Dr Meducci vet's blog: August 2011

Are fungal infections contagious? (vet facts)

8:45 AM | Labels: contagious, fungal infection, infection

I remembered during mycology class, my lecturer told us that fungal infections are NOT contagious, however when we discussed it with other lecturer, he says that fungal infection indeed contagious. I was kind of confuse with the terminologies , and usually we refer many diseases with infection rather than contagious. Let's study the simple terms..

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Look over the terminologies first

1.Infectious (infection)

Infectious diseases are caused by microscopic germs (such as bacteria or viruses) that get into the body and cause problems. Some — but not all — infectious diseases spread directly from one person to another. Infectious diseases that spread from person to person are said to be contagious.

Some infections spread to people from an animal or insect, but are not contagious from another human. Lyme disease is an example: You can't catch it from someone you're hanging out with or pass in the street. It comes from the bite of an infected tick.

2.Contagious (contact)

Contagious diseases (such as the flu, colds, or strep throat) spread from person to person in several ways. One way is through direct physical contact, like touching or kissing a person who has the infection.

Another way is when an infectious microbe travels through the air after someone nearby sneezes or coughs. Sometimes people get contagious diseases by touching or using something an infected person has touched or used — like sharing a straw with someone who has mono or stepping into the shower after someone who has athlete's foot. And sexually transmitted diseases are spread through all types of sex - oral, anal, or vaginal.

"and so...are the fungal infections are contagious?"

Fungal infections are caused by contamination with fungi. Spores are the reproductive form of fungus and very resistant towards external influences and therefore, they can live on - almost invisibly - while their growth form has disappeared completely. Furthermore, fungi as such are not contagious, but spores can be transmitted from one person to another and cause a fungal infection in the latter.

Some fungal infections, such as candidiasis and ringworm, can spread from person to person through contact with the infected area. Most infections, however, develop from fungi found naturally on the human body or in the environment. Many fungi that cause systemic respiratory disease are found in soil or in the droppings of animals or birds. Usually they are inhaled after the soil or droppings are disturbed, sending dust and fungal spores into the air.

Usually, fungi and fungal yeasts are not dangerous. Problems only occur when body resistance is weakened. In humans and animals, fungi grasp the opportunity when the skin is broken or body resistance is weakened due to illness or medication such as immunosuppresion caused by virus (FIV or AIDS)

PS: So, both of the terminologies can be used to describe the fungal infections weather it is contagious or not; it depends on how the way we want to explain it.

Sources: kidshealth.org, fungal infections, janssen, -cilag.com, fungal infection, www.humanillness.com

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Avian female reproductive system

8:25 PM | Labels: Avian female reproductive system

During my second industrial training at chicken breeder farm, I always wondering how the reproductive system if avian works. I studied carefully about it, and it was very short of time that I forgot to post about it. This is very important because of the bird's unique reproductive system compared to other mammals.

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Avian female reproductive system

The avian reproductive system is VERY different from that of mammals. While mammals typically give birth to their offpsring, the offspring of birds develop outside the body of the parents - in eggs. When carried in the womb, mammalian embryos receivet heir daily requirement for nutrients directly from their mother via the placenta. For birds,however, all the nutrients that will be needed for the embryo to fully develop must be provide in the egg before it is laid.

Interior view of chicken's egg before and after incubation

The female reproductive system of the chicken is shown below. It is divided into two separate parts: the ovary and the oviduct.In almost all species of birds, including chickens,only the left ovary and oviduct are functional.Although the embryo has two ovaries and oviducts, only the left pair (i.e., ovary and oviduct) develops. The right typically regresses during development and is non-functional in the adult bird. There have been cases, however,where the left ovary and oviduct have been damaged and the right one has developed to replace it. In some birds, such as hawks, it is the right, and not the left, ovaryand oviduct that typically develops. Kiwis are unique in that both the left and right ovaries develop, though it is only the left oviduct thatdevelops. Ova from both ovaries will passdown the same oviduct, though not typically atthe same time.

Chicken female reproductive system

1. Ovary

The ovary is a cluster of developing yolks or ova and is located midway between the neck and tail of the bird, attached to the back. The ovary is fully formed although very small when the female chick is hatched. It is made up of 13,000 – 14,000 ova which grow by the addition of yolk fluid. Each ovum (singular of ova) starts out as a single cell surrounded by a vitelline membrane. As the ovum develops, yolk is added. The color of the yolk comes from fat soluble pigments called xanthophylls contained in the hen’s diet.

It is possible to find five stages of development in the active ovary:

Primary follicles – follicles that have not yet commenced to grow

Growing follicles

Mature follicles – follicles ready or nearly so for release

Discharged follicles – where the yolk has just been released

Atretic follicles – those from which the yolk has been released some time ago

It takes approximately 10 days for a yolk to develop from the very small to the normal size found in eggs and during this time it is contained in the follicle. The follicle acts as a sack during this period of development supplying it with the nutrients required for its growth. When a mature follicle is examined an elongated area virtually free of blood vessels will be found on the distal surface of it. This area, called the stigma, is where the follicle normally splits to release the yolk into the oviduct. If, for some reason, the follicle splits at other than the stigma, the numerous blood vessels that rupture will result in free blood being found in the egg i.e. a blood spot will form.

Ovulation is the release of the mature ovum from the ovary into the second part of the female reproductive system, the oviduct. The ovum, which is enclosed in a sac, ruptures along the suture line or stigma. This release of the ova occurs 30-75 minutes after the previous egg has been laid.

2. Oviduct

The second major part of the female chicken’s reproductive system is the oviduct. The oviduct is a long convoluted tube (25-27 inches long when fully developed) which is divided into five major sections. They are the infundibulum or funnel, magnum, isthmus, shell gland, and vagina.

Infundibulum- The first part of the oviduct is 3-4 inches long, and it engulfs the ovum released from the ovary. The ovum or yolk remains in the infundibulum 15-18 minutes. The infundibulum also serves as a reservoir for spermatozoa so that fertilization can take place.

