Diseases caused by Rickettsia and Mycoplasma spp

Diseases caused by Rickettsia and Mycoplasma spp.


Heartwater (Hydropericardium)

"Black dung" when affecting African cattle and buffalo


"Sheep fever" when seen in sheep

Heartwater is an acute, non contagious disease of cattle, sheep, goats, antelopes and wild ruminants. It is caused by the rickettsial organism Cowdria (Rickettsia) ruminantium.


Transmission:

Heartwater is transmitted by various species of Amblyomma ticks. Transstadial transmission of the organism occur in vector ticks.

Antemortem findings :


Peracute form

1. Incubation 14 – 28 days
2. Fever
3. Diarrhoea
4. Convulsions and death

Acute form

1. Fever up to 41.7°C
2. Rapid breathing
3. Lack of appetite, depression and listlessness

Nervous signs include

1. Twitching of the eyelids
2. Protrusion of the tongue
3. Champing of the jaw
4. Walking in circles
5. Paddling with legs in recumbent animals
6. Opisthotonos and convulsions

Postmortem findings :

1. Hydropericardium
2. Hydrothorax
3. Pulmonary edema and ascites
4. Haemorrhagic gastroenteritis
5. Enlarged liver, spleen and lymph nodes
6. Haemorrhage in the abomasum and intestine
7. Edema and haemorrhage of the brain

Judgement :


Carcass of an animal affected with heartwater is condemned in the acute stage of the disease. In a chronic case, the carcass may be approved if adequately bled and muscles are wholesome in colour and texture. The affected organs are condemned.


Differential diagnosis :



Peracute form of heartwater should be differentiated from anthrax. The acute nervous form of the disease is differentiated from tetanus, rabies, cerebral trypanosomiasis, strychnine poisoning, piroplasmosis, theileriosis, lead and organophosphate poisoning, parasitism, arsenical poisoning and poisoning with certain plants.





Fig. 63 : Heartwater Cowdria ruminantium in bovine brain smear (arrow).



Q fever (Queensland fever, Nine mile fever, American Q fever, Australian Q fever)


Q fever is a disease of cattle, sheep, goats, donkeys, camels, fowl, dogs, cats, pigeons and humans. It is caused by Coxiella burnetii. Q fever is an occupational disease of livestock personnel. farmers and laboratory personnel.

Transmission :

Ticks spread infection to cattle which develop mild disease. The faeces deposited on animal hide by ticks may be the source of infection for humans. Q fever is also transmitted by inhalation or dust contaminated with infected animal secreta or excreta. Healthy animals may serve as a carrier and shed the organism in milk, urine, faeces, placenta and fetal fluids. They harbour the infection and no clinical signs are observed. Contaminated meat and water are further means of infection read.

field cases there are no clinical signs of this disease. In the disease produced by the inoculation of cows via the udder the clinical signs may include:

1. Acute mastitis
2. Loss of appetite and depression
3. Serous nasal and lacrimal discharge
4. Difficult breathing
5. Atony of the rumen
6. Abortion in pregnant cows

No gross lesions are reported in cattle.

Discussions :
Coxiella burnetii is highly resistant and was isolated from farm soil 6 months after the removal of animals. It may persist in the udder up to 3 years. The temperatures of milk pasteurisation (in bulk at 63°C for 30 minutes or the common method at 72°C for 15 seconds) kill this agent in milk. Vaccination will reduce shedding of organisms in milk.

This disease in humans has a sudden onset and is characterized by loss of appetite, weakness and generalized malaise lasting from 1 – 2 weeks. Pneumonia may also be present. Death may be caused by endocarditis in older people. More severe symptoms of Q fever are noticed.

Contagious bovine pleuropneumonia

This is an acute, subacute or chronic highly infectious disease of cattle caused by Mycoplasma mycoides var, mycoides.

Transmission :


Aerosol and droplet infection from the infected animals. The recovered animal called "lungers" act as carriers and shedders, especially under stress.


