CANINE GASTROENTERITIS: OVERVIEW
Gastroenteritis = inflammation of the stomach and intestines → vomiting, diarrhea, dehydration, and sometimes hemorrhage.
Causes are broadly infectious (bacterial, viral, parasitic) or noninfectious (dietary, toxic, immune-mediated) — we’ll focus on bacterial and viral infectious causes.
BACTERIAL PATHOGENS CAUSING GASTROENTERITIS IN DOGS
Pathogen | Gram Stain / Type | Transmission | Key Pathogenesis | Clinical Features | Notes / Diagnosis |
Salmonella spp. | Gram–negative rod | Fecal–oral (contaminated food, raw meat, environment) | Invades intestinal mucosa → inflammation → diarrhea (may be bloody) | Acute enteritis, fever, vomiting, diarrhea ± sepsis | Zoonotic; culture from feces; some carriers asymptomatic |
Campylobacter jejuni / upsaliensis | Gram–negative curved rod | Fecal–oral; contaminated food, water, feces | Colonizes ileum, jejunum, colon → mucosal inflammation | Mucoid or watery diarrhea, sometimes bloody; more severe in puppies | Often self-limiting; zoonotic potential |
Clostridium perfringens (Type A, C) | Gram–positive spore-forming rod (anaerobic) | Endogenous overgrowth or contaminated food | Produces enterotoxin (CPE) and α-toxin → mucosal necrosis | Acute or chronic large-bowel diarrhea; mucus, fresh blood | PCR or ELISA for toxin genes; often secondary to diet/stress |
Clostridium difficile | Gram–positive spore-forming rod | Opportunistic; antibiotic-associated | Toxin A/B → cytotoxic to enterocytes → pseudomembranous colitis | Diarrhea post-antibiotic therapy | Detection of toxins A/B by PCR or ELISA |
Escherichia coli (Enteropathogenic, Enterotoxigenic, etc.) | Gram–negative rod | Fecal–oral; neonatal infection common | Toxin-mediated secretory diarrhea or mucosal attachment/effacement | Watery diarrhea in young pups; dehydration | Culture + toxin or virulence gene typing; less common in adults |
Yersinia enterocolitica / Y. pseudotuberculosis | Gram–negative rod | Fecal–oral (contaminated meat, water) | Invades ileum/lymphoid tissue → inflammation | Rare; diarrhea ± mesenteric lymphadenitis | Can infect immunocompromised dogs; zoonotic |
Helicobacter spp. (H. felis, H. heilmannii, H. bizzozeronii) | Gram–negative spiral | Endogenous colonization of stomach | Mucosal irritation → gastritis (may accompany enteritis) | Vomiting, anorexia, variable diarrhea | Detected via biopsy, urease test, PCR |
VIRAL PATHOGENS CAUSING GASTROENTERITIS IN DOGS
Virus | Virus Type | Transmission | Key Pathogenesis | Clinical Features | Notes / Diagnosis |
Canine Parvovirus Type 2 (CPV-2) | Non-enveloped ssDNA virus (Parvoviridae) | Fecal–oral; highly contagious | Infects crypt epithelial cells in small intestine → villous atrophy, necrosis → malabsorption and diarrhea | Severe hemorrhagic diarrhea, vomiting, fever, leukopenia, dehydration; high mortality in puppies | ELISA (fecal antigen), PCR; survives in environment for months |
Canine Coronavirus (CCoV) | Enveloped ssRNA virus (Coronaviridae) | Fecal–oral | Infects mature villous enterocytes (vs. crypt cells in parvo) → villous blunting | Mild, self-limiting diarrhea (esp. young dogs) | Co-infection with parvovirus worsens disease |
Canine Distemper Virus (CDV) | Enveloped ssRNA virus (Paramyxoviridae) | Aerosol or secretions | Infects lymphoid + epithelial + CNS tissues | Fever, vomiting, diarrhea, ocular/nasal discharge, neuro signs, hyperkeratosis | PCR or immunofluorescence; systemic disease |
Rotavirus | Non-enveloped dsRNA virus (Reoviridae) | Fecal–oral | Infects tip of villi in small intestine → malabsorptive diarrhea | Mild diarrhea in neonates, self-limiting | Detected by EM or antigen ELISA; rare clinically important |
Adenovirus type 1 (CAV-1, infectious canine hepatitis) | Non-enveloped dsDNA virus (Adenoviridae) | Urine, feces, saliva | Primary hepatic infection; enteritis possible | Vomiting, diarrhea, abdominal pain, “blue eye” (corneal edema) | PCR or serology; controlled by vaccination (CAV-2 cross-protects) |
Category | Information |
Scientific Name | Feline leukemia virus (FeLV) |
