Clostridial Diseases: Causes, Symptoms & Diagnosis PDF

CLOSTRIDIAL GROUP OF DISEASES  CLOSTRIDIUM  Clostridium are sprouting , anaerobic bacteria rather larger size  They occur singly, in pairs, or in chains  Commonly found in soil and intestinal tract of human and animals  Divided in 2 groups  Those produce disease through tissue...

CLOSTRIDIAL GROUP OF DISEASES  CLOSTRIDIUM  Clostridium are sprouting , anaerobic bacteria rather larger size  They occur singly, in pairs, or in chains  Commonly found in soil and intestinal tract of human and animals  Divided in 2 groups  Those produce disease through tissue invasion  By the production of toxin  LIST OF CLOSTRIDIAL DISEASES Sl Clostridia Diseases no. 1 Clostridium chauvoei Blackquarter/ blackleg 2 C. septicum Malignant oedema, Braxy 3 Cl. hemolyticum Bovine bacillary hemoglobinuria 4 Cl. novyi Black disease, wound infection (gas gangrene) 5 Cl. botulinum Botulism 6 Cl. tetani Tetanus 7 Cl. Perfringens (Type A-E) 8 Cl. difficile Pseudomembranous colitis  BLACK QUARTER  Synonym: Blackleg, quarter ill  BQ is an acute, infectious, highly fatal disease of mainly cattle  Sometimes sheep, goat, and rarely horses  Besides cattle, BQ is most common in sheep  The disease is characterized by inflammation of skeletal and cardiac muscles, severe toxaemia and a high mortality  Occurs mostly in the rainy season  Most common in young animals, 6 months to 2 yrs of age, on a good nutrition  Etilogy: Clostridium chauvoei  A gram positive, spore forming, rod shaped bacterium  Spores are highly resistant to environmental changes and disinfectants and persists in the soil for many years  Spread:  Soil borne infection  Ingestion of spores  In sheep: wound infection is always there eg. Skin wounds at shearing, docking and of the navel at birth PATHOGENESIS  Ingestion of the spore Multiple in the intestine Cross the intestinal mucosa and enters into the general circulation Deposited in the no. of tissues and organs, including skeletal muscles Spores remain dormant until damaged to muscle sets up an appropriate anaerobic environment for germination and proliferation Multiply and release toxins locally Alpha Beta Gamma Delta Necrotizing and hemolytic Severe necrotizing myositis (myonecrosis) and systemic toxaemia Results in death  CLINICAL SIGNS  The disease is acute, usually fatal and affected animals are often found dead before signs of illness are seen  Lameness, high fever (1060F), and visible swelling of muscles were observed  Shoulder, pectoral , and hindquarter (gluteal) muscles are most commonly involved  In early stage, the swelling is hot and painful to touch but soon becomes cold and painless, and edema and emphysema can be felt  LESIONS  The lesion consists of crepitant swelling (making a crackling sound) in the muscles particularly of the extremities  Clotting of the blood occurs rapidly  Incision of the affected muscles reveals the presence of dark brown or dark red, swollen tissue, streaked black  Some areas appear moist, and on pressure, yield dark, gas filled exudate  Other group of muscles are dry and sponge-like with numerous gas bubbles  A peculiar rancid or sweetish odour may be noticed  The heart is dark and friable with ulcerative endocarditis  Why affected muscles are black in color??  The toxins causes muscle necrosis producing H2S gas, and hemolysis liberating haemoglobin  The iron part of the haemoglobin and the H2S gas combine to produce iron sulfide (FeS) and H2  This iron sulfide imparts a black color to the muscle  MICROSCOPICALLY  Gas bubbles are seen as spherical spaces, separating muscle bundles and fascia  Irregular areas of necrosis, and collections of neutrophils and lymphocytes along the muscle septa  Gram positive organisms can be demonstrated in sections, appearing singly or in small, irregular clumps DIAGNOSIS  Presumptive diagnosis can be made on the basis of lesions  Isolation and identification of the bacteria BRAXY/BRADSOT  An acute infectious disease of sheep characterized by haemorrhagic abomasitis, toxaemia and high mortality rate  Etiology: Clostridium septicum  Mainly seen in Scotland and Scandinavia  Host:  Mainly young sheep are affected  Occurs during the winter months  Pathogenesis:  Ingestion of frozen grass or feed causes primary abomsitis which permits invasion of C. septicum resulting in fatal toxaemia  Clinical signs:  Sudden death with no clinical signs  Gross lesions:  The wall of the abomasum is thickened, oedematous, and haemorrhagic  Diagnosis:  Based on gross lesions  Confirmatory diagnosis is made on the basis of isolation and identification of the organism BOVINE BACILLARY HAEMOGLOBINURIA  Synonym: red water disease or infectious icterohaemoglobinuria  An acute highly fatal toxaemia of cattle and sheep   The disease is characterized clinically by high fever, haemoglobinuria, jaundice and by presence of necrotic infarcts in the liver  Etiology: Cl. haemolyticum PATHOGENESIS  Following ingestion, organisms multiply in the intestinal tract and enter into the systemic circulation  Localizes in the liver and remains latent until an appropriate anaerobic environment develops  Multiply and release exotoxins (Beta toxin)  Causes liver damage, with production of a characteristic infarct, haemolysis and death CLINICAL SIGNS  Clinically characterized by sudden haemoglobinuria, fever, anaemia and death within a day or two  Lesions:  Large area of necrosis in the liver, resembling