Antemortem findings :

1. Incubation: acute 10 – 14 days, chronic 3 – 6 months
2. Morbidity: 90 % in susceptible cattle
3. Mortality: 10 – 50 %
4. Fever
5. Depression
6. Lack of appetite and loss of weight
7. Coughing on exercise
8. Shallow rapid respiration, grunting and gurgling
9. Extended neck, lowered head and open mouth
10. Arched back and outward rotated elbow
11. Arthritis in young animals

Postmortem findings :

1. Fibrinous inflammation of the pleura (pleuritis)
2. Straw coloured fluid in the thorax (Fig. 64)
3. Lobar pneumonia with red hepatization, marbled appearance of lung lobules (Fig. 65) due to thickening of interlobular septae and interlobular pulmonary edema
4. Enlarged mediastinal lymph nodes
5. Walled-off sequestra formation in chronic cases
6. Haemorrhage in the heart
7. Arthritis and tenosynovitis

Judgement :

Carcass of an animal affected with contagious bovine pleuropneumonia is condemned if the disease is associated with fever, inadequate bleeding of carcass, serous infiltration of the brisket and emaciation. Recovered animals showing no generalized signs of the disease are approved and the affected organs are condemned.

Differential diagnosis :



Shipping fever (Pasteurellosis). East coast fever, foreign body pneumonia, IBR, tuberculosis, chlamidial infections and lungworms




Fig. 64: Contagious bovine pleuropneumonia. Straw coloured fluid in the thorax and partial lung hepatization.






Fig. 65: Contagious bovine pleuropneumonia. Lobar pneumonia with red hepatization and marbled appearnce of lung lobules

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9:25 PM

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Anthrax

 

 

Anthrax is a peracute disease of ruminants manifested with septicemia, sudden death and tarry blood from the body openings of the cadaver. It is caused by Bacillus anthracis.

TransmissionMan may contract anthrax by inhalation, ingestion and through a wound in the skin. Biting flies have been shown to be transmitters.

Ante-mortem findingsThe peracute and acute forms in cattle and sheep are without clinical signs. Death may follow in the acute form after 1 - 2 hours of illness. The acute form lasts about 48 hours.

In pigs and horses this disease is usually localized and chronic and is often characterized by swelling around the throat and head.

Ante-mortem findings in pigs:
1. Incubation 1 - 2 weeks
2. Edematous swelling of the throat and neck
3. Swallowing and breathing difficulties
4. Death due to choking or toxaemia
5. Septicemia is not observed.

Post-mortem findings1. Dark-tarry blood discharge from body orifices
2. Absence of rigor mortis
3. Haemorrhage of the mucous and serous membranes, lymph nodes and subcutaneous tissue
4. Enlarged spleen
5. Severe haemorrhagic enteritis
6. Degeneration of the liver and kidneys
7. Bloating and rapid decomposition of carcass
8. Localized lesions in the intestine of pigs (dysentery)

JudgmentCondemnation of the carcass and its parts by burning or burial. If disposed by burial, the carcass should be buried at least 6 feet below ground. The site should be surrounded by a foot thick layer of quicklime.

Differential diagnosisPeracute blackquarter and septicaemic form of other diseases. In splenic enlargement as seen in babesiosis, anaplasmosis and leucosis, spleen consistency is firm. In anthrax, the spleen is soft and upon incision the pulp exudes like thick blackish-red blood.

DiscussionIf an animal has died from an unknown cause in an abattoir's pen or in the stockyard, a blood smear from the tip of the ear should be examined to eliminate anthrax as a cause of death. All measures should be taken to prevent further contact with the carcass. The orifices of the nose, vulva and anus should be packed with cotton swabs to eliminate further spillage of discharge. The carcass must not be opened. Due to insufficient oxygen supply in the closed carcass, spores of B. anthracis will not be formed and the organism will be killed. The spilled discharge is firstly removed by drying with sawdust and sand and is then destroyed together with the carcass. The carcass is wrapped in thick plastic sheets and destruction is performed under the supervision of an appropriate government official.

