Clostridium Bacteria & Black Quarter

• Clostridium is a sprouting, anaerobic bacterium of larger size.
• Individual clostridium can occur singly, in pairs, or in chains.
• Clostridium is commonly found in soil and the intestinal tract of humans and animals.
• Clostridium is divided into two groups, some produce disease via tissue invasion and others via toxin production.

List of Clostridial Diseases

• Clostridium chauvoei causes Blackquarter/blackleg.
• C. septicum causes Malignant oedema and Braxy.
• Cl. hemolyticum causes Bovine bacillary hemoglobinuria.
• Cl. novyi causes Black disease and wound infection (gas gangrene).
• Cl. botulinum causes Botulism.
• Cl. tetani causes Tetanus.
• Cl. Perfringens (Type A-E) causes Enterotoxaemia
• Cl. difficile causes Pseudomembranous colitis.

Black Quarter

• Black Quarter (BQ) is also called Blackleg or quarter ill.
• BQ is an acute, infectious, and highly fatal disease that mainly affects cattle.
• Sheep, goats, and horses can sometimes be affected by Black Quarter.
• Besides cattle, Black Quarter is most common in sheep.
• The disease is characterized by inflammation of skeletal and cardiac muscles, severe toxaemia, and a high mortality rate.
• Black Quarter occurs mostly in the rainy season and is most common in young animals aged 6 months to 2 years with good nutrition.
• The etiology of Black Quarter is Clostridium chauvoei.
• Clostridium chauvoei is a gram-positive, spore-forming, rod-shaped bacterium.
• The spores of Clostridium chauvoei are highly resistant to environmental changes, disinfectants and can persist in the soil for many years.
• Black Quarter is spread through soil-borne infection, and ingestion of spores.
• In sheep, wound infection is the typical route, such as skin wounds at shearing, docking, and of the navel at birth.

Pathogenesis of Black Quarter

• Spores are ingested and multiply in the intestine.
• The bacteria cross the intestinal mucosa, entering the general circulation.
• They are deposited in tissues and organs, including skeletal muscles but remain dormant.
• When muscle gets damaged, anaerobic conditions encourage germination and proliferation.
• The bacteria multiply and release toxins locally like Alpha, Beta, Gamma, and Delta toxins.
• The toxins cause necrotizing and hemolytic effects.
• Severe necrotizing myositis (myonecrosis) and systemic toxaemia occur.
• Death results from Black Quarter.

Clinical Signs of Black Quarter

• The disease is acute and is usually fatal; affected animals are often found dead before signs of illness are seen.
• Lameness, high fever (106°F), and visible swelling of muscles are observed.
• Muscles of the shoulder, pectoral region, and hindquarter (gluteal) are most commonly involved.
• In the early stages, the swelling is hot and painful to the touch.
• The swelling soon becomes cold and painless, with edema and emphysema that can be felt.

Lesions of Black Quarter

• The lesion consists of crepitant swelling that makes a crackling sound in the muscles, particularly of the extremities.
• Clotting of the blood occurs rapidly after death.
• Incision of the affected muscles reveals dark brown or dark red, swollen tissue, streaked black.
• Some areas appear moist and yield dark, gas-filled exudate when pressed.
• Some muscle groups are dry and sponge-like with numerous gas bubbles.
• A peculiar rancid or sweetish odour may be noted.
• The heart is dark and friable with ulcerative endocarditis.
• Affected muscles are black due to muscle necrosis, which produces H2S gas by toxins, and hemolysis liberating hemoglobin.
• The iron portion of hemoglobin combines with H2S gas, making iron sulfide (FeS) and H2 impart a black color to the muscle.

Microscopic Features of Black Quarter

• Gas bubbles appear as spherical spaces which separate muscle bundles and fascia.
• Irregular areas of necrosis, along with neutrophils and lymphocytes are seen along the muscle septa.
• Gram-positive organisms can be demonstrated appearing singly or in small, irregular clumps.

Diagnosis of Black Quarter

• Presumptive diagnosis is made based on lesions.
• Isolation and identification of the bacteria are key for confirming.