Magnum- The next section of the oviduct is the magnum which is 13 inches long and is the largest section of the oviduct as its name implies (from the Latin word for ‘large’). The ovum or yolk remains here 3 hours during which time the thick white or albumen is added.

Isthmus- The third section of the oviduct is the isthmus which is 4 inches long. The ‘egg’ remains here for 75 minutes. The isthmus, as its name implies, is slightly constricted (The term ‘isthmus’ refers to a narrow band of tissue connecting two larger parts of an anatomical structure). The isthmus is where the inner and outer shell membranes are added.

Shell gland- The next section of the oviduct is the shell gland or uterus. The shell gland is 4-5 inches long, and the ‘egg’ remains here for 20 plus hours. As its name implies, the shell is placed on the egg here. The shell is largely made up of calcium carbonate. The hen mobilizes 47% of her body calcium from her bones to make the egg shell, with the diet providing the remainder of the required calcium. Pigment deposition is also done in the shell gland.

Vagina- The last part of the oviduct is the vagina which is about 4-5 inches long and does not really play a part in egg formation. The vagina is made of muscle which helps push the egg out of the hen’s body. There are also glands located in the vagina where spermatozoa are stored.

Near the junction of the vagina and the shell gland, there are deep glands lined with simple columnar epithelium. These are the sperm host glands, so called because they can store sperm for long periods of time (10 days to 2 weeks!). When an egg is laid, some of these sperm can be squeezed out of the glands into the lumen of the tract, so that they can migrate farther up the oviduct to fertilize another egg. This is one of the really remarkable things about birds; the sperm remain viable at body temperature.

In hens, ovulation usually occurs in the morning and under normal daylight conditions, almost never after 3:00 PM. The total time to form a new egg is about 25-26 hours. This includes about 3½ hours to make the albumen, 1½ hours for the shell membranes, and about 20 hours for the shell itself.

Ovulation for the next egg of a clutch occurs within an hour of laying the previous egg, and so that each day the hen gets later and later in her timing; she "runs behind," like a clock that is improperly adjusted. Eventually she gets so far behind schedule that she would have to ovulate later than 3:00 PM. Since hens do not typically ovulate after 3:00 PM, the next ovulation is delayed and egg laying is interrupted.

Occasionally, a hen will produce double-yolked eggs. This phenomenon occurs primarily due to the age of the hen, but can also be related to genetics. Young hens sometimes release two follicles from the ovary in quick succession. The highly active ovary due to high activity of reproductive hormones in peak egg production can also be a factor.

Double-yolked eggs are larger in size than single yolk eggs. Double-yolked eggs are not suitable for hatching. There is typically not enough nutrients and space available for two chicks to develop to hatch. It has happened, but it is rare.

It is rare, but not unusual, for a young hen to produce an egg with no yolk at all. Yolkless eggs are usually formed when a bit of tissue is sloughed off the ovary or oviduct. This tissue stimulates the secreting glands of the different parts of the oviduct and a yolkless egg results.

Things occasionally go wrong when an egg shell is being developed. The most obvious relates to shell texture. Occasionally the shell becomes damaged while still in the shell gland and is repaired prior to being laid. This results in what is known as a ‘body check.’ Occasionally there will be ‘thin spots’ in the shell or ‘ridges’ will form. The shells of such eggs, though not cracked, are weaker than ‘normal’ eggs and should not be used as hatching eggs.

From left: body check, thin spot, ridges

A second category of problems is abnormal shape. To be considered a hatching egg, the egg should be the typical ‘egg shape.’ Abnormally shaped eggs should not be used as hatching eggs. In many cases it is not clear which is the large end (and eggs should be incubated large end up) or they may not properly fit in the egg trays.

From left: Football shaped and pear shaped eggs.

Ps: Maybe you're not familiar with the terms, click here for more details

Sources: Reproduction;PoultryHub, Female reproductive system, poultry production manual, the university of Kentucky

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Blackleg disease

8:33 PM | Labels: Blackleg disease, clostridium chauvoei

I came across this disease when I read my old bacteriology notes.

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Blackleg disease

Blackleg is a highly fatal disease of young cattle caused by the spore forming, rod shaped, gas producing bacteria Clostridium chauvoei. The spores of the organism can live in the soil for many years. The bacteria enters the calf by ingestion and then gains entrance to the body through small punctures in the mucous membrane of the digestive tract. Cattle that are on a high plane of nutrition, rapidly gaining weight and between 6 months and 2 years of age are most susceptible to the disease. The disease is not transmitted directly from sick animals to healthy animals by mere contact.

The name ‘blackleg’ derives from the fact that the site of infection is often a leg muscle, and that the affected muscle is dark in colour.

Extensive necrosis of the leg musculature with a blackish-red discoloration with a "bubbly" appearance

Etilogy

C chauvoei is found naturally in the intestinal tract of animals. It probably can remain viable in the soil for many years, although it does not actively grow there. Contaminated pasture appears to be a source of organisms. Outbreaks of blackleg have occurred in cattle on farms in which recent excavations have occurred, which suggests that disturbance of soil may activate latent spores. The organisms probably are ingested, pass through the wall of the GI tract, and after gaining access to the bloodstream, are deposited in muscle and other tissues.

The spore or dormant form of the cell exists under conditions where the vegetative state cannot. When the vegetative cells grow in high numbers, the bacteria produce toxins.Under ideal conditions, the bacteria form spores which allow the bacteria to survive in dormant state until exposed to conditions that can support their growth.

C. chauvoei

The bacteria is a Gram-positive (blue), anaerobic rod-shaped bacillus

How does the bacteria affect the animal?

Bacterial spores are eaten in contaminated feed or soil. The spores then enter the bloodstream and lodge in various organs and tissues, including muscles. Here they lie dormant until stimulated to multiply, possibly by some slight injury to the animal. The injury reduces blood flow to the area, thereby reducing the supply of oxygen to the tissues. In the absence of oxygen, the spores germinate and multiply. As they grow, the bacteria produce toxins which destroy surrounding tissues(that's why the muscle become black in color). The toxins are absorbed into the animal’s bloodstream which makes the animal acutely sick and causes rapid death.