Viral Family | Retroviridae, subfamily Orthoretrovirinae, genus Gammaretrovirus |
Genetic Type | Enveloped, single-stranded positive-sense RNA virus (diploid RNA genome); replicates via reverse transcription into DNA provirus |
Species Affected | Domestic cats (Felis catus) and some wild felids (e.g., lynx, lions) |
Age Affected | Most susceptible: kittens <6 months (immature immune system); adults less susceptible but can be infected under high exposure or immunosuppression |
Zoonotic | No — FeLV infects only felids |
Distribution | Worldwide, though prevalence varies; higher in multi-cat environments, outdoor, or shelter cats |
Condition Caused | Chronic, systemic viral infection causing immunosuppression, bone marrow suppression, and neoplasia (especially lymphoma and leukemia) |
Transmission | Primarily via saliva (grooming, biting, sharing bowls); also by nasal secretions, milk, urine, feces; transplacental and lactogenic transmission possible |
Tissue Tropism | Lymphoid tissues, bone marrow, salivary glands, thymus, intestine, spleen, and hematopoietic cells |
Lesions | - Lymphoid tumors (especially multicentric, thymic, alimentary lymphoma) - Bone marrow hypoplasia or dysplasia - Pale mucous membranes, splenomegaly, lymphadenopathy - Opportunistic infections due to immunosuppression |
Pathogenesis | 1. Virus enters via oronasal route → infects oropharyngeal lymphoid tissue. 2. Replication in lymphocytes and macrophages → primary viremia. 3. If not cleared, infection spreads to bone marrow and salivary glands → persistent viremia. 4. Integration of proviral DNA into host genome → latent or progressive infection. 5. Outcomes: • Abortive infection – virus eliminated. • Regressive infection – latent provirus, no viremia. • Progressive infection – persistent viremia, disease. • Focal/atypical infection – restricted to specific tissues. |
Predisposing Factors | Young age, outdoor access, multi-cat households, concurrent infections (esp. FIV), poor vaccination, stress, immunosuppression |
Epidemiology | - Prevalence ~1–6% in healthy cats; higher (up to 20%) in sick or high-risk populations. - Transmission requires close contact; virus is labile in the environment (survives only minutes). |
Clinical Signs | - Lethargy, weight loss, fever, anorexia - Chronic or recurrent infections (URTI, stomatitis, abscesses) - Pale mucous membranes (anemia) - Lymphadenopathy, splenomegaly - Neoplasia (especially lymphoma, leukemia) - Reproductive failure, fading kittens |
Common Lab Findings | - Non-regenerative anemia, pancytopenia - Leukopenia or lymphocytosis - Thrombocytopenia - Hyperproteinemia (due to neoplasia or inflammation) - Positive FeLV antigen test (p27) |
Diagnosis | - Screening: ELISA or SNAP test for FeLV p27 antigen (blood). - Confirmatory: IFA (detects intracellular antigen), PCR (proviral DNA), or virus isolation. - Bone marrow cytology for leukemia or dysplasia. |
Treatment | - No curative therapy. Supportive management includes: • Treat secondary infections (antibiotics, antivirals). • Maintain nutrition, minimize stress. • Antiviral drugs (e.g., zidovudine/AZT, interferon-ω) may help some cases. - Isolation from uninfected cats to prevent spread. |
Prognosis | Guarded to poor for persistently viremic cats (median survival ≈ 2–3 years after diagnosis). Regressively infected cats may live normal lives. |
Vaccination | Yes, effective vaccines available (killed or recombinant). Recommended for kittens and at-risk cats. Vaccination does not interfere with p27 antigen testing. Immunity is good but not absolute; booster as per risk/exposure. |
Category | Information |
Scientific Name | Feline immunodeficiency virus (FIV) |
Viral Family | Retroviridae, subfamily Orthoretrovirinae, genus Lentivirus |
Genetic Type | Enveloped, single-stranded positive-sense RNA virus (diploid genome); replicates via reverse transcription into DNA provirus (integration into host genome) |
Species Affected | Domestic cats (Felis catus); similar lentiviruses exist in wild felids (e.g., lions, pumas) |