Braxy/Bradsot

• This is an acute infectious disease of sheep marked by haemorrhagic abomasitis, toxaemia and high mortality.
• Braxy is caused by Clostridium septicum.
• This disease is mainly seen in Scotland and Scandinavia.
• Young sheep are most commonly affected.
• Braxy typically occurs during the winter months.
• The pathogenesis involves ingestion of frozen grass or feed, causing primary abomasitis.
• The abomasitis results in the invasion of C. septicum, leading to fatal toxaemia.

Clinical Signs of Braxy/Bradsot

• Sudden death often occurs with no prior clinical signs.

Gross Lesions of Braxy/Bradsot

• The wall of the abomasum is thickened, oedematous, and haemorrhagic.

Diagnosis of Braxy/Bradsot

• Diagnosed based on gross lesions.
• Confirmatory diagnosis relies on isolation and identification of the organism.

Bovine Bacillary Haemoglobinuria

• It is also called red water disease or infectious icterohaemoglobinuria.
• This is an acute, highly fatal toxaemia of cattle and sheep.
• Clinically, it is marked by high fever, haemoglobinuria, jaundice, and necrotic infarcts in the liver.
• The causative agent is Cl. haemolyticum.

Pathogenesis of Bovine Bacillary Haemoglobinuria

• Following ingestion, organisms multiply in the intestinal tract and enter systemic circulation.
• The bacteria localize in the liver and remain latent until anaerobic conditions develop.
• It involves multiplication and release of exotoxins, particularly Beta toxin.
• Liver damage occurs with a characteristic infarct, triggering haemolysis and death.

Clinical Signs of Bovine Bacillary Haemoglobinuria

• The disease is clinically characterized by sudden haemoglobinuria.
• Look for fever, anaemia, and death, typically within a day or two.

Lesions of Bovine Bacillary Haemoglobinuria

• There are a large area of necrosis present in the liver, resembling an infarct.
• Microscopically, the necrotic tissue contains gram-positive bacilli surrounded by a polymorphonuclear infiltrate.

Black Disease

• Also called infectious necrotic hepatitis.
• It is an acute, fatal infection mainly of sheep and rarely cattle.
• Clostridium novyi is the causative agent of black disease.
• It is widely distributed in soil and is a common inhabitant of the intestinal tract of sheep.
• Black disease spread through ingestion of spores.

Pathogenesis of Black Disease

• The disease developes following ingestion spores
• Spores pass through the intestinal wall and lodge in the liver, where they stay as latent infection.
• Anaerobic conditions caused by migrating liver flukes activate the bacteria.
• Toxins released include alpha and beta toxins.
• The alpha or lethal toxin is the main necrotizing agent.

Clinical Signs of Black Disease

• It includes sudden death.
• Black disease typically lasts for only 1-2 days.

Lesions of Black Disease

• It shows characteristic multiple foci of necrosis in the liver.
• Petechiae are seen on the epicardium, endocardium, and hydropericardium.
• Subcutaneous venous congestion causes a dark discolouration of the skin, hence the name black disease.

diagnosis of Black Disease

• It's based on history and clinical signs.
• Diagnosis occurs through gross lesions and bacterial isolation/identification.
• FAT can also be used for diagnosis.

Tetanus

• Tetanus is a highly fatal infectious disease caused by the exotoxin of C. tetani.
• C. tetani is a gram-positive, sporulating anaerobe.
• The spores of C. tetani are terminal, giving the organism a drum-stick appearance.
• Tetanus is occurs worldwide.
• Horses and mules are most susceptible to tetanus.
• Sheep, goats, dogs and swine can also be affected.
• Cattle are the least susceptible.
• Birds are resistant to tetanus.
• Infection usually occurs through wound contamination.
• Wounds sustained during shearing, docking, and castration can provide entrance.