Symptoms of disease

The first sign observed is usually lameness, loss of appetite, rapid breathing and the animal is usually depressed and has a high fever. Characteristic swellings (edema) develop in the hip, shoulder, chest, back, neck or elsewhere. First the swelling is small, hot and painful. As the disease progresses, the swelling enlarges and becomes spongy and gaseous. If you press the swelling, gas can be felt under the skin.

The rapid accumulation of gas under the skin and in the body cavity gives the carcass a bloated appearance, with the limbs spread apart and pointing upwards. There may be a frothy, blood-stained discharge from the mouth, nostrils and anus.

If the skin over the affected area is removed, excess bubbly bloodstained fluid can be seen, and the muscle immediately below will be dark in colour. However, when the affected muscle is inside the carcass, such as when the heart muscle is affected, no external evidence of the disease is found.

discoloration of skeletal muscle

The animal usually dies in 12 to 48 hours. In most cases the animal is found dead without being previously observed sick. The speed with which blackleg kills usually makes individual treatment useless.

Treatment

The speed with which blackleg kills usually makes individual treatment useless. In some cases, however, animals treated early with penicillin (antibiotic) may survive, although they often suffer permanent deformity due to partial or complete destruction of muscles.

Prevention

The only effective means of controlling blackleg is by vaccination. Several makes of multivalent vaccine (‘5 in 1’ or ‘7 in 1’) are available commercially and care should be taken to follow the manufacturer’s instructions. The most commonly used clostridial vaccination in cattle is the 7-way type which protects against Clostridium chauveoi (blackleg), Clostridium septicum and Clostridium sordelli(malignant edema), Clostridium novyi (black disease), and three types of Clostridium perfringens (enterotoxemia).

Calves should receive two doses of blackleg vaccine. Two vaccinations 1 month apart are essential to provide the best protection.
A booster vaccination 12 months later should provide lifelong immunity to blackleg.
It is desirable to give the initial two doses of vaccine before young cattle reach their most susceptible age of six months.
To await the occurrence of blackleg before vaccinating is unwise, as vaccines take 10–14 days before they begin to provide immunity.

7 ways types of blackleg vaccination

IMPORTANT!!

Carcasses of animals known to have died from blackleg should not be opened. Opening the carcass can liberate bacteria which will form spores that will contaminate the ground and subsequently infect other cattle. Also, do not drag carcasses along the ground. If possible, burn or deeply bury the carcasses where they lie.

Sources: Cattle Diseases:Blackleg cattletoday.info, The Merck veterinary manual, blackleg in cattle, thedairysite.com

PS: TO MY MUSLIM READERS, HAPPY EID FITRI!!

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Ketosis in cattle

4:08 PM | Labels: ketosis in cattle

moo moo...ketosis?

Ketosis is a fairly common disease among adult cattle, although usually it occurs in dairy cattle. Ketosis typically occurs the first six weeks of parturition.It occurs in dairy cattle because of their inability to intake enough nutrients to meet their energy needs.This can lead to hypoglycemia which is a pathologic state produced by a lower than normal level of glucose.That in turn leads to the formation of ketone bodies from the body and fat stores. Although they are only broken down for energy to used by the heart and brain in the times of low glucose levels. Ketosis is not an immediate thing like many other illnesses, it gradually occurs.

The postpartum period is a critical stage of lactation for a high producing dairy cow. This period is characterized by drastic metabolic changes, immunosuppression, negative energy balance (NEB) and elevated levels of stress, which can lead to increased incidence of diseases and decreased animal efficiency.

At the time of calving and onset of lactation, the animal's nutritive and metabolic requirements are increased about 100 percent partly because of the loss of sugar, protein, and fat in the milk and partly because of the increased metabolic work associated with the production and secretion of milk.

For every 20 pounds of milk produced, approximately 1 pound of glucose, 0.8 pound of fat, and 0.7 pound of protein are withdrawn from the animal. Those withdrawals are from the animal's available resources. If the dietary intake is adequate, the animal remains normal. If the diet is too poor to maintain approximately normal levels of blood glucose and liver glycogen, an imbalance in metabolism develops.This upset is indicated by the existing anorexia (loss of appetite), hypoglycemia, and depletion of liver glycogen. In response to these disturbances, compensatory metabolic adjustments are initiated and tend to correct the imbalance.

The high energy demand during this period of glucose shortage triggers a compensatory process of nutrient partitioning and fat mobilization. During this period of glucose shortage, fat is mobilized as an alternative source of energy. It is used as a fuel for basic cell functions in addition to providing energy to maintain milk production.

Feed intake, or lack thereof, is a critical component in the onset of ketosis. In all cows, dry matter intake begins to decline approximately one month prior to calving, although many people will not notice this decline until several days prior to calving. as feed intake declines and galactopoeisis begins, body fats are mobilized, resulting in an increase in circulationg NEFA levels. NEFAs (nonstrerified fatty acid) themselves are mild appetite suppressants, so they continue to hamper feed intake. NEFAs are also the primary substrate for the production of ketone bodies via ketogenesis. Ketones are potent appetite suppressants, so an increase in their presence also decreases intake.

Once calving occurs, milk production places significant pressure on the liver to supply large quantities of glucose which are required for lactose production in the milk synthesis process, as well as the normal glucose that is required for cellular metabolism. Part of that glucose is utilized as body fats are mobilized and converted back to a readily useable energy form by the liver. If liver function is impaired due to poor prepartum management, then ketosis may result, usually in the first several weeks of lactation. These cows often have a history consistent with adequate to excessive body condition at calving that is then lost very rapidly, often resulting in a significantly thinner cow at the time of physical examination.