An open carcass facilitates exposure of B. anthracis to air and consequently, spores are formed within a few hours. Anthrax spores are resistant to heat and disinfectants and may survive in a suitable environment for years.

The abattoir's pen or stockyard area suspected of being in contact with an anthrax animal should be disinfected with 10 % NaOH or 5 % formaldehyde and cleaned. This cleaning should also include the cattle trucks or cars used for the transportation of infected animals.

All personnel that were in contact with anthrax or that handled contaminated material, are also subjected to decontamination. The arms and hands should be washed with liquid soap and hot water. After they have been rinsed, they should be immersed for about one minute, in an organic iodine solution or 1 p.p.m. solution of mercuric perchloride or other acceptable agents. This is followed by a potable water rinse. Clothing of the personnel involved should also be cleaned and thoroughly disinfected by boiling.

If the carcass is discovered on the killing floor, all operations must cease. The carcass and its parts including hides, hooves, viscera and blood must be condemned and destroyed. The carcasses which have been dressed by the same abattoir employees prior to or after the affected carcass must also be condemned and destroyed. Those carcasses which had been dressed before the affected carcass may have a second option of being salvaged with sterilization. They must be boiled for a minimum of 3 hours if contamination occurred with blood splashes. If impractical, these carcasses may be used for "canned meat" for which heat treatment is recommended.

Disinfection of equipment used for the dressing of a diseased carcass as well as the infected abattoir area, should be done with 5 % solution of sodium hydroxide (NaOH). This disinfectant is used because of its action on fat and grease removal. Heat in the form of a blowtorch can be used for disinfecting buildings.

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9:18 PM

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Cat Restraint

Cat Restraint


1. Catching Cats

A. NO cat will respond solely to verbal command
B. Cats will often try to find a place to hide rather than run away

a. May respond with ears laid back, hissing, scratching and biting at an extended hand

b. Most cats will cower, lowering their body to the floor and scooting backwards

C. You may also try throwing a towel or blanket over the animal, then attempt to grasp the scruff, towel and all

2. Restraint Aids

A. Cat muzzle

a. Covers eyes and mouth leaving a little hole for the nose

b. Unfamiliar surroundings may startle cats; they may feel more secure if they can’t see what’s going on

B. Cat bag

a. May give the cat a sense of security

b. Confines the 4 weapons (feet with claws)

c. Zippers allow utilization of specific body areas

C. Towels

a. Readily available

b. Can be used like a "baby blanket" wrapping claws and allowing them to gouge at the material instead of you

D. Restraint for examination

a. Any type of physical restraint must be used with caution, cats stress very easily

b. Allowing some supervised freedom is sometimes the best method

E. Restraint for Venipuncture

1. Cephalic restraint.

Place one hand around the head and jaw from the bottom of the jaw. Use other hand to extend the leg and hold off the cephalic vein at the top of the leg.

2. Jugular withdrawal

a. You should stretch forefeet over edge of table for better control

b. Keep paws from slipping by placing one of your fingers in between the cat’s feet

c. While restraining for the jugular, you should hold the cat’s head with the palm of one hand over the top of the head

d. The jaw of the zygomatic arch is grasped with the thumb on one side and 2 or 3 fingers on the other side

NOTE: This leaves the index finger free for scratching the cat’s nose to distract the cat from the procedure

3. "Stretch" restraint - can be used for medial saphenous withdrawal or injection

a. The "stretch" restraint is the best method utilized



b. Grab the cat at the scruff of the neck with one hand



c. With your other hand grab the two rear legs again slipping a finger in between his paws



d. Lay animal on its side, using the forearm of the hand holding the scruff to support the back