Age Affected | More common in adult male cats (4–8 years) due to fighting behavior; kittens can be infected via bite or rarely perinatally |
Zoonotic | No — infects only felids, not humans |
Distribution | Worldwide, prevalence variable (2–10% of cats globally; higher in outdoor/aggressive males) |
Condition Caused | Chronic, lifelong immunodeficiency syndrome (similar to HIV in humans) → predisposes to secondary infections, neoplasia, and neurologic disease |
Transmission | Mainly via bite wounds (saliva, blood); virus in WBCs and saliva. Vertical (transplacental or lactogenic) and sexual transmission are rare. |
Tissue Tropism | Lymphoid tissue, T lymphocytes (especially CD4⁺ T cells), macrophages, dendritic cells, and CNS glial cells |
Lesions | - Lymphadenopathy (early) - Lymphoid depletion (chronic) - Opportunistic infections (gingivitis, stomatitis, dermatitis) - Bone marrow suppression - Neoplasia (esp. lymphoma) - CNS changes (encephalitis, demyelination in some cats) |
Pathogenesis | 1. Virus enters via bite wound → infects CD4⁺ T cells, macrophages, and dendritic cells. 2. Local replication → spread to lymph nodes → viremia. 3. Initial acute phase: transient fever, lymphadenopathy, leukopenia. 4. Asymptomatic (latent) phase: months–years, slow CD4⁺ T-cell loss. 5. Terminal phase: immunodeficiency → chronic infections, anemia, neoplasia. 6. Integration into host genome → lifelong infection. |
Predisposing Factors | Outdoor access, male sex (fighting), high-density housing, lack of neutering, co-infection with FeLV or other pathogens |
Epidemiology | - Prevalence higher in free-roaming intact males. - Virus is labile in environment (dies within minutes outside host). - Not easily spread by casual contact (requires inoculation via wounds). |
Clinical Signs | Three phases: Acute: fever, malaise, lymphadenopathy. Latent (asymptomatic): months to years, clinically normal. Chronic/terminal: weight loss, chronic gingivitis/stomatitis, recurrent infections (skin, respiratory, urinary), diarrhea, anemia, neurologic or behavioral changes, ocular disease. |
Common Lab Findings | - Lymphopenia (esp. ↓ CD4⁺ T cells) - Anemia, neutropenia possible - Hyperglobulinemia (polyclonal gammopathy) - Positive FIV antibody test (ELISA) - Occasionally mild thrombocytopenia |
Diagnosis | - Screening: ELISA or SNAP test for FIV antibodies (detects host Ab to viral proteins; most cats remain seropositive for life). - Confirmatory: Western blot or PCR (detects viral DNA/provirus). - Kittens from infected queens may test positive up to 6 months (maternal antibodies). |
Treatment | - No cure. Supportive and symptomatic care: • Control secondary infections (antibiotics, antifungals). • Good nutrition and stress minimization. • Antiviral drugs (e.g., zidovudine [AZT], interferon-ω) may improve quality of life in some cases. - Keep infected cats indoors to prevent spread. |
Prognosis | Variable: many cats live for years (5–10+) in good health if supportive care and stress minimization are provided. Progression to terminal immunodeficiency depends on viral strain, host immune status, and coinfections. |
Vaccination | Available (killed vaccine) but limited use: - Efficacy is variable (60–80%). - Vaccination induces antibodies indistinguishable from natural infection → complicates testing. - Recommended only for high-risk cats (outdoor, aggressive). - Routine vaccination not universally recommended. |
Category | Information |
Scientific Name | Rabies virus |
Viral Family | Rhabdoviridae, genus Lyssavirus |
Genetic Type | Enveloped, single-stranded, negative-sense RNA virus; bullet-shaped virion; non-segmented genome |
Species Affected | All mammals, including cats, dogs, bats, raccoons, skunks, foxes, cattle, humans; birds and reptiles are resistant |
Age Affected | All ages are susceptible; unvaccinated, outdoor, and feral cats at highest risk |
Zoonotic | YES — Highly zoonotic (fatal to humans if untreated) |
Distribution | Worldwide, except in some rabies-free regions (e.g., Australia, New Zealand, Japan, UK, parts of Scandinavia); endemic in much of Africa, Asia, and the Americas |