Cows with elevated BCS at calving (BCS ≥ 4.0) had elevated levels of circulating ketone bodies in plasma. They were at the highest risk of developing clinical and subclinical ketosis compared to cows classified as either a moderate or thin BCS prior to calving. Ketosis is an undesirable condition with a severe impact on animal performance and consequently on the economic well being of dairies.

Conditions when ketosis is likely to occur

Late pregnant cows, ewes and does in the last six weeks of pregnancy grazing dry poor quality pasture (less than 1,000-1,500kg DM/ha), stubbles or green pasture (less than 800kg DM/ha).
Fat cows, ewes or does (ie fat score greater than 3.5-4) or light cows, ewes or does on very poor pasture.
Twin-bearing ewes or does.
Previous history of pregnancy toxaemia.
Cold wet windy weather.
Extensive grazing situations where the last third of pregnancy coincides with a late break in the season followed by cold weather leading to little pasture growth.
Short periods without feed (yarding).
Stress (due to climatic conditions, handling, being chased or management procedures).
Heavy worm infestation.

Symptoms

decreased appetite,
marked weight loss,
decreased milk production,
acetone odor of breath,
nervousness,
hard, mucus covered feces.

For confined cattle, usually decreased appetite is the first sign that they might have ketosis. Also if they are fed in components such as part forage, part grain, they will tend to go for the forage more than they will go for the grain.If you fed your cattle in herds, then usually you will see reduced milk production,lethargy and an somewhat "empty" appearing abdomen.When cattle are physically examined with having ketosis they may appear sightly dehydrated.

Treatment

IV administration of 500 ml of 50% dextrose solution. This treatment allows rapid recovery but the effects are often producing results beyond itself therefore relapses of ketosis are pretty common.Another treatment that can be used is the administration of glucocorticoids such as dexamethasone or isoflupredone acetate via intramuscular.

In mild cases of ketosis you may give your cow 250-400g/dose of propylene glycol orally. Propylene glycol acts a glucose precursor and therefore may be combine with other treatments and can be administered twice a day. However accidentally overdose cow with propylene glycol it will lead to central nervous system depression.

Prevention

Due to the increased energy demand required before calving, strategies to prevent metabolic diseases must focus on the nutritional management of the dry and transition cow. The goals of these diets are to provide all required nutrients and to adapt the rumen for future diet changes as cows advance through these lactation stages.

To prevent metabolic disorders, diets must be properly formulated to accomplish this goal and to minimize DMI reduction.Managing BCS towards the end of the previous lactation is an important management practice to minimize ketosis and other postpartum metabolic diseases.

Probiotics have been shown to promote a positive appetite in animals during times of stress. Feeding probiotics to cattle 2 weeks prior to freshening can help maintain DMI’s through this phase resulting in a better energy balance. This concentrate of good bacteria can help stimulate the gut and perk the animal’s appetite within a few hours.

Sources: ketosis in cattle: symptoms and treatment, helium.com, understanding and dealing with ketosis probiotic smart.com, ketosis in daity cattle, cattlenetwork.com, dairyketosis; cat.vet.upenn.edu, pregnancy toxemia;meat and livestock australia, ketosis in cattle for animal disease; Joseph A. Dye and Robert W. Doughtry

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Toxicology: Methemoglobinemia

3:28 PM | Labels: methemoglobinemia

It was 5.30 am when I see this word!

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Methemoglobinemia

Methemoglobinemia is a blood disorder in which an abnormal amount of hemoglobin builds up in the blood. Hemoglobin is the oxygen-carrying molecule found in red blood cells. In some cases of methemoglobinemia, the hemoglobin is unable to carry oxygen effectively to body tissues.

(Ps: In this topic I only emphasized on the effects of toxins associated with methemoglobinemia)

Methemoglobinemia is a clinical syndrome caused by an increase in the blood levels of methemoglobin secondary to both congenital (chronic) changes in hemoglobin synthesis or metabolism, or acute imbalances in reduction and oxidation reactions (redox imbalance) induced by the exposure to several chemical agents. Central cyanosis unresponsive to the administration of oxygen, which can cause a reduction in oxygen delivery, is the main characteristic of methemoglobinemia. Its prevalence is difficult to determine because it encompasses mild cases, which are probably underdiagnosed, and fatal cases; it frequently presents in the preoperative period and should be known to every anesthesiologist.

Methemoglobinemia occurs when red blood cells (RBCs) contain greater than 1% methemoglobin. This occurs from either congenital changes in methemoglobin affecting synthesis and metabolism or from exposure to toxins that acutely affect redox reactions involving methemoglobin. It is important to realize that methemoglobin is a naturally occurring oxidized metabolite of hemoglobin and physiologic levels (< 1%) are normal. Problems arise when levels increase, as methemoglobin does not bind oxygen, thus leading to a functional anemia.

The molecule of Hb is a tetramer composed of alpha, beta, gamma, or delta chains. The most common form of Hb in adults (HbA) consists of two α and twoβ chains. Each Hb chain is formed by a globin polypeptide linked to a prosthetic heme group, which is formed by a complex of a protoporfirin IX ring and one atom of ferrous iron (Fe+2). Thus, each Hb molecule has four atoms of iron. Each ferrous iron can reversibly link one O2 molecule, for a total of four molecules of O2 transported by each Hb molecule.

Normal haemoglobin

Methemoglobin has an oxidized ferric iron (Fe +3) rather than the reduced ferrous form (Fe 2+) found in hemoglobin. This structural change is responsible for methemoglobin's inability to bind oxygen. In addition, ferric iron has slightly greater affinity for oxygen due to its chemical structure, thus shifting the oxygen dissociation curve of partially oxidized hemoglobin molecules to the left, resulting in decreased release of oxygen in tissues. The findings of anemia and cyanosis despite oxygen treatment result from both of these effects.

In theory, any oxidizing agent can lead to the formation of MetHb. Hemoglobin is constantly being oxidized; however, natural reducing systems maintain the levels of MetHb under 1%.