Pathogenesis of Tetanus

• The spores of Clostridium tetani can enter primarily through wound infections.
• Leukocytes engulf the spores.
• Under anaerobic conditions, the spores vegetate and release toxins locally.
• Key toxins include tetanolysin (a hemolysin), tetanospasmin (neurotoxin), and fibrinolysin.
• The toxins are transported via the axons of peripheral nerves.
• They then travel to the spinal cord and brain.
• There, they interfere with the release of neurotransmitters.
• This interference leads to prolonged spasmodic muscle contractions.
• Death results from asphyxia due to the fixation of respiratory muscles.

Clinical Signs of Tetanus

• Look for prolonged spasmodic contractions of muscles, along with limb extension, stiffness, & immobilisation.
• Mastication muscles are commonly impacted, immobilizing the jaws and creating lockjaw.

Lesions of Tetanus

• There aren't any specific gross or microscopic lesions produced by tetanus.

Diagnosing Tetanus

• A history containing natural or artificial wounds is key.
• Diagnose based on clinical signs, isolation and identification of bacteria.

Botulism

• Botulism originated from the Latin word Botulus, sausage, due to its link to sausage ingestion.
• It is a rapidly fatal motor paralysis caused by ingesting the toxins of Clostridium botulinum.
• Clostridium botulinum is a gram-positive, spore-forming obligate anaerobe.
• There are 7 toxigenic strains of C. botulinum which include A-G.
• It results almost always from eating preformed toxin in food sources.
• C. botulinum spores only proliferate in dead animal or plant matter.
• Its source of infection is almost always carrion.

Pathogenesis of Botulism

• Disease results due to ingestion of preformed toxin in food.
• Bacteria produce extremely potent neurotoxins.
• Toxins bind where they cause nerve blockage at the peripheral nerve endings.
• Inhibition of acetylcholine release happens at the parasympathetic and motor nerve ends.
• The inhibition of acetylcholine then causes muscle paralysis.

Clinical Signs of Botulism

• The incubation period is typically 1-5 days.
• Clinical signs include descending and symmetrical paralysis.
• Paralysis impacts neck, pharynx, tongue, and limbs, and may result in dropping of head as well as dyspnoea.
• Botulism is also called Lamsiekte in South Africa, Bulber paralysis in Australia, and Loin that affect disease.
• There are no particular anatomical abnormalities or lesions to be observed.

Diagnosis of Botulism

• Diagnosed through history and clinical signs.
• Diagnosis occurs through toxin neutralization test.

Enterotoxaemia

• Is also called over eating disease or pulpy this kidney Disease.
• This is an acute toxaemia that affects sheep, goats, and cattle.
• It's characterized by sudden death and brief nervous symptoms, which is caused by Cl. Perfringens type D.
• There are five strains A, B, C, D, and E.
• Yellow lamb disease is caused by type A, while lamb dysentery is caused by type B.
• A C type infection is called Struck.

Clinical Signs of Enterotoxaemia

• It includes Convulsions, coma followed by death.
• The disease can be identified by pushing the head in one direction, which is referred to as blind staggers.
• You may also see anorexia, diarrhoea, or hyperglycaemia.

Pathogenesis of Enterotoxaemia

• It results after concentrated or extremely starchy feeding.
• An impaction and Stasis then follow up in the alimentary that area.
• The organism then favours luxurious growth of its toxins and liberating of toxins.
• Alpha, beta, gamma, and epsilon are the potent growth, and epsilon is the most absorbent.
• It results in a focal and symmetric absorbtion of the toxins in the intestine, which causes an intestinal permeability.

Lesions of Enterotoxaemia

• Petecheal hemorrhages occur on the epicardial's surface, Serous surfaces of the intestine, abdominal muscles and the diaphragm, and the thymus glands.
• Soft, enlarged, friable kidneys result in pulpy kidney, especially in young animals.
• This is an example of premature post mortem autolysis.

Diagnosis of Enterotoxaemia

• Sudden death with lambs and diarrhea, particularly increased glycosuria, is indicative of this.
• Diagnosis occurs through Gross Lesions in an Isolation and identification of the bacteria.
• Testing also helps in confirming such diagnosis.

Explore Clostridium bacteria characteristics, disease mechanisms, and Black Quarter (Blackleg). Learn about the spread, pathogenesis, and diagnosis of necrotizing myositis in animals, including key post-mortem findings.