Adult Gastrointestinal diseases

Salmonellosis

  • Overview: caused by many serotypes; >2500 known serotypes; some are zoonotic. In cattle, the most common Salmonella enterica serotypes are Typhimurium, Dublin, and Newport. Contamination risk: approximately 5-20% of dairy cattle feed may be contaminated. Generally tolerable unless the animal is immunocompromised.

  • Transmission: fecal-oral; also via milk/colostrum.

  • Diagnosis:- Fecal culture with enrichment broth to increase sensitivity, followed by PCR

    • Blood culture

    • Serological tests

  • Clinical signs (systemic and GI):- Systemic/endotoxemia signs: fever, tachypnea, tachycardia, scleral injection, depression, weakness, shock

    • Diarrhea: often-putrid or foul odor; watery-mucoid with possible fibrin and blood; maldigestion due to loss of mucosal epithelial cells; may be secretory if enterotoxin produced; inflammatory diarrhea possible

  • Treatment:- Aggressive fluid therapy

    • NSAIDs

    • Antibiotics guided by culture & sensitivity

  • Prevention & control on farm:- Manage infected animals (identify, isolate or cull, vigorous treatment for systemic disease, retest carriers)

    • Calf management: biosecurity, sanitation in calving area, early separation of calves from carrier dams, pasteurization of colostrum, vaccination considered for young animals

    • Cow management: vaccination before calving may be considered; reduce stress; biosecurity to prevent introduction and spread; avoid random mixing

    • Farm biosecurity: protect feed and water from fecal contamination; clean and disinfect contaminated buildings

    • Worker safety: communicate zoonotic risk and enforce hygiene and PPE

    • Vaccination: consideration mentioned but not definitively established

  • Outbreak considerations:- Measures to reduce shedding and transmission; identification and segregation of carriers; overall stress reduction

Johne’s Disease

  • Etiology: caused by Mycobacterium avium subspecies paratuberculosis (MAP); tiny rod-shaped bacterium; primary lesion is chronic proliferative enteropathy primarily of the small intestine.

  • Herd prevalence: high; in the US, about 80% of herds affected at some level.

  • Transmission: ingestion is the primary route; via manure, contaminated milk, water, and feed. Intrauterine transmission occurs in about 25% of calves from infected cows.

  • Infection dynamics: infection generally occurs when young; clinical signs (CS) appear later due to long incubation period; CS include chronic protein-losing enteropathy.

  • Clinical signs: chronic diarrhea (often with a poor appetite but weight loss), edema (submandibular/bottle jaw) due to hypoproteinemia, progressive weight loss despite good appetite

  • Diagnosis:- Presumptive dx based on clinical signs

    • Culture: isolate MAP from manure, tissue, or environmental samples (slow growth)

    • PCR: feces

    • Serology: ELISA or AGID (Agar Gel Immunodiffusion) on milk or blood

    • Biopsy: terminal ileum, ileocecal and mesenteric LNs

  • Treatment & prognosis: treatment is not recommended; infection is typically managed to reduce spread; clinical disease leads to thickened, corrugated ileum

  • Herd eradication strategies (control program):- Goal: curtail spread of infection; often federal-state-industry coordinated

    • Strategies include: closed herds; testing replacements; clean water; rest pastures with slurry/manure applied (3–12 months); protect calves/young cattle from infection; good hygiene and biosecurity

Winter dysentery

  • Etiology: bovine coronavirus (BCoV); environmental stability: heat-sensitive, but can survive in cold temperatures; easily inactivated by common disinfectants

  • Transmission: fecal-oral

  • Epidemiology: outbreaks occur in adult lactating dairy cows during winter; associated with close confinement and handling of manure; incidence of D+ spreads with respiratory signs (co-occurring resp signs may be observed)

  • Incubation and shedding: incubation 3-8 days; fecal and nasal shedding occur for 1-4 days

  • Morbidity/Mortality: high morbidity: 30-50%; mortality low: around 2%

  • Clinical signs: sudden onset anorexia, decreased milk production, diarrhea, fever

  • Diagnosis: viral detection methods such as electron microscopy, ELISA, RT-PCR on intestinal tissues, feces, rectal or nasal swab- Sample collection window: within 1-3 days after onset; samples stored in PBS or culture medium and can be frozen for shipment

  • Treatment: supportive care with IV or oral fluids, NSAIDs, antibiotics as needed, and possible transfaunation

  • Vaccination: no vaccines have proven effective against WD

Malignant catarrhal Fever (MCF)