NOTE: The "Stretch" method can also be used for any task if more than supervised freedom is required on a rowdy cat

 
F. Chemical Restraints

1. Ketamine

a. IV injection

b. IM injection - extremely irritating, causes immediate pain, take precautions in restraining

c. Causes tetany when used alone

d. Reduces blink reflex

e. Apply opthalmic ointment

2. Acepromazine

a. May be used alone or combined with ketamine to reduce rigid effect

                    b. May be given IM or subcutaneously

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9:13 PM

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immunity

 lymph node

thymus


 

bone marrow


 

spleen

 

blood cells

Examples of Eosinophils

 

 

Example of a Basophil

Examples of Lymphocytes

Examples of Monocytes

Examples of Neutrophils

immune system

 :

Innate immunity

Signal Transduction Pathways in Innate Immunity

Adaptive (acquired) immunity  

Antibodies

Antibody-mediated (humoral) immunity is regulated by B cells and the antibodies they produce. Cell-mediated immunity is controlled by T cells. Antibody-mediated reactions defend against invading viruses and bacteria. Cell-mediated immunity concerns cells in the body that have been infected by viruses and bacteria, protect against parasites, fungi, and protozoans, and also kill cancerous body cells.

Antibody-mediated Immunity

Stages in this process are:

1. antigen detection
2. activation of helper T cells
3. antibody production by B cells

Each stage is directed by a specific cell type.

Macrophages

are white blood cells that continually search for foreign (nonself) antigenic molecules, viruses, or microbes. When found, the macrophages engulfs and destroys them. Small fragments of the antigen are displayed on the outer surface of the macrophage plasma membrane.

Antibodies bind to specific antigens in a lock-and-key fashion, forming an antigen-antibody complex. Antibodies are a type of protein molecule known as immunoglobulins. There are five classes of immunoglobulins: IgG, IgA, IgD, IgE, and IgM

Antibodies are Y-shaped molecules composed of two identical long polypeptide (Heavy or H chains) and two identical short polypeptides (Light or L chains). Function of antibodies includes:

1. Recognition and binding to antigens
2. Inactivation of the antigen

A unique antigenic determinant recognizes and binds to a site on the antigen, leading to the destruction of the antigen in several ways. The ends of the Y are the antigen-combining site that is different for each antigen.

Helper T cells activate B cells that produce antibodies. Supressor T cells slow down and stop the immune response of B and T cells, serving as an off switch for the immune system. Cytotoxic (or killer) T cells destroy body cells infected with a virus or bacteria. Memory T cells remain in the body awaiting the reintroduction of the antigen.

A cell infected with a virus will display viral antigens on its plasma membrane. Killer T cells recognize the viral antigens and attach to that cell's plasma membrane. The T cells secrete proteins that punch holes in the infected cell's plasma membrane. The infected cell's cytoplasm leaks out, the cell dies, and is removed by phagocytes. Killer T cells may also bind to cells of transplanted organs.

The immune system is the major component of this defense. Lymphocytes, monocytes, lymph organs, and lymph vessels make up the system. The immune system is able to distinguish self from non-self. Antigens are chemicals on the surface of a cell. All cells have these. The immune system checks cells and identifies them as "self" or "non-self". Antibodies are proteins produced by certain lymphocytes in response to a specific antigen. B-lymphocytes and T-lymphocytes produce the antibodies. B-lymphocytes become plasma cells which then generate antibodies. T-lymphocytes attack cells which bear antigens they recognize. They also mediate the immune response. Success of organ transplants and skin grafts requires a matching of histocompatibility antigens that occur on all cells in the body. Chromosome 6 contains a cluster of genes known as the human leukocyte antigen complex (HLA) that are critical to the outcome of such procedures. The array of HLA alleles on either copy of our chromosome 6 is known as a haplotype.