NADH-Methemoglobin reductase (NADH-NR) , a system with two enzymes, cytochrome B5 and cytochrome B5-reductase (CB5R), is responsible for the endogenous reduction of MetHb, corresponding to 99% of the reducing activity. NADH-Methemoglobin reductase transfers one electron from NADH to MetHb, changing it into reduced hemoglobin (HHb) (Figure 1). Other systems also help to maintain a low level of MetHb; among them, ascorbic acid, gluthation, and NADPH dehydrogenase should be mentioned. Gluthation reduces several oxidizing substances in the blood before they attack the Hb. However, under normal conditions those pathways are less significant, but become important when NADH-MR is disrupted.

Methemoglobinemia results from a redox imbalance, either due to excessive oxidization of Hb (increased production) or a decrease in the activity of reducing enzymes (decreased metabolism)

Most cases of methemoglobinemia are due to excessive production of methemoglobin following exposure to oxidant drugs, chemicals, or toxins. This increased production of methemoglobin overwhelms the physiologic regulatory mechanisms previously discussed. These agents can cause an increase in methemoglobin levels either by ingestion or by absorption through the skin. Such agents fall into 2 general categories: nitrites or aromatic amines. Dapsone and benzocaine are common causes for methemoglobinemia.

Blood: methemoglobulin(left) and normal blood (right)

Substances that can cause methemoglobinemia

Inorganic agents
- Nitrates – Fertilizers, contaminated well water, preservatives, industrial products
- Chlorates
- Copper sulfate – Fungicides
Organic nitrites/nitrates
- Amyl nitrite
- Isobutyl nitrite
- Sodium nitrite
- Nitroglycerin
- Nitroprusside
- Nitric oxide
- Nitrogen dioxide
- Trinitrotoluene (TNT), combustion products
Others
Local anesthetics – Benzocaine, lidocaine, prilocaine, phenazopyridine (Pyridium)
Antimalarials – Primaquine, chloroquine
Rasburicase
Antineoplastic agents – Cyclophosphamide, ifosfamide, flutamide
Analgesics/antipyretics – Acetaminophen, acetanilid, phenacetin, celecoxib
Zopiclone
Herbicides – Paraquat (dipyridylium)
Methylene blue (high dose or in G6PD deficient patients)
Indigo Carmine (Indigotindisulfonate)
Resorcinol
Antibiotics – Sulfonamides, nitrofurans, P-amino-salicylic acid, Dapsone
Industrial/household agents – Aniline dyes, nitrobenzene, naphthalene (moth balls), aminophenol, nitroethane (nail polish remover)

Symptoms of methemoglobinemia

Symptoms are proportional to the methemoglobin concentration and include skin color changes (cyanosis with blue or grayish pigmentation) and blood color changes (brown or chocolate color) at methemoglobin levels up to 15%. As levels of methemoglobin rise above 15%, neurologic and cardiac symptoms arise due to hypoxia. levels above 70% are usually fatal.

Bluish faces

Diagnosis

There are many differential diagmosis, I only emphasize diagnosis in animals only.

The potassium cyanide test can distinguish between methemoglobin and sulfhemoglobin. After the addition of a few drops of potassium cyanide, methemoglobin turns bright red, but sulfhemoglobin remains dark brown. This is due to the binding of methemoglobin to cyanide, forming cyanomethemoglobin, which is bright red in color. Sulfhemoglobin, on the other hand, is inert and does not bind cyanide.

Treatment

If methemoglobinemia is the result of toxin exposure, then removal of this toxin is imperative. Further ingestion or administration of the drug or chemical is to be avoided. If the substance is still present on the skin or clothing, the clothing should be removed and the skin washed thoroughly. These patients may be unstable and should be in a closely monitored situation with oxygen supplementation as needed.

Methylene blue is the primary emergency treatment for documented, symptomatic methemoglobinemia. The methylene blue dose is 1-2 mg/kg administered as a 1% solution in intravenous saline over 3-5 minutes. This dose may be repeated at 1 mg/kg every 30 minutes as necessary to control symptoms. Doses of methylene blue should not exceed 7 mg/kg, because this agent in itself can be toxic and cause dyspnea, chest pain, and hemolysis.

methylene blue antidot

Methylene blue requires G6PD to work. Therefore, it is not effective in patients who have G6PD deficiency with methemoglobinemia. Additionally, methylene blue administration may cause hemolysis in these patients.

Sources: methemoglobulin from diagnosis to treatment; Revista Brasileira de Anesthesiologia, methemoglobinemia,evidence-based care review, Habib Ur Rehman, methemoglobinemia, emedicine.medscape.com

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Breeding system

6:11 AM | Labels: breeding system

One day, a guy asking me on facebook. "What is nucleus breed?". I simply replied "Pure breed". Then he asked again "Is this same as inbreeding?" then I realized maybe I gave him inaccurate answer. I had had a rough time in genetic during my sophomore years. When he asked me that question, he gave me idea to revise back basic principle of breeding system; the one I have forgotten for quite some time.

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Breeding system (as described in sheep breeding system)

Animal breeding is a branch of animal science that addresses the evaluation of the genetic value of domestic livestock. A breed is a group of domestic animals with a homogeneous appearance, behavior, and other characteristics that distinguish it from other animals.

1. Pure breeding

Pure-breeding is the mating of rams and ewes of the same breed or type. A purebred flock can be managed as a single flock because all ewes and rams are of the same breed. The goal of purebred sheep production is to provide superior genetics (seedstock) to the commercial sheep industry. Seedstock are marketed as rams and replacement ewes to other seedstock producers or to commercial sheep operations.

Pure bred merino sheep

Pure bred charollais ram

2. Inbreeding

Inbreeding is a system of breeding in which closely related animals are mated. This includes sire to daughter, son to dam, and brother to sister. Technically, inbreeding is defined as the mating of animals more closely related than the average relationship within the breed or population concerned. The primary genetic consequence of inbreeding is to increase the frequency of pairing of similar genes.

