed in the bursa of Fabricus. A slight decrease in the number of lymphocytes (arrow on Fig. 2M) at 1 dpi, necrosis of lymphocytes and lymphocytes decreased significantly (arrow on Fig. 2N) at 3 dpi, at 5 dpi, microscopic lesions were serious and massive lymphocytic necrosis (many cells have dissolved and disappeared) (arrow on Fig. 2O). The lesions of the brain were slight compared to those of the spleen and bursa of Fabricus. The tissue edema (increasement of perivascular gap, arrow on Fig. 2Q) was found at 1 dpi, and neuronophagia (microglia proliferation with the phagocytosis of necrotic neurons, arrow on Fig. 2R) and perivascular inflammatory infiltrates (arrow on Fig. 2S) were detected at 3 and 5 dpi, respectively, suggesting a mild viral encephalitis during the infection. No microscopic lesions were observed in the control group (Fig. 2D,H,L,P,T). Overall, our results indicate that DPV could cause pathological lesions in a variety of tissues, specially the spleen and bursa of Fabricus with serious lesions, which indicated DPV might target the immune organs.

Figure 2: Pathological changes of the DPV-infected ducks at the different time points.

(A) Mild granular degeneration of myocardial fibers at 1 dpi; (B) A small amount of erythrocyte infiltration at 3 dpi; (C) Myocardium haemorrhage at 5 dpi; (E) Fatty degeneration in the liver at 1 dpi; (F) Fatty degeneration and focal necrosis of hepatocyte at 3 dpi; (G) Hepatocyte necrosis with hemorrhage at 5 dpi; (I) Slight congestion in the white pulp of the spleen at 1 dpi; (J) Necrotic foci of lymphocyte at 3 dpi; (K) Lymphocytic necrosis with diffuse hemorrhage at 5 dpi; (M) Slight reduction of lymphocytes in the bursa of Fabricus at 1 dpi; (N) Lymphocytes dissolved and disappeared, the number decreased significantly at 3 dpi; (O) Serious necrosis of lymphocytes at 5 dpi; (Q) Brain edema at 1 dpi; (R) Neuronophagia of the brain at 3 dpi; (S) Perivascular inflammatory infiltrates at 5 dpi. D, H, L, P, and T represent the heart, liver, spleen, bursa of Fabricus, and brain of ducks from the control group, respectively. Magnification, ×400 .

Diagnosis Although a presumptive diagnosis of duck plague may be made on the basis of characteristic internal lesions, final diagnosis can only be made by virus isolation and identification. Ducks, geese, and swans that have characteristic signs or lesions should be euthanized and shipped to a qualified diagnostic laboratory as quickly as possible. Submit whole birds rather than tissues. When this is not possible, the liver should be removed, wrapped in clean aluminum foil, and then placed in a plastic bag and frozen for shipment. The remainder of the carcass should be incinerated if possible and the area and instruments used to process the carcass disinfected. Take particular care in preserving and packaging specimens to avoid their decomposition during transit and contamination of the shipping containers (see Chapter 2, Specimen Collection and Preservation, and Chapter 3, Specimen Shipment).

Control The primary objectives for duck plague control activities are to minimize exposure of the population-at-risk at the outbreak site and to minimize the amount of virus present in the environment as a source for potential exposure of waterfowl that may use the site in the near future. Control of duck plague outbreaks requires rapid response and aggressive actions to prevent disease spread and establishment. Birds with inapparent duck plague infections are probably the major reservoir of this disease and they pose the greatest problem for disease prevention and control. Clinically ill birds actively shed the virus and are recognized as sick birds. However, asymptomatic healthy duck plague carriers can shed the virus periodically, but they are not overtly identifiable. Therefore, destruction of infected flocks, including eggs, is recommended whenever possible because infected birds that survive are likely to become carriers and can initiate subsequent outbreaks. New technology provides promise for determining whether or not there are carriers in a flock. The success of new technology for detecting carriers will allow selective euthanization of those birds and not the remainder of the flock. Duck plague virus is hardy, and it can remain viable for weeks under certain environmental conditions; for example, the virus could be recovered from Lake Andes water held at 4 °C for 60 days under laboratory conditions. Duck plague virus is instantly inactivated at pH 3 and below and at pH 11 and above. Therefore, rigorous decontamination of infected waters (for example, by chlorination) and grounds (that is, by raising pH) and burning or decontamination of physical structures, litter, and other materials at outbreak sites should be carried out to the extent practical. Carcass collection should be thorough and incineration used for disposal. Personnel and equipment used at outbreak sites should be decontaminated before leaving the site to prevent mechanical spread of the virus to other waterfowl areas; chlorine bleach and phenol base disinfectants are suitable for this (see Chapter 4, Disease Control Operations). A low virulence live-virus vaccine has been developed for combating duck plague in the domestic white Pekin, but this vaccine has not been proven entirely reliable in protecting other species of ducks and geese. It should not be considered as a means of controlling or preventing outbreaks in migratory birds. The close association between duck plague outbreaks and captive waterfowl, especially muscovy and mallard, needs to be considered. Waterfowl release programs should not use birds or eggs from flocks with a history of this disease unless the flock has subsequently been shown by adequate testing and other technical assessments to be free of duck plague. Birds scheduled for release should be confined for at least 2 weeks before release. Birds that die during this period should be submitted to a qualified disease diagnostic laboratory. If duck plague is found to be the cause of death in any of these birds, none of the remaining birds should be released. Also, managers of areas for wild waterfowl should not permit the maintenance of domestic waterfowl, especially muscovy ducks, on the area or waterfowl display flocks that have not been certified free of duck plague.