  • Forms:- Sheep-associated MCF (North America): caused by ovine herpesvirus type 2; cattle and other wild ruminants are affected when in contact with sheep/goats (asymptomatic carriers)

    • Wildebeest-associated MCF: may occur outside Africa in zoological settings; caused by alcelaphine herpesvirus type 1; transmission via direct or indirect contact, aerosols, nasal or ocular secretions

  • Incidence and prognosis: low morbidity but high mortality

  • Clinical signs: profuse oculo-nasal discharge, diarrhea, oral and nasal erosions, corneal opacity, enlarged superficial lymph nodes, hyperemic coronary bands with lameness, hematuria, dermatitis, encephalitis

  • Treatment: supportive care only

  • Prognosis: poor

Clostridial disease

  • Overview: histotoxic clostridia produce exotoxins causing localized tissue necrosis and systemic toxemia; enterotoxic clostridia are common in gut in low numbers

  • Key organisms and associated syndromes:- Histotoxic clostridia

    • Clostridium chauvoei
      True blackleg; C. septicum
      False blackleg; Clostridium novyi; C. novyi type B
      Black disease (infectious hepatic necrosis); C. sordellii; C. perfringens type A and type D (and E in some contexts)

    • Clostridium chauvoei/C. septicum/C. novyi/C. sordellii are linked to myonecrosis, malignant edema, gas gangrene, etc.

    • Clostridium perfringens types A, C, D, E cause various hemorrhagic enteritis, abomasal ulcers, gas gangrene, yellow lamb disease, lamb dysentery, enterotoxemia in several species

    • Enterotoxic clostridia: C. perfringens types A, B, C, D, E with distinct toxin profiles (A: alpha; B: alpha+beta+epsilon; C: alpha+beta; D: alpha+epsilon; E: alpha+iota) and related diseases as summarized below

  • Diseases and toxins (Table-style summary):- Type A: Alpha toxin; diseases include hemorrhagic enteritis in cattle; abomasal tympany/ulcers in neonatal calves; gas gangrene; yellow lamb disease; lamb dysentery

    • Type B: Alpha, beta, epsilon toxins; enterotoxemia of foals

    • Type C: Alpha, beta toxins; necrotic hemorrhagic enterotoxemia of calves, lambs, kids, foals, piglets

    • Type D: Alpha, epsilon toxins; enterotoxemia of sheep, goats, cattle; abomasal tympany and ulcers in calves; enteritis in rabbits

    • Type E: Alpha, iota toxins; enterotoxemia-like disease

  • Major clostridial conditions and examples:- Clostridium chauvoei: True blackleg (rapid onset, muscle necrosis, swelling in hindquarters/neck, rapid carcass decomposition)

    • Clostridium septicum: Malignant edema; braxy-type lesions; wound-associated infection with rapid spread along fascial planes; may cause enteric abomasitis in lambs

    • Clostridium novyi: Black disease (infectious necrotic hepatitis), often following liver damage from Fasciola hepatica

    • Clostridium novyi type B: Very similar to Black disease; high fatality, rapid course in livestock

    • Clostridium haemolyticum (Bacillary hemoglobinuria): Associated with liver fluke infections; hemoglobinuria (“red water”); tachycardia/tachypnea; hepatic infarcts on necropsy

    • Clostridium sordellii: part of histotoxic clostridia group; systemic toxaemia

    • Clostridium haemolyticum: Bacillary hemoglobinuria (see above)

    • Clostridium botulinum, Clostridium tetani: Botulism and lockjaw; vaccine and toxin considerations are used in some contexts

  • Diagnosis: history of rapidly progressing signs; fecal culture + toxin expression (where applicable); necropsy findings; culture from lesions

  • Treatment: supportive care; antibiotics such as penicillin; antitoxins or anti-toxin products; surgical/clinical management depending on lesion

  • Prevention and vaccination: vaccines are available for some Clostridia in cattle (bacterin-toxoid vaccines) and are used as part of herd programs; specific products mentioned include:- Clostridium chauvoei-septicum-novyi-perfringens types C & D bacterin-toxoid (for veterinary use)

    • Mannheimia haemolytica bacterin-toxoid (used alongside Clostridial vaccines in multi-disease programs)

    • One Shot Ultra® 7 (vaccine mix by Zoetis) containing multiple clostridial antigens

  • Practical notes: vaccination is part of disease prevention, though not all diseases may be covered in a single product; vaccination schedules and product choice depend on regional risk and herd history

Hemorrhagic bowl syndrome (HBS)