The large number of alleles involved mean no two individuals, even in a family, will have the same identical haplotype. Identical twins have a 100% HLA match. The best matches are going to occur within a family. The preference order for transplants is identical twin > sibling > parent > unrelated donor. Chances of an unrelated donor matching the recipient range between 1 in 100,000-200,000. Matches across racial or ethnic lines are often more difficult. When HLA types are matched survival of transplanted organs dramatically increases. 

Antigens

Antigen Matching

antigen action

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9:08 PM

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Icterus

Icterus (Jaundice)

Icterus is the result of an abnormal accumulation of bile pigment, bilirubin, or of haemoglobin in the blood. Yellow pigmentation is observed in the skin, internal organs (Fig. 22, 23), sclerae (the white of the eye), tendons, cartilage, arteries, joint surfaces etc. Icterus is a clinical sign of a faulty liver or bile duct malfunction, but it may be also caused by diseases in which the liver is not impaired. Jaundice is divided into three main categories (Fig. 24).

1. Prehepatic jaundice (haemolytic icterus)
2. Hepatic jaundice (toxic icterus)
3. Posthepatic jaundice (obstructive icterus)

Fig. 22: Jaundice of an aged cow caused by liver disease. Note yellow discoloration of body fat, lungs, heart and kidneys.







Fig. 23: Yellow discoloration of pig viscera and carcass caused by cirrhosis of the liver.









Fig. 24: Classification of jaundice

1. Pre-hepatic:
2. Hepatic:
3. Post-hepatic

Prehepatic jaundice occurs following excessive destruction of red blood cells. Tick-borne diseases such as Babesia ovis and Anaplasmosis cause this type of icterus, which is one of the main causes of carcass condemnation in Southern Africa due to prevalence of these parasites. Overproduced blood pigment, which cannot be metabolized in the liver, builds up in the blood (haemoglobinemia). It is excreted by the kidneys into the urine (haemoglobinuria). Normal urine colour changes and becomes bright red to dark red.

Hepatic jaundice occurs due to direct damage to liver cells as seen in liver cirrhosis (Fig. 23), systemic infections, and in chemical and plant poisoning. In sheep, jaundice may have been caused by phytogenic chronic copper poisoning.

Liver function is impaired and the liver is unable to secrete bile pigments. Obstructive jaundice occurs when the drainage of the bile pigment bilirubin is blocked from entry into the intestine. This usually occurs due to the obstruction of the hepatic ducts by a tumour, by parasites such as flukes or by gall stones. Obstruction may also occur due to an inflammation of the bile ducts. In hogs, mature ascarides may occlude the bile ducts.


Judgement :


Animals suspected to have icterus should be treated as "suspects" on antemortem examination. On postmortem examination, the carcass and viscera with haemolytic, toxic icterus and obstructive icterus are condemned. Less severe cases are kept in the chiller for 24 hours. Upon re-examination, the carcass may be approved or condemned depending on the absence or presence of pigment in the tissue. If the obstructive icterus disappears after 24 hours, the carcass and viscera can be passed for human food.

A simple laboratory test will help to make an objective test for bile pigment icterus. Two drops of serum are mixed on a white tile with two drops of Fouchets agent.² A blue/green precipitate is positive for bile icterus.

² Fouchets Reagent Trichloroacetic acid.25 gmFeCl₃ (10 % solution)10 mlDistilled water100 ml

Differential diagnosis :



Yellow fat in animals with heavy corn rations, nutritional panniculitis (yellow fat disease, steatitis) and yellow fat seen in extensive bruises. In yellow fat disease, the fat has a rancid odour and flavour upon cooking.

To differentiate icterus from the normal colour of fat of certain breeds, the sclera, intima of the blood vessels, bone cartilage, liver, connective tissue and renal pelvis should be examined. If yellow discoloration is not noted in these tissues, icterus is not present.

Icterus should not be confused with yellow fat disease in hogs fed predominantly on fish by-products or by the yellowish appearance of tissue caused by breed characteristics or nutritional factors.

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8:49 PM

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