Condition Caused | Rabies (acute fatal viral encephalitis); characterized by progressive neurological dysfunction and behavioral changes |
Transmission | - Bite wounds (virus in saliva of infected animal) - Less commonly via scratches or mucous membrane contact with saliva - Transplacental and aerosol transmission are extremely rare |
Tissue Tropism | Neural tissue (CNS and peripheral nerves), salivary glands (for shedding), muscle tissue at inoculation site |
Lesions | - Gross lesions: Often minimal; sometimes self-inflicted trauma, bite wounds. - Histologic lesions: Nonsuppurative encephalitis, neuronal degeneration, perivascular cuffing, microgliosis, and characteristic Negri bodies (eosinophilic intracytoplasmic inclusions, esp. in hippocampus and cerebellar Purkinje cells). |
Pathogenesis | 1. Virus inoculated via bite → replicates locally in myocytes. 2. Enters peripheral nerves at neuromuscular junctions (via nicotinic acetylcholine receptors, NCAM, p75NTR). 3. Retrograde axonal transport to CNS → replication in neurons (brainstem, hippocampus, cerebellum). 4. Centrifugal spread via peripheral nerves to salivary glands, cornea, skin, etc. 5. Virus shed in saliva → transmission to new host. 6. Death from progressive encephalitis and neuronal dysfunction. |
Predisposing Factors | - Lack of vaccination - Outdoor access or contact with wildlife reservoirs (bats, skunks, raccoons) - Geographic residence in endemic areas |
Epidemiology | - Cats are the most commonly rabid domestic animal in the U.S. (due to lower vaccination compliance vs. dogs). - Major reservoirs vary by region: bats (Americas), dogs (Asia/Africa), foxes (Europe), mongooses/skunks/raccoons (Americas). - Virus is highly neurotropic and fatal once symptoms appear. |
Clinical Signs | Incubation: 3–8 weeks (can range days–months). Prodromal phase: 1–3 days: behavior change, fever, dilated pupils, vocalization. Excitative (furious) form: aggression, hyperreactivity, biting, hypersalivation, incoordination. Paralytic (dumb) form: ataxia, weakness, paralysis (especially facial and laryngeal muscles), dysphagia, drooling, coma. Cats often alternate between furious and paralytic stages. |
Common Lab Findings | No characteristic hematologic abnormalities; diagnosis relies on virus detection rather than routine lab tests. |
Diagnosis | Postmortem diagnosis definitive. - Direct fluorescent antibody test (dFA): gold standard (detects viral antigen in brain tissue). - RT-PCR: detects viral RNA in brain, saliva, or tissues. - Histopathology: Negri bodies in brain neurons (confirmatory if present). - Immunohistochemistry may also be used. Antemortem testing in animals is unreliable. |
Treatment | No effective treatment once clinical signs develop. - Euthanasia recommended for suspected rabid cats. - Supportive therapy is ineffective — infection is almost invariably fatal. - Post-exposure prophylaxis applies only to humans or vaccinated animals before symptom onset. |
Prognosis | Grave (100% fatal) once clinical signs appear. |
Vaccination | Highly effective, inactivated vaccines available. - Core vaccine for cats. - Initial vaccination at ≥12 weeks, booster at 1 year, then every 1–3 years (depending on vaccine type and regulations). - Essential for both individual and public health protection. |
Category | Information |
Scientific Name | FVRCP = Feline Herpesvirus-1 (FHV-1) + Feline Calicivirus (FCV) + Feline Panleukopenia Virus (FPV) |
Viral Family | - FHV-1 → Herpesviridae (subfamily Alphaherpesvirinae) - FCV → Caliciviridae - FPV → Parvoviridae (genus Parvovirus) |
Genetic Type | - FHV-1 → Enveloped, double-stranded DNA virus - FCV → Non-enveloped, single-stranded positive-sense RNA virus - FPV → Non-enveloped, single-stranded negative-sense DNA virus |
Species Affected | Domestic cats (Felis catus); some wild felids can also be infected (especially FPV) |
Age Affected | All ages susceptible, but kittens are at greatest risk for severe disease; older cats can have recrudescence (FHV-1) or mild infection |