sources :

http://www.merckvetmanual.com/poultry/duck-viral-enteritis/overview-of-duck-viral-enteritis

https://www.nature.com/articles/srep32183#f1

http://www.michigan.gov/dnr/0,4570,7-153-10370_12150_12220-26644–,00.html

https://www.dwhc.nl/en/diseases/anatid-herpesvirus/

https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/ps/92/11/10.3382/ps.2013-03356/2/poultrysci92-2892.pdf?Expires=1502736226&Signature=RxTOdrqFFtrEizIKzOck6JCjX0h-u0BwlCI7jk2q1TpV2Ef3-fkSPAvhx5x3NJEkUO~Bzkx-2On5xEMS26DwoDpOoQE~LAK7xGYO57kSruOnrv-bl5xLpGGVc6u73uF5nBrTym3xdjrJ1iQ~70oHySQkCYthuoNTpdH5XWH8~7N1eWEsAb5jKuzOhEnvegUxPUMQXJ4uwInZu5yo0-enyBat5Bv4yyG74TZ9lcn2mhjSM255~phnMrqNuxTZfCygiplHdy87mDzT2yNVCSKXEqVM-H4NtosqNUyiFwtxi5iEhPjY5Z00dPn4Cm35nmGXs8APxrOPGAZkKEtALLqGzA__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q

http://aciar.gov.au/files/node/571/pr117-chapter3.pdf

https://web.oie.int/eng/normes/MMANUAL/2008/pdf/2.03.07_DVE.pdf

http://saspjournals.com/wp-content/uploads/2015/06/SJAVS-23B253-255.pdf

http://www.tandfonline.com/doi/pdf/10.1080/01652176.2017.1298885

https://www.nwhc.usgs.gov/publications/field_manual/chapter_16.pdf

http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.03.07_DVE.pdf

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On the subject of souvenirs for our listeners, check out our new Radio Slovakia International keyrings!

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Day 7/52 of productivity/until my flight home. (8th Nov) Microbiology notes for the final in General Microbiology, making my winter season of exams a lot easier if I can pass it on the 9th Nov, a lot of cramming and a late night ahead. Pokémon 007; Squirtle. Week 7/52 meant a cheeky mini ski and snowboard trip to Donovaly resort in Slovakia for the weekend.

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Day 6/52 of productivity/until my flight home. (7th Nov) A full day of uni was more than I could handle and so most of the evening was spent sleeping off illness. Some last minute cramming for the nutrition credit was managed though! Pathophysiology credit from before was passed as well! Pokémon 006; Charizard. Week 6/52 of 2016 was the week little Kitler/Sofia entered my life as a foster.

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Day 5/52 of productivity/until my flight home. (6th Nov) Finally feeling better and managed to finish my flashcards for the Nutrition credit test on the 8th. Pokémon 005; Charmeleon. Week 5/52 of 2016 was back to university and goodbye to the worst subject and exam of my life, Biochemistry!

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Day 4/52 of productivity/until my flight home. (5th Nov) Fever rages on but some cards written out to revise for a Nutrition credit on cattle for Tuesday 8th. Pokémon 004; Charmander. Week 4/52 of 2016 was spent getting some quality rest with the face of this blog, before summer semester!

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Day 3/52 productivity/until my flight home. (4 Nov) Still sick with a fever meant getting up a little early to read some more toxicology before the test- I think certain topics should be banned before normal waking hours! Test passed though! Pokémon 003; Venusaur. Week 3/52 of 2016 was spent back in the family home in Plymouth, which meant back to work at the shelter, and more puppy cuddles in the kennels.

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Day 2/52 of productivity/until my flight home. (3 Nov) Had a fever but made it to a farm trip for Animal Hygiene and made some brief notes for a Toxicology credit exam the next day. Pokémon 002; Ivysaur. Week 2/52 of 2016 was spent enjoying and leaving the most magical place on earth- Tromsø.