Inbreeding is essential to the development of prepotent animals — animals that uniformly "stamp" their characteristics on their progeny. Inbreeding may also be used to uncover genes that produce abnormalities or death — genes that, in outbred herds, are generally present in low frequencies. Inbreeding is suggested for only highly qualified operators who are making an effort to stabilize important traits in a given set of animals.

In general, inbreeding results in an overall lowering in performance: vigor, disease resistance, reproductive efficiency, and survivability. It also increases the frequency of abnormalities. For example, the spread of spider lamb disease in black-faced sheep is believed to be the consequence of inbreeding.

3. Linebreeding

Linebreeding is a system of breeding in which the degree of relationship is less intense than in inbreeding and is usually directed towards keeping the offspring related to some highly prized ancestor. The degree of relationship is not closer than half-brother half-sister matings or cousin matings, etc. Line breeding is a mild form of inbreeding.

The benefit of linebreeding is the production of more consistent offspring. It also have a chance to reinforce desired characteristics and eliminate health problems one has to have a thorough knowledge of both pedigrees of both sire and dam for at least 5 generations.

Breeders can assure uniform of quality without asking the inherent danger of inbreeding. This techniques appears to be the best compromised between inbreeding and doubts between outcrossing and outbreeding.

4. Outbreeding

Out-breeding is the mating of animals of the same breed but which have no closer relationship than at least 4 to 6 generations. Outbreeding is the recommended breeding practice for most purebred sheep breeders.

5. Crossbreeding

Crossbreeding is the mating of rams and ewes of different breed compositions or types. However, it does not denote indiscriminate mixing of breeds, but rather is a systematic utilization of different breed resources to produce crossbred progeny of a specific type. Crossbreeding is used extensively in the commercial sheep industry and the majority of slaughter lambs are crossbred.

Crossbreeding offers two distinct advantages:

1)heterosis

2)breed complementarity.

Heterosis or hybrid vigor is the superiority of the crossbred offspring. Mathematically, heterosis is the difference in performance between the crossbred and the average performance of its purebred parents.

There are effects of heterosis in the crossbred offspring, crossbred dam, and crossbred ram. In general, crossbred individuals tend to be more vigorous, more fertile and grow faster than purebreds.

Effects of heterosis tend to be large for traits that are lowly heritable (e.g. reproduction) and small for traits that are highly heritable (e.g. growth, carcass, and wool). The effects of heterosis are cumulative. Heterosis can be maximized by mating crossbred ewes to a ram of another breed to produce crossbred offspring. Composite breeds such as the Katahdin and Polypay capture most of the benefits of heterosis.

ewe with crossbred lambs

Hybrid vigor

crossbred Dorper ram

The second major advantage of crossbreeding lies in the ability to utilize breed complementarity. All breeds have strengths and weaknesses. No one breed excels in all relevant traits. Thus, production can be optimized when mating systems place breeds in roles that maximize their strengths and minimize their weaknesses.

Mating Polypay ewes to Suffolk rams is an example of matching complementary strengths of breeds to optimize efficiency of a production system. This cross takes advantage of the reproductive efficiency and moderate maintenance costs of Polypay ewes while producing Suffolk-sired lambs to meet market requirements for fast-growing, heavy muscled lambs.

The efficiency of this cross would be much greater than the reciprocal mating of Suffolk ewes to Polypay rams. The latter cross would produce genetically equivalent market lambs (half Suffolk and half Polypay), but fewer lambs would be sold and production costs greatly increased due to higher feed requirements of heavy Suffolk ewes compared to Polypay ewes.

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Crossbreeding system

There are several systematic crossbreeding systems. Terminal crossing makes maximum use of both heterosis and breed complementarity. It may utilize two, three, or four breeds, and can be as simple as crossing two pure breeds.

3-ways cross lambs

1.Terminal crossing

In terminal crossing, all of the crossbred offspring are sold and replacement ewe lambs must be purchased or produced in the flock by mating a proportion of the flock to rams of the same breed. In a three or four breed terminal crossbreeding system, crossbred ewes and crossbred rams can be utilized in the system to maximize heterosis.

2.Rotational crossing

Rotational crossing will also maintain high levels of heterosis. Rotational crossing involves alternating the use of rams of two, three, or more breeds. Ewes are mated to rams of the breed which they are least related. It works best when breeds which function acceptably as both ram and ewe breeds, are utilized.

3.Roto-terminal crossing

Roto-terminal crossing involves both terminal crossing to produce market lambs and rotational crossing to produce ewe lambs. The best ewes in the flock would comprise the nucleus flock. They would be used to produce replacement ewes. The rest of the ewes in the flock would be bred to a terminal sire to produce market lambs.

4.Grading up

Grading up denotes the repeated crossing of ewes and their female progeny to rams of a single breed, with the ultimate objective of creating a flock that is indistinguishable from purebred flocks of the ram breed. It is used when only rams of the breed of interest are available or affordable.

Grading up to Dorper

5.Composite breeds

Crossbreeding is also used to form new or "composite" breeds. Once the crossbred base population has been formed, the flock is managed as a purebred flock. This is how many new breeds are created.Many of the aforementioned crossbreeding systems are difficult to accomplish in a small flock, which may only have the option of one or two breeding groups. The purchase of replacement females would enable the use of a terminal crossing program. Alternating the use of ram and ewe breeds would maintain maternal and growth characteristics in the flock.

Polypays: A composite breed

Ps: I am not expert in genetics, references is needed to guide the detail explanations of breeding system

Sources: sheep 201; A beginner's guide to raising sheep,

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Hypersensitivity

8:15 AM | Labels: Hypersentivity

I remembered one day we have oral immunology test with Dr Ali, everyone was busy with the notes and trembling their fingers trying to memorize the notes. The topic that we prayed that it wouldn't ask by him was hypersensitivity and autoimmunity. It was funny, because we only understand Type 1 (at that time) and hoping type 2,3 and 4 will not come out. Now I decided to post immunology hypersensivity for home revision.