Zoonotic | No — all three viruses are feline-specific |
Distribution | Worldwide; highly prevalent where vaccination rates are low |
Condition Caused | Combined term “Feline Upper Respiratory Disease Complex” + Feline Panleukopenia (enteritis) - FHV-1 → Feline viral rhinotracheitis - FCV → Feline calicivirus infection (oral/respiratory disease) - FPV → Feline panleukopenia (“feline distemper”) |
Transmission | - FHV-1 & FCV: Direct contact with ocular/nasal/oral secretions; aerosol droplets; fomites. - FPV: Fecal–oral route (highly stable in environment). - All three can spread via contaminated bedding, bowls, grooming tools, etc. |
Tissue Tropism | - FHV-1: Upper respiratory tract epithelium, conjunctiva, cornea, trigeminal ganglia (latent infection) - FCV: Oral and respiratory epithelium, lungs, synovium (some strains), endothelium (in virulent systemic FCV) - FPV: Rapidly dividing cells—intestinal crypts, bone marrow, lymphoid tissue, developing cerebellum (in fetuses/neonates) |
Lesions | - FHV-1: Ulcerative keratitis, conjunctivitis, rhinitis, tracheitis. - FCV: Oral ulcers (tongue, hard palate), interstitial pneumonia, arthritis. - FPV: Villous atrophy, necrosis of intestinal crypts, bone marrow depletion, cerebellar hypoplasia (if in utero infection). |
Pathogenesis | FHV-1: Inhalation → replication in nasal/oral mucosa → cell lysis → necrosis → latent infection in trigeminal ganglion → recrudescence with stress. FCV: Oral/nasal infection → replication in epithelial cells → cell lysis → oral ulcers, sometimes systemic vascular damage. FPV: Ingestion → replication in lymphoid tissue → viremia → attacks rapidly dividing cells → leukopenia, intestinal crypt necrosis, cerebellar damage. |
Predisposing Factors | - Lack of vaccination - Stress (especially for FHV-1 reactivation) - Overcrowding, shelters, catteries - Co-infections (FeLV, FIV) - Poor sanitation, malnutrition |
Epidemiology | - FHV-1 & FCV cause >80% of feline upper respiratory infections. - FPV outbreaks still occur in unvaccinated populations; virus is environmentally resistant (can persist ≥1 year). |
Clinical Signs | FHV-1 & FCV (Upper Respiratory Complex): - Sneezing, nasal discharge, conjunctivitis, ocular discharge, fever, lethargy, anorexia. - FHV-1: corneal ulcers, blepharospasm, hypersalivation. - FCV: oral ulcers, lameness (transient arthritis), pneumonia in virulent strains. FPV: Fever, vomiting, diarrhea, dehydration, severe leukopenia, sudden death, cerebellar ataxia (kittens). |
Common Lab Findings | - FHV-1/FCV: Mild leukocytosis or neutrophilia; secondary bacterial infection possible. - FPV: Severe leukopenia and neutropenia, dehydration, hemoconcentration, possible anemia. |
Diagnosis | - FHV-1/FCV: Clinical signs, PCR or viral isolation from swabs, fluorescent antibody tests, or cytopathic effects in culture. - FPV: Leukopenia + fecal ELISA (parvovirus antigen), PCR, or virus isolation; necropsy shows intestinal crypt necrosis and bone marrow depletion. |
Treatment | - Supportive: Fluids, nutritional support, antibiotics for secondary infections. - FHV-1: Antivirals (famciclovir, lysine supplementation). - FCV: Supportive care; antivirals less effective. - FPV: Aggressive fluid therapy, broad-spectrum antibiotics, antiemetics, isolation. |
Prognosis | - FHV-1/FCV: Usually good with care; may become chronic carriers. - FPV: Poor in unvaccinated kittens (mortality up to 90%); better if intensive care started early. |
Vaccination | Core vaccine (FVRCP): - Modified-live or killed combination vaccines available. - Initial series: Start at 6–8 weeks → booster every 3–4 weeks until 16–20 weeks. - Booster: 1 year later, then every 3 years (per guidelines). - Prevents disease and reduces viral shedding, though does not always prevent infection or carrier state (esp. FHV-1/FCV). |
Horses are hindgut fermenters.
Their gastrointestinal tract hosts a complex, highly specialized microbial population, especially in the cecum and large colon, where fermentation of fibrous plant material occurs.