an infarct  Microscopically, the necrotic tissue contains gram positive bacilli and surrounded by a polymorphonuclear infiltrate. BLACK DISEASE  Also known as infectious necrotic hepatitis  It is an acute fatal infection of sheep and rarely cattle  Etiology: Clostridium novyi  Widely distributed in soil and common inhabitant of the intestinal tract of sheep  Spread:  Ingestion of spores PATHOGENESIS  Following ingestion  Pass through the intestinal wall and lodge in the liver  Where they remain as latent infection  An anaerobic environment produced by migration of liver flukes activates the bacteria  Release exotoxins, which includes alpha and beta toxins  Alpha or lethal toxin is the main toxin which is necrotizing CLINICAL SIGNS  Sudden death  The disease lasts for 1-2 days  Lesions:  Characteristic multiple foci of necrosis in the liver  Petechiae on the epicardium, endocardium and hydropericardium  Subcutaneous venous congestion causes a dark discoularation of the skin, therefore called as black disease DIAGNOSIS  History and clinical signs  Gross lesions  Bacterial isolation and identification  FAT in smears or sections of the liver TETANUS (LOCK JAW)  Tetanus is a highly fatal infectious disease caused by the exotoxin of C. tetani  C. tetani is a gram positive, sporulating anerobes  The spores are terminal giving the organism a drum stick like appearance  Incidence: word wide distribution  Horses and mules are most susceptible  Sheep, goat, dogs and swine may also be affected  Cattle least susceptible  Birds are resistant  Routs of infection:  Almost always by way of wound infection  Wounds that occur during shearing, docking and castration may serve as portals of entrance PATHOGENESIS  Entry through wound infection Engulfed by the leukocytes In favorable anaerobic condition spores vegetate and liberate toxins locally Tetanolysin (a hemolysin) Tetanospasmin (neurotoxin) Fibrinolysis Toxins are absorbed by the axons of the peripheral nerves Passage centripetally to the neurons of the spinal cord and the brain Interfere with the release of neurotransmitter Leads to prolonged spasmodic contraction of muscles Death occurs from asphyxia due to fixation of the muscles of respiration  CLINICAL SIGNS  Characterized by prolonged spasmodic contractions of muscles, with extension of limbs, stiffness and immobilization  The muscles of mastication are often affected, immobilizing the jaws, hence the name lockjaw  Lesions:  No specific gross and microscopic lesions are produced DIAGNOSIS  History of any natural or artificial wounds  Clinical signs (wooden-horse posture and symptoms of asphyxiation)  Isolation and identification of the bacteria  BOTULISM  Originated from the Latin word Botulus meaning sausage, because of its association with ingestion of sausage  Botulism is a rapidly fatal motor paralysis caused by ingestion of the toxins  Etiology: Clostridium botulinum  7 toxigenic strain A-G  Spread:  Almost always result from the ingestion of preformed toxin in a food source  C. botulinum a spore forming anerobe proliferates only in decaying animal or plant material  Source of infection is almost always carrion  PATHOGENESIS Ingestion of preformed toxin in food source Produce numerous extremely potent neurotoxins Toxins act at the peripheral nerve endings, where they get bound and cause nerve blockage Inhibits the release of acetylcholine at the parasympathetic and motor nerve ends Causing muscle paralysis  CLINICAL SIGNS  Incubation period: 1-5 days  The clinical signs are characterized by a descending and symmetrical paralysis  There is paralysis of the muscles of the pharynx, tongue, limbs and neck with dropping of head, dyspnoea etc.  Butulism is also known as Lamsiekte in South Africa, Bulber paralysis in Australia, and Loin disease in the US  Lesions:  No characteristic gross and microscopic lesions are noted  Diagnosis  History and clinical signs  Toxin neutralization test  ENTEROTOXAEMIA  Synonym: Over eating disease or Pulpy kidney Disease  It is an acute toxaemia of sheep and goat also of cattle characterized by brief nervous symptoms and sudden death  Etiology: Cl. Perfringens type D  Five strains A,B,C,D, and E  Type A- Yellow lamb disease  Type B- Lamb dysentery  Type C- Struck CLINICAL SIGNS  Convulsion, coma followed by death  Some animals, show a desire to push the forehead against a solid wall, such animals being referred to as blind staggers  Sometimes, anorexia and diarrhoea  There is usually hyperglycaemia and glycosuria  PATHOGENESIS Feeding of excessive amount of starchy diet or concentrate Stasis and impaction of the alimentary tract Favors luxuriant growth of the organisms and liberation of toxins Alpha, beta, gamma and epsilon (most potent) Absorption of the toxin in the intestine Causes increase permeability and adsorptive power of the intestinal mucosa Results in diarrhoea and focal symmetrical encephalomalacia in the brain LESIONS  Petecheal hemorrhages beneath the epicardial and endocardial surfaces, serous surfaces of the intestine, abdominal muscles, diaphragm and thymus  Kidneys are soft, enlarged and friable particularly in young animals giving rise to the name pulpy kidney disease  This is the result of early postmortem autolysis DIAGNOSIS  Sudden death of lambs with diarrhoea and prolonged glycosuria is highly suggestive  Gross lesions  Isolation and identification of the bacteria  Biological test  Neutralization test