Ps: I am still giggling to myself! haha

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Hypersensitivity Type 1

Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 - 12 hours).

Urticaria (bee sting)

conjuctivitis

Immediate hypersensitivity is mediated by IgE. The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils. A biopsy of the reaction site demonstrates mainly mast cells and eosinophils.

The mechanism of reaction involves preferential production of IgE, in response to certain antigens (often called allergens). The precise mechanism as to why some individuals are more prone to type-I hypersensitivity is not clear. However, it has been shown that such individuals preferentially produce more of TH2 cells that secrete IL-4, IL-5 and IL-13 which in turn favor IgE class switch. IgE has very high affinity for its receptor (Fcε; CD23) on mast cells and basophils.

Cross-linking of IgE and allergens (substance enhance allergic reaction)

Such cross-linking leads to rapid degranulation (60-300 secs) of the mast cells and the release of primary inflammatory mediators stored in the granules. These mediators cause all the normal consequences of an acute inflammatory reaction - increased vascular permeability, smooth muscle contraction, granulocyte chaemotaxis and extravasation etc.

Mast cell activation via Fc epsilonRI also leads to the production of two other type of mediators. These secondary mediators, unlike the stored granule contents, must be synthesised de novo and comprise arachadonic acid metabolites (prostaglandins and leukotrienes) and proteins (cytokines and enzymes).

Primary mediators
Histamine		Vascular permeability, sm contraction
Serotonin		vascular permeability, sm contraction
ECF-A		eosinophil chaemotaxis
NCF-A		neutrophil chaemotaxis
proteases		mucus secretion, connective tissue degradation
	Secondary mediators
Leukotrienes		vascular permeability, sm contraction
Prostaglandins		vasodilation, sm contraction, platelet activation
Bradykinin		vascular permeability, sm contraction
Cytokines		numerous effects inc. activation of vascular endothelium, eosinophil recruitment and activation

Allergens

Numerous ideas have been put forward as to what property might distinguish antigens which stimulate a sufficient IgE response to generate type I hypersensitivity (allergens) from those antigens which rarely or never do so. However no common property has yet been discerned. below is a list of common allergens.

Systemic Anaphylaxis

The consequences of a generalised reaction are potentially fatal. Ingestion of nuts or seafood, insect bites (venom), and drug injection may all cause life-threatening reactions in highly sensitised individuals. Death in such cases is due to systemic release of vasoactive mediators leading to general vasodilation and smooth muscle contraction resulting in sudden loss of blood pressure, massive oedema and severe bronchiole constriction (systemic anaphylaxis).

Hypersensitivity Type 2

Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity.

Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples. The reaction time is minutes to hours. Type II hypersensitivity is primarily mediated by antibodies of the IgM or IgG classes and complement. Phagocytes and NK cells may also play a role. Type 2 is also known as autoimmunity as it attack self-antigen of the cell.

The Fab portion of the antibody binds to epitopes on the "foreign" cell. The NK cell then binds to the Fc portion of the antibody. The NK cell is then able to contact the cell and release pore-forming proteins called perforins, proteolytic enzymes called granzymes, and chemokines. Granzymes pass through the pores and activate the enzymes that lead to apoptosis of the infected cell by means of destruction of its structural cytoskeleton proteins and by chromosomal degradation. As a result, the cell breaks into fragments that are subsequently removed by phagocytes. Perforins can also sometimes result in cell lysis.

ADCC (Antibody dependent cell cytotoxicity)-induced by NK cell during cell apoptosis

Apoptosis occurs when certain granzymes activate a group of protease enzymes called caspases that destroy the protein structural scaffolding of the cell, degrade the cell's nucleoprotein, and activate enzymes that degrade the cell's DNA. As a result, the infected cell breaks into membrane-bound fragments that are subsequently removed by phagocytes. If very large numbers of perforins are inserted into the plasma membrane of the infected cell, this can result in a weakening of the membrane and lead to cell lysis rather than apoptosis. An advantage to killing infected cells by apoptosis is that the cell's contents, including viable virus particles and mediators of inflammation, are not released as they are during cell lysis.

The lesion contains antibody, complement and neutrophils. Diagnostic tests include detection of circulating antibody against the tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence. The staining pattern is normally smooth and linear, such as that seen in Goodpasture's nephritis (renal and lung basement membrane) (figure 3A) and pemphigus (skin intercellular protein, desmosome)

Mechanism of Hypersensitivity Type 2

Hypersensitivity Type 3

Type III hypersensitivity is also known as immune complex hypersensitivity. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs (e.g., aspergillosis), blood vessels (e.g., polyarteritis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms.

Serum sickness (arthus reaction)

The reaction may take 3 - 10 hours after exposure to the antigen (as in Arthus reaction). It is mediated by soluble immune complexes. They are mostly of the IgG class, although IgM may also be involved. The antigen may be exogenous (chronic bacterial, viral or parasitic infections), or endogenous (non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE). The antigen is soluble and not attached to the organ involved. Primary components are soluble immune complexes and complement (C3a, 4a and 5a). The damage is caused by platelets and neutrophils. The lesion contains primarily neutrophils and deposits of immune complexes and complement. Macrophages infiltrating in later stages may be involved in the healing process.

It is now thought that this form of hypersensitivity has a lot in common with type I except that the antibody involved is IgG and therefore not prebound to mast cells, so that only preformed complexes can bind to the low affinity FcgammaRIII.

Watch Type 3 hypersensitivity animation

Large quantities of soluble antigen-antibody complexes form in the blood and are not completely removed by macrophages. These antigen-antibody complexes lodge in the capillaries between the endothelial cells and the basement membrane. The antigen-antibody complexes activate the classical complement pathway and complement proteins and antigen-antibody complexes attract leukocytes to the area. The leukocytes then discharge their killing agents and promote massive inflammation. This leads to tissue death and hemorrhage. This is also example of autoimmunity.