Distribution of Microflora Along the Equine GIT
GIT Region | pH | Microbial Load | Dominant Microbes | Main Functions |
Stomach | 2–6 | Relatively low | Lactobacillus, Streptococcus, Lactobacillus salivarius, yeasts | Initial fermentation of soluble carbohydrates; some lactic acid production. |
Small Intestine | 7–8 | Moderate | Lactobacillus, Enterococcus, Bacillus, small numbers of coliforms | Enzymatic digestion of starch, protein, fats — limited microbial fermentation. |
Cecum | 6.5–7 | Very high | Fibrolytic bacteria (e.g. Ruminococcus flavefaciens, Fibrobacter succinogenes), methanogens, protozoa, anaerobic fungi | Fermentation of cellulose & hemicellulose → VFA production (acetate, propionate, butyrate). |
Large Colon | 6.8–7 | Very high | Similar to cecum; large anaerobic population; Clostridium, Bacteroides, Prevotella, Streptococcus bovis | Continuation of fermentation; microbial protein synthesis; VFA absorption. |
Small Colon / Rectum | 6.5–7 | Decreasing | Similar to colon but less dense; Enterococcus, Lactobacillus | Final water absorption; fecal formation. |
Major Groups of Microbes in the Equine Hindgut
Group | Role | Examples |
Bacteria (10⁹–10¹⁰ per gram) | Cellulose, starch, sugar fermentation | Ruminococcus flavefaciens, Fibrobacter succinogenes, Lactobacillus, Bacteroides |
Protozoa | Starch and fiber fermentation, stabilize pH | Entodinium, Isotricha |
Anaerobic fungi | Fiber degradation, aid cellulolytic activity | Neocallimastix, Piromyces |
Methanogens | Use hydrogen to form methane | Methanobrevibacter spp. |
Yeasts | Carbohydrate fermentation, may stabilize microflora | Saccharomyces cerevisiae |
Functions of Normal Microflora
Fermentation of plant fiber → production of volatile fatty acids (VFAs):
Acetate (energy, lipid synthesis)
Propionate (gluconeogenesis)
Butyrate (energy for colonocytes)
Synthesize B vitamins (e.g. B₁₂, biotin, folate)
Synthesize microbial protein (limited absorption in hindgut)
Prevent colonization by pathogens (competitive exclusion)
Maintain mucosal health via short-chain fatty acids and immune modulation
Disturbance of Microflora — Pathological & Physiological Conditions
Sudden Dietary Change
Example: abrupt shift from hay to grain, or lush pasture
Increase in readily fermentable carbohydrates (starch, sugars) reaching the hindgut.
Rapid proliferation of lactic acid–producing bacteria (Streptococcus bovis, Lactobacillus).
Drop in pH (acidosis) → death of fiber-digesting bacteria.
Endotoxin and exotoxin release → systemic inflammation → laminitis.
Loss of protozoa and anaerobic fungi due to acid intolerance.
Clinical outcome: Colic, diarrhea, hindgut acidosis, laminitis.
Fasting / Anorexia
Reduced substrate for fermentation → microbial die-off.
Reduced VFA production, energy imbalance.
Shifts toward proteolytic bacteria (ammonia producers).
Impaired mucosal barrier → risk of endotoxemia.
Clinical outcome: Poor appetite recovery, increased gut permeability.
Antibiotic Therapy
Broad-spectrum antibiotics (e.g. oral trimethoprim-sulfa, penicillin) can kill commensal anaerobes.
Allows overgrowth of pathogenic bacteria, e.g. Clostridium difficile, Clostridium perfringens.
Toxin production → antibiotic-associated colitis.
Clinical outcome: Severe diarrhea, endotoxemia, colitis.
Stress (Transport, Surgery, Disease)
Increased catecholamines and cortisol → altered gut motility, perfusion, and immunity.
Dysbiosis due to reduced motility and mucosal ischemia.
May lead to overgrowth of Clostridium spp. or Salmonella.
Clinical outcome: Stress-related colitis, “travel colic”.
Feed Restriction or Low-Fiber Diet
Reduced cellulose fermentation → decreased fibrolytic bacteria.
Relative increase in proteolytic species.
Less VFA → reduced mucosal trophic effect.
Clinical outcome: Poor performance, altered manure consistency.
Parasitism or Inflammation
Mucosal damage from parasites (e.g. Strongylus, Cyathostomes) alters the microenvironment.
Increased mucus, pH shifts → dysbiosis.
May favor facultative pathogens (E. coli, Salmonella).
Clinical outcome: Chronic diarrhea, weight loss.
Age and Development
COLITIS - CAUSES
Bacteria: Salmonella, Clostridium difficile, Clostridium perfringens, E. coli, Lawsonia intracellularis, Neorickettsia risticii (Potomac Horse Fever)
Viruses: rotavirus in foals, coronavirus
Parasites: small strongyles