  • Overview: sporadic, frequently fatal enteric disease affecting dairy cattle; commonly 3–4 months into lactation; higher prevalence reported in Brown Swiss

  • Pathophysiology: massive hemorrhage into the small intestine with intraluminal formation of large clots and blood casts, causing obstruction

  • Etiology: potential association with Clostridium perfringens type A; exact pathogenesis not fully clarified

  • Clinical signs:- Per-acute onset of progressive weakness

    • Abdominal distension with transient abdominal sounds (pings)

    • Fluid splashing sounds on auscultation

    • Often mistaken for obstruction; death within 24–48 hours if not treated

  • Rectal exam: ruminal gas accumulation; otherwise normal

  • Diagnosis: transabdominal ultrasound showing dilated loops of small intestine

  • Treatment: primarily medical and supportive; surgical options (massage the clot or remove affected bowel) are considered but often futile and unrewarding

  • Prognosis: poor without rapid intervention; high fatality risk

Rectal prolapse

  • Etiology/risk factors:- Tenesmus due to conditions like coccidiosis or colitis

    • Dysuria from cystitis, urolithiasis, dystocia, neoplasia

    • Neuropathy (e.g., estrus-related riding, spinal tumors/abscesses)

    • Chronic coughing from BRD

    • Tail docking too short (especially in small ruminants)

    • Genetic susceptibility

  • Diagnosis: direct visual inspection of prolapse

  • Classification (by structure/anatomy):- Type I (I): Prolapse of rectal mucosa only (small, usually intermittent)

    • Type II (II): Prolapse of mucosa and full-thickness rectum (complete prolapse); length variable; can be intermittent

    • Type III (III): Type II with prolapse of large colon (intussusception of large colon into rectum); longer, more painful; signs progress rapidly

    • Type IV (IV): Type III with anal sphincter intact causing constriction of rectum and colon (intussusception through anus)

  • Clinical features: similar across types with progression in higher types

  • Treatment: patchwork of approaches depending on severity- Clean the prolapse; osmotic agent; lubrication

    • Replace the prolapse; purse-string suture pattern using umbilical tape to secure

    • Surgical amputation if irreducible

    • Rectal ring to prevent recurrence (temporary measure)

    • Treat underlying cause of prolapse

  • Prognosis: recurrence is common; underlying cause must be addressed to reduce recurrence

Knowledge Check (study prompts)

  • Scenario: A 4-year-old Holstein Friesian cow recently aborted at 7 months gestation, followed by decreased milk production and DMI; vitals show fever (T = 103.8F), tachycardia, tachypnea, and absent ruminal motility; foul-smelling diarrhea with hematochezia observed.- Top differential diagnosis?

    • This agent can cause endotoxemia. List the clinical signs of endotoxemia.

    • What herd-level precaution should be discussed with the herd manager and relayed to workers on the dairy?

    • How would you diagnose this pathogen?

Notes on connections, implications, and practical planning

  • Zoonosis and biosecurity are recurring themes across Salmonellosis and other enteric diseases; emphasize PPE and hygiene for farm workers and visitors.

  • Early calf management and calving area biosecurity are critical in Johne’s disease and Salmonellosis control programs; milk/feed handling and colostrum processing (pasteurization) reduce transmission risk.

  • Winter dysentery highlights how environmental conditions and housing can drive outbreaks; emphasize management changes during winter to reduce stress and exposure.

  • Clostridial diseases illustrate the value of vaccination programs (bacterin-toxoid vaccines) as preventative measures; vaccination strategies should be tailored by region and herd history.

  • HBS underscores the importance of prompt differential diagnosis of acute, rapidly progressive diarrhea with severe intestinal hemorrhage; ultrasound can aid in distinguishing from simple obstructions.

  • Rectal prolapse management depends on the stage (type) and underlying cause; proactive prevention includes minimizing straining factors and timely treatment of underlying diseases.

Quick reference numbers (for review)

  • Salmonella feed contamination risk: 5-20%

  • MAP herd prevalence in the US: 80%

  • Johne’s disease calves: intrauterine infection rate around 25%

  • Winter dysentery morbidity: 30-50%; mortality about 2%

  • Calf separation and colostrum pasteurization recommended as part of MAP control and Salmonella prevention plans (numbers variable by herd and protocol)

  • Pasture rest after slurry/manure application: 3–12 months

"Note: This summary consolidates content from the provided transcript pages (1–30) into study-ready notes with major and minor points, clinical details, diagnostic approaches, treatment strategies, and practical herd management considerations for bovine gastrointestinal diseases."