The Arthus reaction

The Arthus reaction is the name given to a local type III hypersensitivity reaction. It is easy to demonstrate experimentally by subcutaneous injection of any soluble antigen for which the host has a significant IgG titre. Because the FcgammaRIII is a low affinity receptor and because the threshold for activation via this receptor is considerably higher than for the IgE receptor the reaction is slow compared with a type I reaction, typically maximal at 4-8hrs, and consequently more diffuse. The condition extrinsic allergic alveolitis occurs when inhaled antigen complexes with specific IgG in the alveoli, triggering a type III reaction in the lung, for example in 'pigeon fanciers lung' where the antigen is pigeon proteins inhaled via dried faeces. Complement is not required for the Arthus reaction, but may modify the symptoms.

Systemic reaction of type 3 hypersensitivity

The presence of sufficient quantities of soluble antigen in circulation to produce a condition of antigen excess leads to the formation of small antigen-antibody complexes which are soluble and poorly cleared. In the normal animal these complexes fix complement but experiments in animals genetically deficient in C3 or C4 have shown that complement is not required for pathology to be observed following antibody-antigen complex challenge. The major pathology is due to complex deposition which seems to be exacerbated by increased vascular permeability caused by mast cell activation via FcgammaRIII. The deposited immune complexes trigger neutrophils to discharge their granule contents with consequent damage to the surrounding endothelium and basement membranes. The complexes may be deposited in a variety of sites such as skin, kidney and joints. Common examples of generalised type III reactions are post-infection complications such as arthritis and glomerulonephritis.

Type 4 hypersensitivity

Type IV hypersensitivity is also known as cell mediated or delayed type hypersensitivity. The classical example of this hypersensitivity is tuberculin (Montoux) reaction which peaks 48 hours after the injection of antigen (PPD or old tuberculin). The lesion is characterized by induration and erythema (abnormal redness and inflammation of skin)

Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, histoplasmosis, toxoplasmosis, leishmaniasis, etc.) and granulomas due to infections and foreign antigens. Another form of delayed hypersensitivity is contact dermatitis (poison ivy, chemicals, heavy metals, etc.) in which the lesions are more papular. Type IV hypersensitivity can be classified into three categories depending on the time of onset and clinical and histological presentation

Table 3 - Delayed hypersensitivity reactions
Type	Reaction time	Clinical appearance	Histology	Antigen and site
contact	48-72 hr	eczema	lymphocytes, followed by macrophages; edema of epidermis	epidermal ( organic chemicals, poison ivy, heavy metals, etc.)
tuberculin	48-72 hr	local induration	lymphocytes, monocytes, macrophages	intradermal (tuberculin, lepromin, etc.)
granuloma	21-28 days	hardening	macrophages, epitheloid and giant cells, fibrosis	persistent antigen or foreign body presence (tuberculosis, leprosy, etc.)

This is the only class of hypersensitive reactions to be triggered by antigen-specific T cells. Delayed type hypersensitivity results when an antigen presenting cell, typically a tissue dendritic cell which has picked up antigen, processed it and displayed appropriate peptide fragments bound to class II MHC is contacted by an antigen specific T_H1 cell patrolling the tissue. The resulting activation of the T cell produces cytokines such as chemokines for macrophages, other T cells and, to a lesser extent, neutrophils as well as TNFbeta and IFNgamma. The consequences are a cellular infiltrate in which mononuclear cells (T cells and macrophages) tend to predominate. It is usually maximal in 48-72 hours.

The problem which this explanation faces is the rarity of antigen-specific T cells. Despite the fact that "memory T cells", unlike naive T cells, do circulate through tissues, there is some doubt that a single T cell could initiate the event. The answer to this conundrum may lie in the recent observations that at least some Type IV reactions absolutely require the presence of 'natural' IgM antibody for initiation. Due to the nature and kinetics of the reaction it is still believed that activation of memory TH1 cells is primarily responsible for propagating the reponse, but initiation may require IgM and probably also complement. One theory is that limited IgM-antigen complexes in local capilliaries may lead to a limiting, localised complement activation within the vessel activating the vascular endothelium and thus recruiting inflammatory cells including memory T cells.

The classical example of delayed type hypersensitivity is in tuberculosis.The tuberculosis skin test is a test used to determine if someone has developed an immune response to the bacterium that causes tuberculosis (TB). The tuberculin skin test is based on the fact that infection with M. tuberculosis bacterium produces a delayed-type hypersensitivity skin reaction to certain components of the bacterium. The components of the organism are contained in extracts of culture filtrates and are the core elements of the classic tuberculin PPD (also known as purified protein derivative).

This PPD material is used for skin testing for tuberculosis. Reaction in the skin to tuberculin PPD begins when specialized immune cells, called T cells, which have been sensitized by prior infection, are recruited by the immune system to the skin site where they release chemical messengers called lymphokines. These lymphokines induce induration (a hard, raised area with clearly defined margins at and around the injection site) through local vasodilation (expansion of the diameter of blood vessels) leading to fluid deposition known as edema, fibrin deposition, and recruitment of other types of inflammatory cells to the area. An incubation period of two to 12 weeks is usually necessary after exposure to the TB bacteria in order for the PPD test to be positive.

Result Interpretation

A tuberculin reaction is classified as positive based on the diameter of the induration in conjunction with certain patient-specific risk factors. In a healthy person whose immune system is normal, induration greater than or equal to 15 mm is considered a positive skin test. If blisters are present (vesiculation), the test is also considered positive.

Positive test tuberculin: 18mm

Summary of type 4 hypersensitivity

1. Antigen is injected into the subcut tissue and processed by local APC

2. A Th1 effector cell recognizes antigen and releases cytokines which act on vascular epithelium

3. Recruitment of T cells, phagocytes fluid and protein to site of antigen injection causes visible lesion

TH1 Influence of immune response

Summary of hypersensitivity (click)

Sources: Microbiology and immunology online; Univ of south carolina school of medicine; http;//www.-immuno-path.cam.ac.uk, The adaptive immune system; faculty.ccbcmd.edu, tuberculosis skin test medicine.net.com

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